SWEET POISON

DAVID GILLESPIE is a recovering corporate lawyer, cofounder of a successful software company and consultant to the IT industry. He is also a father of six young children (including one set of twins). With such a lot of extra time on his hands, and ! extra "ilos on his waistline, he set out to investigate why he, li"e so many in his generation, was fat. He deciphered the latest medical findings on diet and weight gain and what he found was chilling. #eing fat was the least of his pro$lems. He needed to stop poisoning himself.

Praise for Sweet Poison

%What&s impressive a$out Sweet Poison is that 'illespie turns complex research on what happens to food inside our $ody and its relation to weight gain into a good read.& Sydney Morning Herald %(omprehensive, thought provo"ing and highly reada$le.& The Age %)ye-opening.& Womans Day %*avid 'illespie&s ground$rea"ing $oo" on the dangers of a high sugar inta"e could well revolutionise the way you diet.& A Current Affair %Sweet Poison is a worthy and impassioned effort $y an +ustralian dad to share his surprising discoveries with struggling dieters and provo"e further de$ate a$out the o$esity epidemic.& Australian Bookseller & Pu lisher %I&ve lost ,,"g without $eing on a diet. It&s good to "now this $oo" is non-fiction.& Ste!e "rons MP# Mem er of the Parliamentary "n$uiry into % esity

SWEET POISON
WH- ./'+0 1+2). /. 3+T

*+4I* 'I55).6I)

4I2I7' an im&rint of 6)7'/I7 #882.

3or 5i99ie, +nthony, :ames, 'wendolen, +dam, )li9a$eth and 3inlayson.

4I2I7' 6u$lished $y the 6enguin 'roup 6enguin 'roup (+ustralia) ;<! (am$erwell 0oad, (am$erwell, 4ictoria =,; , +ustralia (a division of 6earson +ustralia 'roup 6ty 5td) 6enguin 'roup (/.+) Inc. =>< Hudson .treet, 7ew -or", 7ew -or" ,!!, , /.+ 6enguin 'roup ((anada) ?! )glinton +venue )ast, .uite >!!, Toronto, (anada 87 1 6 ;-= (a division of 6earson 6enguin (anada Inc.) 6enguin #oo"s 5td @! .trand, 5ondon W(;0 !05 )ngland 6enguin Ireland ;< .t .tephen&s 'reen, *u$lin ;, Ireland (a division of 6enguin #oo"s 5td) 6enguin #oo"s India 6vt 5td ,, (ommunity (entre, 6anchsheel 6ar", 7ew *elhi A,,! !,>, India 6enguin 'roup (7B) C> +pollo *rive, 0osedale, 7orth .hore !C=;, 7ew Bealand (a division of 6earson 7ew Bealand 5td) 6enguin #oo"s (.outh +frica) (6ty) 5td ; .turdee +venue, 0ose$an", :ohannes$urg ;,?C, .outh +frica 6enguin #oo"s 5td, 0egistered 8fficesD @! .trand, 5ondon, W(;0 !05, )ngland 3irst pu$lished $y 6enguin 'roup (+ustralia), ;!!@ (opyright E *avid 'illespie ;!!@ The moral right of the author has $een asserted +ll rights reserved. Without limiting the rights under copyright reserved a$ove, no part of this pu$lication may $e reproduced,

stored in or introduced into a retrieval system, or transmitted, in any form or $y any means (electronic, mechanical, photocopying, recording or otherwise), without the prior written permission of $oth the copyright owner and the a$ove pu$lisher of this $oo". penguin.com.au I.#7D ?>@-,-> -;;@ @C-C

Contents
Introduction Part 1: Why is su ar !a"in you fat# 1 Startin out $ Theories of fatness % &o' 'e turn food into ener y ( )sin stored ener y * +at !a"es you fat , or does it# - .ioche!istry 1/1 0 &oney 'ithout 1ees 2 Porrid e in the arteries 3 4ore "i55ers Part $: What can you do# 1/ What a1out e6ercise# 11 A reci7e for co5d tur"ey 1$ So is this a diet# 1% A5ternati8es to fructose 1( It9s a55 a1out !oney Notes Ac"no'5ed e!ents

Introduction
I still remem$er the day 5i99ie told me. .he had a stunned, almost fearful expression on her face and was unsure of herself in a way I had rarely seen in my wife of ,= years. 8ur fifth and assumedly last child had Fust $een turned into twins with a wave of the ultrasound wand. In a$out eight months, we were to $ecome parents of six children under nine years of age. I was a$out !"g overweight, and had struggled with my weight for as long as I could remem$er (except for a $rief period during university when I managed to snare 5i99ie). I had tried most things, from reducing fat in my diet to not eating to regularly attending the gym and wal"ing the dog. .ometimes I had had limited success (a few "ilograms here and there), $ut it was mostly small $ac"ward steps on my ever-accelerating Fourney to o$esity and $eyond. With the weight came lethargy and sleeping pro$lems. +s any parent could attest, getting enough sleep and having the energy to get through the day is difficult at the $est of times, let alone when you&re starting out in the red. I was going to have to $e a dad to twin $a$ies and four other young children and I couldn&t see myself managing it carrying ! extra "ilos, feeling lethargic and not sleeping. +t the time, the +t"ins diet was $eginning to ta"e off, with all manner of people touting it as a miracle diet. 1y uncle had recently undergone heart surgery and was now on +t"ins. He had lost a vast amount of weight and was tuc"ing into $acon and eggs every morning for $rea"fast. This loo"ed li"e a diet I could really enFoy. I immediately cut out all car$s and, lo and $ehold, I started losing weight li"e never $efore (although I suspect it was $ecause I found it almost impossi$le to find any food I wanted to eat that did not contain car$ohydrates). I spent

a couple of wee"s feeling li"e I was starving to death. The weight was coming off $ut the willpower reGuired to stay on the diet was overwhelming (not to mention the nasty side effects that eliminating fi$re from my diet was having). I started to loo" for alternatives. +t first low-'I diets seemed appealing, $ecause they at least allowed you to eat some car$ohydrates, $ut almost no foods were la$elled with 'I indicators and the maths involved in calculating it myself was $eyond me. When chocolate spreads advertised their low-'I levels, I "new that if a food that was half sugar and half fat could earn a low-'I la$el, the 'I calculation was pro$a$ly almost meaningless for dieters. I had $een reading a lot a$out (harles *arwin&s life and his wor"s on evolution. *arwin&s theories held that all characteristics of modern animals were survival responses developed slowly over millennia. +s a result, we (and all animals) are woefully inadeGuate at dealing with sudden changes in the environment. +fter reading a$out these theories, it had occurred to me that my weight gain, and that of most other people in our society, could not possi$ly $e down to a lac" of willpower alone (since willpower, or the lac" of it, would $e an evolved characteristic that could not suddenly have changed in Fust a few hundred years). In a desperate attempt to find a way to "eep up the weight loss without having to stay on the car$-free diet, I started to read up on human meta$olism. I Guic"ly came to the conclusion that I would have to learn a whole new voca$ulary to understand most of what was $eing written. However, I was $eginning to get the vague feeling that many in the medical profession too" for granted a fact that was a complete mystery to the rest of us. .tudy after study seemed to $e pointing to the inescapa$le conclusion that the fructose part of sugar was fat-inducing in animals, and pro$a$ly in humans as well. Worse still, it seemed to $e complicit in ma"ing us want to eat more food in general.

+lthough I found many studies within the medical fraternity $ac"ing this line of thought, documents written for the rest of us were almost impossi$le to find. Those that did exist were, more often than not, rants against sugar in general without any explanation as to why it was $ad for us. I immediately changed from eliminating car$s to Fust eliminating foods with added sugar A at last I could eat $read again. It was impossi$le to remove all sugar $ecause everything seems to contain it, so I set myself a limit of no more than ,!g of sugar in a meal (a$out the amount of fructose in an apple). This simply meant I no longer ate sweets and $iscuits or dran" Fuice and soft drin". The weight loss continued, $ut the diet was a lot easier to stic" to. +fter a few months, I was so used to not having sugar that it too" no willpower at all to refuse it. In fact, on the few occasions I did try chocolates, they tasted un$eara$ly sweet. I&ve now lost the !"g and, more importantly, no longer worry a$out weight gain at all. I "now that I can eat when I feel hungry and stop eating when I feel full and I will not put on weight. I can eat whatever I li"e whenever I feel li"e eating, as long as it does not include sugar. I have no urge to eat when I&m not hungry, I no longer feel lethargic or sleep deprived (other than as would $e expected for a father of six), and no unnecessary exercise was involved at all. #y far the greatest $enefit has $een the a$ility to trust my own $ody to let me "now when to eat and when not to. It&s a feeling I&ve never experienced $efore. 6eople o$viously noticed the change in my appearance and energy levels, and as"ed me what I had done. %I stopped eating sugar& seemed too trite and forwarding them medical Fournal articles Fust a little $it over the top, so I decided the story of the sweet poison had to $e written in language we all could understand.

PA:T 1 W&; IS S)GA: 4A<ING ;O) +AT#

1= STA:TING O)T
8ne of the first articles I came across during my %neteducation& was a $oo" written over ! years ago with the catchy title The Sa''harine Disease. This Guaintly written ,;?page $oo", authored $y .urgeon-(aptain (leave of Her 1aFesty&s 7avy in ,?CC, caught my eye $ecause it contained a theory that there was a strong lin" $etween evolution and diet. This matched up with some of the thoughts I had $een having after reading a$out (harles *arwin&s theories on evolution. The good doctor was saying that the human $ody, having evolved in an environment of a largely wholegrain, vegeta$le and (occasional) meat diet, was ill-eGuipped to deal with the highly processed sugar and refined flour diet of the twentieth century. *r (leave had decided, after a lifetime of treating sic" sailors (he was C! when he wrote the $oo"), that a huge num$er of modern diseases were directly caused $y the overconsumption of sugar and refined flour. He $lamed sugar and flour for the headline diseases li"e o$esity, coronary disease and dia$etes. #ut he also threw in peptic ulcer, constipation, haemorrhoids and varicose veins, as well as appendicitis, gallstones, urinary tract infection, inflammation of the large

intestine and, of course, dental cavities, among others. This $oo" was clearly written with a medically trained audience in mind, so I don&t recommend it for a relaxing read in front of the fire. I&m certainly no doctor and I came across this $oo" at the very $eginning of my reading, so most of its analysis went straight over my head. There was, however, one graph A that&s right, I went straight for the pictures A that really got me interested in the theory $ehind *r (leave&s %saccharine disease&. (hapter ; contained a graph that showed that sugar consumption in )ngland had risen eightfold $etween ,@,< and ,?<<. The average inha$itant of the #ritish Isles was consuming Fust ,<l$ (a$out >"g) of sugar in ,@,>. #y ,?<<, their inta"e was almost ,,!l$ (<!"g). The steady upward march had only $een $riefly interrupted $y the intervention of the two world wars. The .urgeon-(aptain was convinced that this rise in sugar consumption, along with a similar trend in the consumption of refined white flour, was entirely responsi$le for the raft of illnesses that he collectively du$$ed %the saccharine disease&. *r (leave had noticed that all of the diseases he was including were virtually nonexistent prior to ,?!! and he simply put two and two together. The diseases were increasing at a$out the same rate as the consumption of sugar and refined flour. +ccording to him, it was the concentration ($y refinement) that was the pro$lem with $oth sugar and flour. When sugar is refined from cane or sugar $eet, ?? per cent of the original food (mostly the fi$re) is removed, leaving only the sugar syrup. .imilarly, $y the time white flour is created, ?! per cent of the $ran has $een removed. The thin"ing was that $y removing the fi$re, we were ma"ing food much easier to digest. .ugar and flour would $e reduced to glucose $y the $ody and, without the fi$re to slow things down, the glucose would hit our $loodstream very Guic"ly. *r (leave felt this would %upset the evolutionary adaptation in the pancreas Hwhere itI is held J to

cause the disease&. The solution was o$vious to (leave. :ust add $ran to everything you eat. 5egend has it that while serving as the ship&s doctor a$oard the $attleship (ing )eorge * during World War II, he would have large sac"s of $ran $rought on $oard to %prescri$e& to the crew. I thin" he could have counted himself luc"y that the worst nic"name he acGuired as a result was %the $ran man&. I was intrigued $y the enormous growth in sugar consumption shown in the graph. .ugar consumption was clearly growing at an extraordinary rate and some of *r (leave&s other graphs showed that dia$etes and other diseases were growing at similar rates. #ut I was less convinced $y his argument that adding $ran to your diet to counteract the excess sugar and flour was the secret to avoiding so many diseases. I needed to understand more a$out the chemistry involved in digestion $efore I was prepared to start pouring $ran on my chocolate ice-cream. This, unfortunately, would involve my getting very close to some su$Fects that I had avoided since I almost failed #iology and (hemistry in high school. #ut I am one of those people who can&t leave a pro$lem alone until I am convinced I have wor"ed out a logically consistent argument for how the whole system wor"s. +nd *r (leave&s clogged-up pancreas wasn&t doing it for me. #y the time you get to the end of this $oo", you&ll figure out (as I did) that *r (leave wasn&t too far from the mar". +ll right, it&s called %meta$olic syndrome& rather than %the saccharine disease&, and it&s a part of sugar that&s the pro$lem, not refined flour and sugar. #ut the pancreas does play a role and fi$re is part of the prevention. He got close to the right answer from his o$servations, $ut (as with most things in life) the details were significantly more complex than I am sure he ever imagined.

There is no shortage of %educational& resources a$out human digestion on the internet. +fter reading a few of the more %interesting& theories a$out digestion and how it wor"s, I decided to stic" to sites that doctors seemed to regard as authoritativeD mostly medical Fournals, or sites run $y people who pu$lish articles in medical Fournals. /nfortunately, all of these articles appeared to have $een written on the presumption that I had completed six years of medical school and practised gastroenterology (the study of the human digestive system) and endocrinology (the study of the human hormone-producing organs) for at least ;! years. I had a steep learning curve ahead of me and it too" me a long time to get up to speed, loo"ing up every second word on Wi"ipedia along the way. I won&t $ore you with the detail of all the false starts and $lind alleys, $ut here is what I discovered (in )nglish rather than 5atin and 'ree"). The sugar that *r (leave was tal"ing a$out is common ta$le sugar, the white (or $rown) stuff some of us add to our cup of tea in the morning to ma"e it a $it more pleasura$le to drin". It&s the same sugar that, in +ustralia and the /nited 2ingdom, is added to most foods that reGuire sweetening. In the /nited .tates they use a cheaper su$stance called high-fructose corn syrup (H3(.) for sweetening processed food. H3(. is, for all practical purposes, identical to sugar, despite what some of the more excita$le we$sites would have you $elieve. #ut more on that later J It seems cocoa, tea and coffee merchants were in fact almost single-handedly responsi$le for introducing sugar into the )nglish (and hence the western) diet. +s anyone who has tried even %@! per cent cocoa& dar" chocolate will attest, cocoa is a pretty $itter pill to swallow without sugar. #ut add some of the sweet stuff and suddenly you have a product that flies off the shelves. The same goes for tea and coffee, so the only way the merchants $ringing these new foods into the western world

could convince people to drin" their newly introduced $itter $everages in the sixteenth century was to suggest the addition of the newly discovered sweetener, cane sugar. .ometimes it&s called caster sugar or raw sugar or $rown sugar or white sugar, $ut it&s all the same stuff. It&s what most of us thin" of when as"ed to descri$e sugar. .cientists call ta$le sugar (and all its variants) %sucrose&. The group of compounds with chemical properties li"e ta$le sugar are generically called %sugars& $y chemists and nutritionists. This ma"es it all pretty confusing since what ordinary people call sugar and what scientists and nutritionists call sugar are in fact two different ($ut overlapping) things. .ucrose (ta$le sugar) is a dou$le sugar (disaccharide A 5atin for two sugars). This simply means that it is made up of two %simple sugars& A glucose and fructose A Foined together at the molecular level. :ust as this is starting to sound confusing, it turns out that our digestive system doesn&t $other remem$ering complex names either. To your digestive system there is no such thing as sucrose. When you eat a teaspoon (<g) of sucrose, your $ody %sees& ;.<g of glucose and ;.<g of fructose. There are only three important simple sugarsD glucose, fructose and galactose. +ll of the other %sugars& you are li"ely to encounter in daily life are simply com$inations of these three. 3or example, the %sugar& you see on the la$el of a carton of mil" is lactose. 5actose is half glucose and half galactose. 1altose, the sugar in $eer, is two molecules of glucose Foined together in an unusual way. .imple sugars li"e glucose and fructose can also $e present in nature in their uncom$ined form. 1ost fruit, for example, contains some sucrose, some fructose and some glucose. To our digestive system, however, the sucrose is Fust a $undle of more fructose and glucose.

This food , Contains , 1il" and dairy foods #eer

Which 1rea"s do'n to , 'alactose K glucose 'lucose K glucose

5actose 1altose

Ta$le sugar, $rown sugar, .ucrose caster sugar, etc.

'lucose K fructose

3igure ,.,D +ll those different %oses& $rea" down to one of three important sugars.

'lucose is $y far the most plentiful of the simple sugars. 6retty much every food (except meat) contains significant Guantities of glucose. )ven meat (protein) is eventually converted to glucose $y our digestive system. It&s a pretty important sugar to humans. 6ure glucose tastes slightly sweet, $ut would $e $arely noticea$le to the sugar-saturated palate of the modern human. +ustralian readers who have recently $een to the pharmacist will insist this is not true, citing a $rand of Felly $ean stoc"ed only $y chemists as evidence to the contrary. /nfortunately, a Guic" loo" at the la$el reveals that the primary ingredient is in fact sugar. The sweetness comes from the fructose part of the molecule. 'alactose is present in our environment in only very small Guantities and is found mainly in dairy products in the form of lactose. 1ost $a$y mammals, including humans, are adapted to survive on lactose when they are young, $ut a$out >! per cent of the world&s adult human population are lactose intolerant and cannot digest lactose or use it for energy production.

6eople with ancestry in northern )urope, the 1iddle )ast and India (the places where people have the longest association with domesticated cattle), however, have a version of the lactose digestion gene that is not disa$led when they grow up. Those people (most of the +ustralian population) are a$le to continue to drin" and eat mil" products comforta$ly into adulthood. Those of us who can digest galactose convert it to glucose and treat it as glucose for all important digestive purposes. )very$ody else lets it pass straight through the digestive system, which is why a primary symptom of lactose intolerance is diarrhoea. 'alactose is slightly less sweet than glucose, $ut it&s still on the sweet side of the palate. If you are not lactose intolerant, pay close attention to the next glass of mil" you consume. -ou will notice an ever so slight sweet tinge to the flavour A it is certainly not sour (at least if you drin" it $efore the use-$y date). 3ructose is also relatively rare in nature. It is found primarily in ripe fruits, which is why it is sometimes call fruit sugar. It is usually found together with glucose and sometimes sucrose. 3ructose tastes a$out C! per cent sweeter than glucose or galactose. In practical terms this means you would need to consume ; teaspoons of glucose to get the same sweetness hit that you would from , teaspoon of fructose. Ta$le sugar, $eing a com$ination of the two, is halfway $etween in terms of sweetness. +s with lactose, consumption of a large amount of pure fructose can result in exceeding the capacity of our intestines to a$sor$ it, resulting in diarrhoea. If, however, fructose is eaten in com$ination with glucose, for example $y eating sugar, then it seems we can a$sor$ virtually unlimited Guantities (more on this later). These three %sugars& ma"e up the vast maFority of the food group we call car$ohydrates (they are made up of 'ar on, hydrogen and oxygen A the %ate& in car$ohydrate indicates the presence of oxygen). The only other significant car$ohydrate is

cellulose, or what we commonly call fi$re (the hard stringy $its of plants). If you&ve ever eaten a lot of $a"ed $eans in a sitting, you&ll "now that humans can&t fully digest fi$re. +nd overconsumption leads to exactly the same result as when a lactoseintolerant person eats too much dairy food A diarrhoea and flatulence. This doesn&t mean fi$re has no purpose in our digestive systemL it&s Fust that we don&t use it for energy. 8nly a$out half the western diet is car$ohydrate $ased. In a normal diet, a further one-sixth of our energy needs are supplied $y protein (predominantly from meat, $ut also from nuts). 6rotein is $ro"en down into amino acids $y our digestive system, some of which are used to $uild up our tissues and some to assist in hormone production. 5eftover amino acids are converted to glucose and used for energy in exactly the same manner as with car$ohydrate digestion. The remaining third of our food is fat. 3at is $ro"en down into fatty acids $y our digestive system. 1ost fatty acids are used to ma"e all the chemicals we use to digest everything else, and some are used for energy. This food J #read Contains >!ost5y? Which 1rea"s , do'n to , (ar$ohydrate 'lucose K fi$re

1il"

'lucose K (ar$ohydrate K fat galactose K fatty acids 6rotein K fat (ar$ohydrate 'lucose K amino acids K fatty acids 'lucose K

1eat (or nuts) 3ruit

fructose K fi$re 4egeta$les (ar$ohydrate 'lucose K fi$re

3igure ,.;D The whole world loo"s li"e glucose to our digestive system.

If you thin" of your $ody as $eing li"e an automo$ile (mine started out as a mini$us), then thin" of it as $eing designed to run on a fuel of pure glucose. 8ur preferred source is car$ohydrates, which can $e $ro"en down easily into glucose, $ut we have some well-designed coping mechanisms to convert other foods to glucose as well. +s far as our $ody is concerned, everything we eat is Fust glucose in disguiseL sometimes it&s wrapped in a $it of fat or a $it of fi$re, sometimes with some %additives& (vitamins) that we can use for running repairs and maintenance, $ut in the end it&s really Fust glucose. 1ost car$ohydrates are $ro"en down into glucose, with a few throwaway molecules of fructose and galactose. )ven the galactose is either converted to glucose or expelled from the $ody. 6rotein is similarly largely reduced to glucose $efore $eing used as fuel. 1ost experts seem to agree that we have existed as a separate species for a$out ,=! !!! years. This ma"es our current ur$an environment and diet (which even with the most optimistic definition has existed for only the last ,! !!! years) almost completely irrelevant in determining the evolved characteristics of our digestive system. We are pro$a$ly genetically identical to the people who first settled in villages in the 7iger delta. +nd ,;! !!! years $efore that, as our fore$ears started roaming the +frican savanna, they had to select things that would provide them with energy from the availa$le food sources and at the same time avoid things that could poison them. 6eople who couldn&t tell the difference generally didn&t last long enough to reproduce. 8ur distant fore$ears had

evolved a handy little energy detector. 3ood that contains glucose tastes slightly sweet to us so, in nature, that taste we descri$e as sweetness is generally a relia$le indicator of the presence of an edi$le high-energy food. 8ur fore$ears learned that the sweeter the food, the more energy it was li"ely to contain. 1illennia of evolution have ensured that we are programmed to see" out sweet sources of food and reFect sour su$stances as $eing pro$a$ly poisonous or at least to $e treated with caution (meaning wait for your neigh$our to give it a go first).

3or all $ut the last few hundred years (a heart$eat on the genetic evolution time scale), really sweet foods have $een difficult to find. The sweetest food we encountered in nature, fruit, had $een an occasional and, depending on where you lived, relatively rare $onus in our diet. The only other way to get a sugar hit in nature involved discussing the matter with a large swarm of disgruntled $ees. Honey is ! per cent fructose, which is why, even despite the difficulty in o$taining it, it was very popular as a food additive $efore the discovery of sugar.

8nce we figured out, towards the end of the nineteenth century, how to ma"e any food artificially sweet $y adding sugar, sugar $ecame a pretty popular %condiment&, as the good *r (leave&s graph clearly showed. 3ood manufacturers were happy to accommodate our preference for sweet foods as soon as it $ecame commercially via$le to produce sugar in large Guantities. #ut more on the commercial side of things later A $ac" to $iology J +s far as I could tell, there was nothing controversial in any of the processes I have descri$ed a$ove. How food is $ro"en down and what supplies us with energy seems well settled (if somewhat opaGuely explained $y most sources). /nderstanding that all food is essentially glucose was an

important foundation for me. (Why doesn&t any$ody tell us this in schoolM 1ay$e they did and I Fust wasn&t listening.) #ut I hadn&t figured out how the pancreas was involved (or even what the pancreas was) and why *r (leave would thin" that sugar consumption would clog it up, with all sorts of disastrous conseGuences. 8r, for that matter, why putting $ran on my food would fix it. (learly further research was reGuired.

$= T&EO:IES O+ +ATNESS
1ost of us don&t eat constantly during the day (unless we are on the %)lvis in the &>!s& diet), so our fuel inta"e is a $it %lumpy&. Three times a day we ta"e in a lot of fuel, which is Fust a$out enough to get us to the next meal. 8ur $ody, however, needs a constant fuel supply that doesn&t change much over time. 5ife would $e pretty strange if we got pea" performance out of our $rain, heart and "idneys only directly after a meal, with performance falling off until we were virtually comatose Fust $efore the next meal came around. It would $e li"e having a car that only wor"ed well Fust after you filled its tan". To ensure the amount of glucose in our $lood (the fuel mix, if you li"e) remains constant, our $ody uses a simple negative feed$ac" system. When we eat, our $lood-glucose levels increase as the food is $ro"en down into its component molecules and a$sor$ed into our $loodstream. +nd it seems this is where the pancreas comes in. The pancreas (from 'ree", meaning %all flesh&, $ecause it loo"s li"e a fleshy lump A $ut then again what organ doesn&tM) is a small organ, a$out ,< to ;<cm long in most of us, tuc"ed in Fust $elow and $ehind the stomach. 8lder readers will "now lam$ and calf pancreas $y the $utcher&s description of %sweet$reads& (which made it a little more salea$le than %pancreas& and definitely more salea$le than %fleshy lump&, I suspect). -ounger readers will have no clue what I&m tal"ing a$out. We are all now too affluent to $other eating offal (unless we freGuent all-you-can-eat esta$lishments where it is presented in gravy or those really fancy restaurants that are trying to ma"e offal trendy again).

+i ure $=1: The pancreas and its neigh$ouring organs A not pretty, $ut then very little $elow s"in level in a human is.

This fairly important piece of offal performs two $asic functions for us. It produces the en9ymes (proteins that accelerate chemical reactions) that $rea" down our food into its component parts $y separating the molecules.

To "eep the num$er of names we have to remem$er to a minimum, the name of the en9yme that $rea"s down a given sugar has the same start to the sugar&s name $ut ends in %ase&. 3or example, the en9yme that $rea"s down lactose into glucose and galactose is called lactase. If you are lactose intolerant, your pancreas can&t produce lactase. This means you are una$le to extract any energy from the lactose and so it passes through the stomach to the intestine unmolested $y en9ymes. If we don&t have the right en9yme, we can&t digest any car$ohydrate other than pure glucose, so en9ymes are pretty crucial to the whole process.

#esides ma"ing the garden shears used to chemically chop up our food, the pancreas also produces the hormones that control the amount of glucose in our $loodstream A the eGuivalent of the throttle in my car analogy. .pecialist cells in our pancreas called the islets of 5angerhans monitor $lood-glucose levels. These cells were named after the 'erman $iologist 6aul 5angerhans, who first descri$ed them in ,@C? as islands of clear cells in the pancreas. 6aul didn&t "now what they were for, $ut the island description stuc" and so did his name. 8ne of the critically important hormones manufactured $y the islets of 5angerhans is insulin (insula is 5atin for %island&). Insulin is a powerful hormone that regulates many processes in the digestive system, $ut its primary function is to reduce glucose concentrations in our $lood. The first and most o$vious way to do this is to use the glucose as fuel. 1ost cells in our $odies use glucose as the main source of energy, $ut without insulin also present in the $lood, the cells have no chemical means of accessing the energy stored in glucose. Insulin acts as a chemical ena$ler that allows the cells to a$sor$ and then convert the glucose to energy. The only significant exception is our $rain. 7eurons (the cells that ma"e up our grey matter) do not need insulin A they can suc" up the glucose and use it directly from the $loodstream.

.ome people need to inFect insulin after a meal $ecause their pancreas is una$le to ma"e its own. +$out one in every <! !!! people is una$le to ma"e insulin $ecause their islets of 5angerhans have $een destroyed $y their own immune system. 6eople who study these things for a living don&t "now why these (usually) young $odies have destroyed their own capacity to produce such a critical hormoneL however, a popular theory is that it is the result of a viral infection in childhood. These people are referred to medically as suffering from insulindependent dia$etes, also called type , dia$etes. This type of dia$etes is really Fust chronic high $lood sugar. 3or those who li"e impressing friends with $ig 'ree" medical words, the technical term is hyperglycaemia (hy&er A excessiveL gly' A sweetL and aemia A related to the $lood). When a person with dia$etes eats, the $lood fills with glucose, $ut without insulin present to ena$le its conversion to energy (or fat, as we shall see later), and $ecause the only maFor organ a$le to use the glucose without insulin is the $rain, the $ody maintains a state of very high $lood sugar. If you have untreated type , dia$etes, you are not expected to have a very long or pleasant life. With most cells having no way to access the glucose in your $lood, it&s the medical eGuivalent of dying of thirst in the middle of the ocean. The $ody would $e in a constant energy crisis $ecause no matter what you ate, you would $e una$le to convert most of the glucose from the food into energy. -ou would $e starving in a sea of food. Humans come eGuipped with a $ac"up system for emergency access to energy Fust in case we find ourselves starving to death (or on a low-car$ohydrate diet A $ut more a$out that later). #ecause the lac" of insulin prevents our $ody from %seeing& the car$ohydrates we have Fust eaten, our $ody, convinced that we are starving, switches to 6lan # A eat our own fat and muscles until some$ody finds some real food. 3at and muscle mass are converted to an alternate fuel called

"etones. +t this point in my reading a light went on for me. + dia$etic&s $ody thin"s it&s starving $ecause it can&t see the glucose in the $loodstream. .imply put, the glucose gets there $ecause the person ate car$ohydrates. If I didn&t eat car$ohydrates in the first place then it&s li"ely that exactly the same effect would $e produced. 1y $ody would thin" it was starving, switch to 6lan # and start actually using up some of my (vast) supply of fat rather than storing more. This explained why low-car$ohydrate diets such as +t"ins wor". I read further. #orn in 8hio in ,?=!, 0o$ert +t"ins graduated from (ornell 1edical (ollege in ,?<< and commenced practice as a cardiologist in 7ew -or". In ,?C=, he got the "ind of shoc" most of us run into at some point. He saw an old photo of himself from two decades earlier, when he had weighed a$out ,<"g less. .purred into action, he started loo"ing into what the medical literature had to say a$out the latest and greatest in weight-loss techniGues. He tried a couple of different diets without any real success, until he read an article in the +ournal of the Ameri'an Medi'al Asso'iation. The article was $y *r :ohn -ud"in, head of the $rand-new *epartment of 7utrition at 5ondon&s Nueen )li9a$eth (ollege. *r -ud"in&s study showed that a diet with unlimited protein and fat $ut little or no car$ohydrates was much more effective than a diet that controlled Foules(calories) or fat inta"e. -ud"in&s article went on to say that when you told people not to eat car$ohydrates, $ut to eat as much fat and protein as they li"ed, they actually ate up to << per cent fewer Foules(calories) overall. +ll of the su$Fects ate less fat, some massively so. +ll of them lost weight. -ud"in concluded that low-car$ohydrate diets wor"ed principally $ecause they reduced overall Foule(calorie) consumption. *r -ud"in&s study was then the most recent in a series of

research proFects aimed at proving or disproving the miraculous effects of the #anting diet, the first diet to suggest that people reduce car$ohydrate inta"e. +lmost ,!! years to the day $efore 0o$ert +t"ins started loo"ing for a solution to his middle-age spread, an )nglish underta"er and coffin ma"er $y the name of William #anting had solved his %corpulence& pro$lem $y limiting his inta"e of car$ohydrates. #orn in ,>?>, when #anting entered his thirties he encountered a pro$lem that was much rarer then than it is now. He started to $ecome overweight. He was advised to increase his %$odily exertion&, which he duly did $y rowing on the near$y river for two hours a day. #ut all this seemed to do was ma"e him even hungrier, which meant that he ate more and $ecame fatter. His medical friends advised him to stop exercising immediately and limit himself to moderate and light food. This he did, only to find that he was constantly hungry and $ro"e out in $oils (which sounds li"e a lot of the diets I tried A perhaps without the $oils). 8ver the next ;! years he tried swimming, wal"ing, ta"ing the sea air, soa"ing himself at the spa, starvation diets and Tur"ish $aths, $ut succeeded in losing Fust ;.<"g. #y ,@C;, at < feet < inches (,C<cm), #anting weighed in at almost ,!!"g A hardly noteworthy $y today&s standards, $ut in ,@C!s )ngland, he would have stood out as $eing particularly o$ese. In +ugust ,@C;, at the age of C< and worried a$out his increasing deafness, #anting consulted *r William Harvey, a noted ear, nose and throat specialist. When #anting appeared in his office complaining of deafness, *r Harvey was Fust as interested in his story of failed diet after failed diet as he was in curing his hearing pro$lem. Harvey also thought that the deafness may well $e caused $y #anting&s o$esity, so he suggested a diet $ased on the theories of *r (laude #ernard, who thought that the liver might produce a sugar-li"e su$stance made from the fats, sugars and starches consumed as part of a %normal& diet. *r Harvey as"ed #anting to avoid $read, $utter,

mil", sugar, $eer, por" and potatoes. This is a strange list to modern eyes, $ut what *r Harvey was restricting was what doctors at the time thought were foods containing %starch& (car$ohydrates). He could eat as much meat or fruit as he wished. +lmost immediately, #anting $egan losing weight and generally feeling much healthier. 8ver the next year he lost weight at a constant rate of a$out half a "ilo a wee". + man who had failed misera$ly for =! years to lose weight was suddenly a$le to lose ;C"g in the space of a single year and cure his deafness. #anting found that, unli"e all the other diets, he didn&t need any willpower to stay on this one A he could eat until he was full and genuinely enFoyed his food. The only adFustment he had to ma"e was to avoid the list of foods *r Harvey had given him. #anting was ecstatic. He was determined that others suffering the %oppression of corpulence& needed to "now his secret, so he funded and pu$lished a $oo" detailing his experience. He never charged for the $oo" $ecause he didn&t want to $e accused of doing it for the money. The #anting diet was so contrary to contemporary thin"ing on weight loss that the medical profession immediately set against #anting and *r Harvey. *r Harvey was not a$le to provide much of a defence. He "new the diet wor"ed $ut he was una$le to explain why. The pu$lic didn&t care whyL repeated successes with the #anting diet were $ecoming newsworthy A or at least gossip-worthy A events, much to the frustration of the medical profession. )nter *r 3elix 7eimeyer from .tuttgart. +ll doctors at the time %"new& that protein was not fatteningL it was only fat and starch that caused you to gain weight. It was thought that fat and starch com$ined with oxygen in the lungs to produce energy, with any excess $ecoming $ody fat. 7eimeyer rec"oned that the reason #anting&s diet wor"ed was $ecause it restricted fat and starch. 7eimeyer created a modified version that insisted on the meat $eing trimmed of all fat. #anting had

never actually concerned himself with fat inta"e, $ut this tiny modification made the 7eimeyer variation of the #anting diet instantly accepta$le to the doctors. #anting lived to the ripe old age of @, at a normal weight and in good health. He was always very critical of the 7eimeyer modification to his diet $ecause he said it unnecessarily complicated what was Guite a simple eating program. #ut in the end 7eimeyer helped #anting&s diet to gain the support of many in the medical profession and ultimately ensured that it helped many more people than those a$le to o$tain one of the ;<!! copies of his $oo". The #anting diet $ecame so popular among the upper classes of 4ictorian )ngland that $eing %on the $ant& $ecame synonymous with dieting well into the ,?;!s and &=!s. Those who spea" .wedish will also recognise anta as the ver$ for %diet&. #anting&s diet was copied many times $efore *r +t"ins read a$out it in the late &C!s. In ,?C!, it was promoted as the %(anadian +ir 3orce *iet&L in ,?C , the %*rin"ing 1an&s *iet&L and in ,?C>, the %*octor&s Nuic" Weight-5oss *iet&. This last diet, also "nown as the .tillman diet after its creator, reGuired the dieter to eat nothing (and I mean nothing) $ut protein. +$solutely no fats and no car$ohydrates were permitted. The .tillman diet was extraordinarily popular in its time, with the $oo" descri$ing the diet selling over <.< million copies. +ll of these diets had their little Guir"s, $ut they all had something in commonD low or no car$ohydrates. They had one other thing in commonD li"e poor old *r Harvey, the medical profession couldn&t provide any reasona$le explanation for why the diet should wor", the theory of fat and starch $eing com$ined in the lungs having long since fallen $y the wayside. +fter reading *r -ud"in&s research, and still having difficulty fitting into his graduation pants, +t"ins decided to give lowcar$ a try. He experienced the same persistent success enFoyed

$y #anting a century earlier. /nli"e .tillman and a raft of others, +t"ins thought he "new why the diet wor"ed. It was all related to insulin production and the creation of a state of "etosis. +t"ins pu$lished his $oo" Dr Atkins Diet ,e!olution in ,?>;, which promoted his new variation on the $y then very old low-car$ohydrate theme. What was uniGue a$out +t"ins& $oo" was not so much the diet itself as the considera$le effort put into descri$ing the meta$olic processes that explained how the diet wor"ed. If *r +t"ins thought he was onto a <.< million $estseller, li"e .tillman Fust five years earlier, he was a$out to $e sadly disappointed. #y ,?>;, fat-mania, driven in large part $y *r +ncel 2eys (a$out whom I will have much more to say later), had well and truly infected the medical esta$lishment. +t"ins was a laughing stoc" for suggesting you could eat as much fat as you li"e. The medical profession %"new& $y then that fat was the cause of most evil. +ll you had to do to lose weight was reduce your fat inta"e and show some willpower (oh, and go to the gym with :ane 3onda). Interest in +t"ins& diet smouldered in cult followings for almost two decades. In the early ,??!s a new version of his $oo" was released. This time, however, the pu$lic was ready to listen. #y then, almost twice as many people needed *r +t"ins& services A and that was after having ta"en the low-fat advice of the medical mainstream for two decades. The +t"ins diet $ecame a worldwide phenomenon, spawning its own series of copycats (the (.I08 diet in +ustralia is a recent variant that isn&t Guite so strict). +lmost two decades down the trac", low-car$ has almost eGualled ($ut not yet displaced) low-fat in the food mar"eter&s lexicon of power mar"eting phrases. .ince the +t"ins $oom in the late &?!s, the medical profession has wor"ed very hard to prove that low-car$ohydrate diets are no more effective than low-fat diets. .tudy after study has

shown that the $ody is perfectly capa$le of getting its Foules(calories) from 6lan # for extended periods and there is no logic to the suggestion that feeding the $ody protein rather than car$ohydrate should produce the results claimed $y the promoters of +t"ins, the Bone, the .outh #each *iet, the (.I08 diet or many of the other modern versions of going on the $ant. The reality is, however, that, at least in the short term, they definitely wor". It seems li"ely to me that what *r -ud"in discussed in the article that first inspired *r +t"ins is in fact the case. When you tell people they can eat as much fat and protein as they li"e, Fust don&t have car$ohydrates, they actually eat fewer Foules(calories). Thin" a$out that for minute and it&s not too surprising. -ou can&t eat fruit, $read, sugar, cereal, potatoes, pasta or pastry. #acon and eggs sounds good for $rea"fast $ut that wears very thin after even a wee" of having it every day A and anyway, who&s got time for that palaver every morningM -ou can&t even get it as a $acon and egg muffin on the way to wor" unless you plan to eat the contents and throw away the muffin. -ou can&t have sandwiches for lunch and you can&t have potatoes for dinner. 1ost of the things we are prepared to eat include car$ohydrates to some degree. 1any of these diets loosen the reins a little and let you "eep eating limited car$ohydrates, $ut if you follow those diets you are not really enacting the "etonic theory. +ll you are really doing is following Fust another Foule(calorie)- or food-limiting diet. 4ery recent research on the precise detail of the $iochemistry of how the $ody turns food into energy has shown that "etonic energy production (from protein and fat) costs more in terms of Foules(calories) used than %normal& car$ohydrate energy production. This means that low-car$ diets should produce weight loss as long as you don&t eat more of other foods to compensate for the energy drain. +nd *r -ud"in&s o$servations seemed to show that, if anything, you would eat less. 1y own personal experience with low-car$ diets lined up with

what *r -ud"in had found. It definitely wor"ed, and I suspect it was $ecause I actually ended up eating less of everything. +fter two days of feeling extraordinarily hungry no matter how much protein or fat I ate, my $ody suddenly turned off the hunger signal A as I was a$out to find out, the feeling of hunger is closely related to the operation of our car$ohydrate regulation system. 3rom that point on, I didn&t feel particularly hungry even if I ate nothing for a whole day. 1y $ody had ample supplies of fat to "eep me going for months, years or pro$a$ly even decades. The trou$le was that the types of food I could eat $ecame very limited. If you rule out everything containing car$ohydrates you are left with pretty much meat, dairy and salad. +nd $elieve me, after a few wee"s of nothing $ut meat, dairy and salad, you get pretty sic" of it. In the past, I had stopped low-car$ diets $ecause I couldn&t stand extended periods of trying to avoid $read, pasta and chippies. 7ow I had found out why it pro$a$ly wasn&t a good idea anyway. 6eople on a low-car$ diet $ecame "etonic Fust li"e untreated dia$etics A $ut hang on, they also eventually died. That seemed li"e a fairly extreme side effect. 3urther reading revealed "etone production is not a $ad thing in the short term. It is a natural response to starvation and it will "eep us alive until we can find the next $unch of $ananas. It&s not, however, a good idea to use "etones as a long-term source of energy. +s the "etones in the $lood $uild up over time, the acidity of the $lood increases significantly, since uric acid production is a $y-product of the process that produces "etones. This eventually leads to widespread tissue damage (particularly highly sensitive tissues such as those involved with eyesight and the "idneys), multiple organ failure and eventually death. High $lood sugar won&t "ill you instantly, $ut within a few months your muscles will $egin to waste, and within a few years "etonic acidity (or "etoacidosis, if you want to get technical) will eventually lead to significant organ

damage, accompanied $y $lindness, and then coma and ultimately death. Hmm, definitely a good idea to leave the +t"ins diet on hold. #ut I wasn&t entirely unconvinced. It might not $e necessary to eat ya" stea"s fed on .wiss glacial water or whatever other fandangled twist every new low-car$ diet came out with, $ut there seemed to $e good reasons why a sensi$le approach to low-car$ eating could well produce the solid results o$served $y so many since 1r #anting. I par"ed that thought in the $ac" of my mind and decided to find out more a$out meta$olism.

%= &OW WE T):N +OOD INTO ENE:G;

In nature, edi$le food is sometimes difficult to o$tain. )volution has ensured that our digestive systems are designed not to waste one Foule(calorie) of the energy we put into our mouths. If glucose, and therefore energy, can $e extracted, then our $odies will extract it and either use it immediately or store it for later. We can store a$out four hours& worth of energy as glucose in our $loodstream. This explains why we position mealtimes at eGuidistant times during our wa"ing hours. .o that we don&t have to get up in the middle of the night to have another meal, we also ma"e another hormone called serotonin, which is released while we are asleep. It tells our stomach we don&t need to eat right now. +s you might imagine, a hormone that tells us not to eat is of enormous interest to researchers in the weight-loss industry A $ut more on that later. If we eat more than four hours& worth of food ($ecause we managed to come across a particularly large dead antelope at lunchtime, for example), our $odies have a couple of energystorage systems to deal with the extra food. I understood this a lot $etter when I thought of myself as $eing li"e a laptop computer. I am a top-of-the-range laptop (of course) with a nice long four-hour $attery life (the eGuivalent of the amount of energy I can store in my $loodstream). Three times a day I plug into the mains for Fust long enough to charge the $attery. #ut I also have a $ag full of spare $atteries. If I have access to multiple power points at my recharge time, I can charge up some of the spare $atteries, Fust in case I&m not a$le to get to a mains supply in a further four hours& time. 1ind you, I have to $e prepared to carry around a $ag of spare $atteries Fust in case. :ust li"e the laptop with the $ag of spare $atteries, we can store

a further ;! hours of energy (five extra $atteries) as a form of solid glucose called glycogen (often called animal starch $y nutritionists or $rown fat $y $utchers). It is stored primarily around the liver and muscles. The liver is the second-largest organ in your $ody (your s"in is the largest). It is the functional eGuivalent of a pool filter in the $ody, cleaning the $lood supply $y removing excess nutrients and poisons a$sor$ed through the stomach and intestinal walls. 8ne of the most important functions of the liver is to manage, recharge and discharge our short-term energy storage (our spare $atteries). If insulin is in the $loodstream (usually $ecause we have Fust eaten), the liver uses the insulin in a chemical reaction that suc"s glucose out of the $loodstream and converts it to long chains of glucose molecules, which are stored as glycogen. :ust in case you are "eeping a list of all these 'ree" and 5atin words, the medical term for this process is glycogenesis, $ut I wouldn&t $other remem$ering that unless you plan to $ecome an endocrinologist (or have easily impressed acGuaintances). .tored glucose in the form of glycogen helps us to smooth out our energy reGuirements. Without it, we would have to eat every four hours or run the very real ris" of running out of the

+i ure %=1: The liver is the dar" grey-coloured organ in this picture.

glucose fuel reGuired to "eep our $rain and internal organs functioning. 'lycogen stores give us the fast-$urn capacity to "eep going for up to ; hours without having to eat at all.

Insulin is such an important protein that it is common to all animals. It wor"s in exactly the same way in worms and fish as it does in mammals. There is only a three-amino-acid difference (out of <,) $etween cow insulin and human insulin. 6ig insulin is an even $etter match, with only a one-amino-acid differential. Today, sufferers of dia$etes don&t inFect pig, cow and fish insulinL they inFect manufactured human insulin. In ,?@;, )li 5illy introduced a genetically engineered copy of human insulin, which has since spawned many similar preparations, and it is now illegal to use anything other than synthetic human insulin in many countries.

'lycogen is not the only energy-storage system we have. We also have the a$ility to store excess energy as fat (and don&t we all "now a$out that). 8nce again, insulin is the trigger for this mechanism. :ust as normal cells need insulin to convert glucose to energy, fat cells need insulin to convert glucose to fat. .o, as well as helping cells that need energy to access the glucose, and converting glucose to glycogen, the third way that insulin helps us reduce the circulating glucose load is to help the fat cells pac" away any excess glucose as $ody fat. 3at is almost twice as dense as car$ohydrate or proteinL a "ilogram of $ody fat stores almost dou$le the energy that a "ilo of muscle or glycogen does. If you stored all excess energy as glycogen rather than fat, it would ta"e up almost twice as much space and weigh almost twice as much. (I&ll $et that&s the first time you&ve thought of $ody fat as $eing a good thing.) 'etting $ac" to my laptop analogy, $ody fat is li"e a super-long-life $attery that ta"es twice as long to charge $ut also lasts twice as long (and only weighs the same as the other $atteries). The good news from a survival perspective is that, unli"e circulating $lood sugar or glycogen, you can store virtually unlimited amounts of $ody fat (well, in theory). It also means that your $ody is designed to ta"e every opportunity to store $ody fat, $ecause you never "now when you&ll $ring down

your next antelope. +t a$out this point in my reading another light went on in my head. .o that was why I "ept getting fatter A I was designed to eat all availa$le food and store it as $ody fat. 1ay$e there were diets that reduced the amount of insulin released after a meal, which would mean that less fat was storedM I started loo"ing and it wasn&t long $efore I stum$led onto 'I diets. 'I stands for glycaemic index and, simply put, it is a measure of the degree to which any given food produces a spi"e in $lood sugar (and therefore insulin). It&s "ind of li"e the different types of fuel you can feed a fire. If you put pine plan"s on the fire, they will $urn very hot and very Guic"ly $ut they will $e used up in minutes. If, however, you put hardwood sleepers on, they will $urn slowly for hours. 5ow-'I foods are hardwood sleepers to our $ody and high-'I foods are pine plan"s. 'I diets effectively treat all of us li"e we are suffering from dia$etes A the theory is that if you aim to "eep $lood-glucose levels and therefore insulin levels low and constant, your appetite will $e largely suppressed and large Guantities of insulin will not $e released and used to create $ody fat. It sounded logical to me, so I immediately started reading a$out the glycaemic index and loo"ing for low-'I foods.

+i ure %=$: + comparison of the effect that the 'I of a food will have on $lood-glucose levels over time. High-'I foods cause a much higher spi"e than low-'I foods.

In ,?@, in the Ameri'an +ournal of Clini'al -utrition, *r *avid :en"ins, a professor of 7utritional .cience at the /niversity of Toronto, was the first to pu$lish a theory a$out the glycaemic index and its effect on diet. *r :en"ins developed the index to help doctors determine what foods were $est for dia$etics. He found that there was no simple rule such as %don&t eat potatoes& or %do eat meat&L rather, all foods produced different $lood-sugar responses $ased on the com$ination of car$ohydrates, fats and proteins, as well as how much indigesti$le fi$re was present. It was, however, left to an +ustralian to develop a comprehensive ta$ulation of the glycaemic index of almost C!! foods. *r :ennie #rand-1iller, an associate professor and head of the teaching and research staff of the Human 7utrition /nit of the *epartment of #iochemistry at the /niversity of .ydney, $ecame the most

vocal champion of using 'I ratings to assess foods when she pu$lished her $oo" The )" .a'tor in ,??C.
/nli"e fat, protein and car$ohydrate measures, the 'I value of a food is relatively difficult to cali$rate. It relies on feeding volunteers foods and measuring their $lood-sugar responses. This is complicated $y the fact that the response will differ from day to day even in the same person. To avoid inconsistency, the $est measures are ta"en over ,! consecutive days and averaged over a group of volunteers. The volunteers are given an amount of the food $eing tested that will deliver exactly <!g of car$ohydrate. .o, for example, if we were testing pasta (;< per cent car$ohydrate) we would give the volunteers ;!!g of pasta to eat). .cientists then compare the $lood-sugar response of the volunteer to the pasta with a standard reference food for that volunteer (glucose is the most common). 6reviously doctors thought that complex car$ohydrates li"e potatoes and rice were a$sor$ed slowly. 'I measurements prove this is not so. 0ice has a glycaemic index of ? (where pure glucose is ,!!), which means that it is very high and will produce an immediate spi"e in $lood sugar. 6asta has a low glycaemic index $ecause it is prepared from crac"ed wheat, not from wheat flour. The method of preparation ma"es a difference to the particle si9e and therefore to the speed at which we can a$sor$ it. To ma"e matters worse, coo"ing the food will sometimes change the glycaemic index. (oo"ed pasta has a higher index than raw pasta, and you can lower the index of any food $y adding fat or fi$re to it, since $oth add weight to the food and lower the percentage of the food that is car$ohydrate. 0emem$er, the 'I only measures the $ody&s response to car$ohydrates.

+t first this diet loo"ed li"e a great idea to meL the pro$lem was that it was very hard to guess what the 'I of any food was going to $e, and I wasn&t prepared to wal" around a supermar"et with *r #rand-1iller&s C!!-item list in my hands. 3ortunately, I was not on my own in wanting 'I information, and some food manufacturers were starting to la$el their foods with 'I values. There was a range of low-'I $reads, and even chocolate drin"s and spreads had low-'I la$els J Hang on a secO What "ind of diet was this that encouraged you to drin" a chocolate drin" that is half sugar and eat a chocolate spread that is half fat and a third sugarM I Guic"ly realised that food manufacturers had figured out that they could la$el their food low 'I $ecause the fat content lowered the 'I rating dramatically. I very much dou$ted that it was *r #rand-1iller&s intent to develop a plan to allow you to eat significant Guantities of fat and sugar and call it a diet. 'I would o$viously $e important to a dia$etic needing to "eep $lood-sugar readings in chec", $ut I struggled with the notion that our predecessors were controlling their $lood sugar through some intuitive sense of the 'I of the foods they encountered on the plains and in the Fungles. We must $e capa$le (at least when healthy) of dealing with $lood-sugar spi"es. I couldn&t $elieve that the only reason we were suddenly all getting fatter was that we were suddenly consuming more potatoes and less pasta (and chocolate spread). It Fust didn&t stac" up logically. (learly I needed to find out more a$out how our $odies deal with car$ohydrates A and stop eating chocolate spread and calling it a diet. It turns out that insulin is the .wiss army "nife of hormones. It doesn&t Fust help cells to ma"e energy and help the liver and fat cells to store energy. It also has some appetite control properties A it stops us eating when we have ta"en on sufficient energy. 8nce insulin is introduced into our $loodstream it interacts with special receptor cells in a part of our $rain called

the hypothalamus. The hypothalamus is a critical and very complex central control unit for the human $ody. .ome of the maFor things it controls are our growth, our $ody temperature, when we sleep, our thirst and, most importantly for this discussion, our hunger.

+i ure %=%: The almond-si9ed hypothalamus is the control centre for most of the $ody&s automatic functions

The hypothalamus is continuously sampling our circulating $lood. 3or example, when it detects foreign cells li"e $acteria or viruses, it turns up our $ody temperature in an effort to "ill them. +nd when it detects insulin in the $lood it tells our $rain we have had enough to eat. +nother part of the hypothalamus then tells the $rain to reduce food inta"e. If the part of the hypothalamus controlling food inta"e is surgically removed in la$oratory animals, the animal stops eating altogether. (While this is pro$a$ly an effective dietary control it&s a little irreversi$le, so put down that scalpel.) (ut out the part that detects insulin and the animal $ecomes o$ese. +s much as we li"e to thin" we are in control of what and when we eat, it

seems to $e an unconscious choice controlled $y a lump of nerve cells that wouldn&t cover a postage stamp. This insulin-induced fullness signal only wor"s for as long as there is excess insulin circulating in the $lood, so it is relatively short term. It is enough to ma"e us push $ac" from the ta$le with the feeling of a full and satisfied tummy. We can consciously fight the fullness signal and eat on regardless (and if this was the only meal we had had for a few days, we pro$a$ly would). In the normal course, however, it seems we are designed to stop when we have had enough, so there goes my %perpetual eating leads to fatness& theory. 3at and glycogen storage are really Fust smoothing and $ac"up systems for storage of occasional excess energy. It seems insulin&s interaction with our hypothalamus would normally ensure we never ate too much more than we needed. To maintain that full feeling for longer than an hour or so after eating, insulin also triggers the release of the hormone leptin, another long-term appetite suppressant. 5eptin is a relative newcomer to our understanding of human appetite. It was first discovered Fust ,= years ago $y *r :effrey 3riedman at 0oc"efeller /niversity, a private institution $ased in 7ew -or" (ity dedicated to $iomedical research. *r 3riedman found that o$ese mice were missing a gene, which he christened the o$ (o$ese) gene. 7ot having the o$ gene meant the mice could not produce a hormone that 3riedman named leptin (from the 'ree" le&tos, meaning thin). When the o$ese mice were continuously inFected with leptin, they Guic"ly reverted to normal $ody si9e. +s you can imagine, the announcement of an inFecta$le su$stance that made o$ese mice thin again made Fust a few headlines in ,??<. /nfortunately, su$seGuent human trials revealed that it only really wor"ed as a cure for o$esity if you were one of the very, very, very small group of humans with the same genetic mutation as those mice (meaning you didn&t have an o$ gene). #y ,??@, the researchers were pretty

much satisfied that inFecting the rest of us with leptin was unli"ely to cure o$esity. 5eptin is produced $y fat cells in response to the presence of circulating insulin. The more insulin in your $loodstream, the more leptin will $e produced. #ecause insulin is swiftly eliminated from the $loodstream $y the various digestive processes, the $ody reGuires a longer-term means of appetite control. 5eptin performs that longer-term function. The insulin gets used up doing other Fo$s, li"e converting glucose to fat and energy, $ut the leptin stays around, continuing to tell the hypothalamus that we are still full. If it weren&t for leptin, the feeling of fullness created $y insulin after a meal would not last. We would $egin to feel hungry again as soon as circulating insulin was used up (an hour or so after a meal). .ince leptin is produced $y fat cells, the more fat you have, the more leptin you will generally have in your $loodstream. In this way, leptin acts li"e a fat meter for the hypothalamus. 5ots of fat translates to lots of leptin, which in turn results in suppressed appetite for longer periods. Theoretically, if you are carrying a little extra, leptin should moderate your food inta"e over the longer term and you should gradually use up your fat stores. It&s a very elegant designL the only trou$le is that something a$out it is clearly not wor"ing $ecause we are all getting fatter. + raft of recent studies have clearly shown that high levels of fatty acids in the arteries $loc" the action of leptin in much the same way that they inhi$it insulin. Insulin resistance means that your immediate appetite control is impaired and will eventually lead to type II dia$etes (see chapters @ and ?). 5eptin resistance means that your $ody loses the a$ility to tell when it has had enough to eat over the medium to long term. If you don&t "now you are full, you Fust "eep eating until suddenly you realise your wedding suit doesn&t fit any more.

(= )SING STO:ED ENE:G;

+$out four hours after we eat (unless we are asleep and therefore using less energy) glucose concentrations in our $lood will $egin to fall $elow a lower threshold. 8nce again, the change in glucose concentration is detected $y our pancreas. #ut this time, instead of releasing insulin into the $lood, it releases a hormone called glucagon. In ,?;=, shortly after insulin was discovered, 6rofessor :ohn 1urlin at the /niversity of 0ochester, 7ew -or", noticed that when the pancreatic extracts were inFected into dia$etic patients, there was a $rief, $ut noticea$le, spi"e in glucose levels Fust $efore the insulin acted to reduce them. He speculated that there might $e another hormone in the pancreatic extracts that had the opposite effect to insulin. He (Guite confusingly) called this hormone glucagon, which is not to $e mixed up with glycogen, the solid form of glucose stored around the liver. 'lucagon was proved to $e a hormone in ,?<? and its role in dia$etes was confirmed in the &C!s and &>!s. #y ,?@<, its role in the digestive system was well understood. 'lucagon is $est thought of as anti-insulin $ecause its effects are almost exactly the opposite of those of insulin. Its purpose is to get glucose concentrations $ac" up to normal levels. If your $lood-glucose levels fall the results can $e disastrous and, unli"e with high $lood glucose, immediate. 'lucose is your fuel. If you run out, you stop. The end. It&s that simple. Too little glucose, called hypoglycaemia (hy&o A too littleL gly' A sugarL aemia A in the $lood), results in very immediate pro$lems for your $rain. 0emem$er, the only fuel your $rain can use is pure glucose. Without it, the $rain $egins to shut down. +t first mental efficiency decreases, then sha"iness and sudden depression occur (hypoglycaemic dia$etics can

sometimes $e mista"en for drun"s when they reach this point), followed Guic"ly $y coma and then death. Type , dia$etics can no more manufacture glucagon than they can insulin. If they inFect too much insulin, they run the real ris" of suffering hypoglycaemic shoc". #lood sugar can $e Guic"ly raised simply $y eating anything containing glucose, which is why this type of dia$etic li"es to have ready access to sweets in case they start to feel di99y. 3or the rest of us, glucagon is a pretty important safety mechanism. To restore our $lood-glucose levels to a normal range, it does a num$er of things. 3irstly, it instructs our liver to access our short-term energy store $y telling it to convert glycogen stores $ac" into circulating glucose. This is the chemical eGuivalent of changing $atteries on my laptop. 'lucagon tells the liver to go into reverse, stop storing glucose and instead start using it. That solves the emergency need for glucose and should "eep us alive long enough to find something new to eat. 0emem$er that, if we are fully charged, we have a good ;! to ; hours of emergency power stored around our liver as glycogen. #ut it doesn&t stop thereD glucagon also tells the liver to convert amino acids (the component parts of proteins) into glucose, and tells our fat cells to release energy. The fat cells release the fatty acids they stored in $etter times and the presence of glucagon allows them to $e separated from their glycerol $ac"$one. The glycerol is then converted to glucose for use as fuel. #ut if that were all the hormone did, we would $e $lissfully unaware $ecause our leptin levels would still $e telling our $rain that we were full. If something weren&t done to tell us to loo" for food, we&d still die, we&d Fust last a $it longer while we ran down our spare $atteries. To stop this from happening, glucagon also stimulates the production of a hormone in the stomach called ghrelin.

With the discovery of leptin, the hunt was on for the appetitestimulating hormone that was leptin&s counterpart. 0esearchers "new that if the hormone could $e identified, it might $e possi$le to suppress its effects in some way. + multi-$illiondollar mar"et $ec"oned for a drug that could suppress appetite and in the mid-,??!s there were plenty of people loo"ing. + team at 1erc" 6harmaceuticals "new that such a hormone must exist, $ecause in ,?? they had identified the receptors for it in the hypothalamus. 0esearch teams were furiously testing tissue samples from organs all over the $ody to attempt to isolate the hormone that instructed the hypothalamus to ma"e us hungry. 1ost teams were searching the hypothalamus itself, $ut in ,???, 1asayasu 2oFima and 2enFi 2angawa at :apan&s 7ational (ardiovascular (entre Fust pipped the 1erc" team at the post and found ghrelin. The hormone they discovered gets its strange name $ecause it interacts with the growth hormone receptor ('H0) in the hypothalamus. 2oFima and 2angawa found it in massive Guantities in the stomach lining (in retrospect, not an entirely strange place to loo" for something that ma"es the tummy rum$le at dinnertime). 'hrelin is produced $y the stomach lining in response to the presence of glucagon in the $loodstream, $loc"ing the action of insulin (and leptin) in the hypothalamus. (irculating leptin levels stay reasona$ly constant most of the time, so our default appetite position is that we are full (or at least not hungry). 'hrelin counteracts the effect of leptin on the hypothalamus, effectively neutralising leptin for a while so we can feel hungry. The release of ghrelin is li"e throwing a %hungry& switch in our $rain. 'hrelin also stimulates our stomachs to contract, giving us that empty gurgling feeling that tells us it&s time to eat. 7ot surprisingly, there has $een a lot of research into a %vaccine& for ghrelin. #etween ,??? and ;!!;, there were no fewer than ,=! pu$lished research articles on ghrelin ( ! of

which were co-authored $y 2angawa). The theory is that if you could $loc" ghrelin&s interaction with the hypothalamus, you&d never feel hungry and, therefore, you wouldn&t eat and wouldn&t get fat. *r 2im :anda from the .cripps 0esearch Institute in 5a :olla, (alifornia, pu$lished results in ;!!> of successful animal testing of a vaccine that trains the immune system to identify and destroy ghrelin. In other words, treat the hormone that ma"es us hungry li"e a $acterial infection and train the $ody to "ill it. 7ow, that sounds good in theory, $ut the one thing I have noticed a$out hormones in all my reading is that they often do much more than one thing. 0emem$er leptinM InFecting it was supposed to stop you getting hungry too. It turns out it doesn&t wor" Guite that way, $ecause it seems that almost none of us has a defective o$ gene. 7evertheless, if you feel li"e turning your $ody into a la$ experiment, you won&t have to wait long. Human trials of a ghrelin vaccine will pro$a$ly have commenced $y the time you are reading this.

In a healthy $ody, insulin and glucagon act in opposing fashion to "eep our $lood-glucose levels (our fuel supply) at constant levels. )ach of these important hormones will trigger either the storage (insulin) or use (glucagon) of the $ody&s short- and long-term energy stores, as well as act on the appetite centre in the $rain to tell us whether to start or stop eating. The insulinPglucagon feed$ac" loop is designed to "eep us on an even "eel, consuming Fust enough energy to "eep our $ody running at the level of activity we choose to pursue. In common with all other animals, we are designed to maintain a normal healthy weight in all $ut exceptional circumstances.

0emem$er, in a normal diet our energy needs are supplied $y car$ohydrate, protein (predominantly from meat) and fat. -our $ody needs fats to function properly. *ietary fat is made up of a variety of fatty acids $onded to a $ac"$one of glycerol. When

we eat fat, it is a$sor$ed $y our upper intestine and transported into our $loodstream as triacylglycerols (three fatty acids tied together $y glycerol, a sugar alcohol of glucose), sometimes called T('s, lipids or fatty acids. The fatty acids are used in the production of cell mem$ranes (our $rain is almost all fat) and are critical for the production of several hormones, which help regulate $lood pressure, heart rate, $lood-vessel constriction and $lood clotting. 3atty acids are also important for the transportation of fat-solu$le vitamins (vitamins +, *, ) and 2) around our $ody. /nused circulating fatty acids are eventually converted $ac" into stored $ody fat. When we eat fat or protein, our upper intestine releases a hormone called cholecysto"inin (which than"fully gets a$$reviated to ((2), from the 'ree" 'hole A $ileL 'ysto A sacL and kinin A moveL technically, %move the $ile sac&. ((2 was originally discovered in ,?;@ and was "nown to induce contractions in the gall $ladder, the small organ $etween the liver and the pancreas (see page ;>, 3igure =.,). It&s a sac that contains a reserve of a$out <!ml of $ile. #ile is used to emulsify any fat that enters our stomach. 0esearchers have "nown since ,?;@ that ((2 triggers the release of digestive en9ymes from the pancreas and $ile from the gall $ladder. 8nly in the last decade has it $ecome clear that in much the same way as leptin does, ((2 also tells the hypothalamus to suppress hunger and ma"e us feel full. We have a well-developed system for accurately detecting when we have had exactly as much food as we need. (ar$ohydrates and proteins are regulated using the insulinPglucagon control of $lood glucose, and fats are regulated $y the similar use of ((2. I was once told that modern passenger aircraft constantly cycle fuel $etween their wing and fuselage tan"s to ensure that the plane is always perfectly $alanced as the fuel is used up. The fuel-management system at wor" in your $ody ma"es that system loo" a$out as

modern as 3red 3lintstone&s car. 0ight now, your $ody is delicately adFusting hormone levels to cycle multiple energy stores up or down $ased on the energy you need, when you last ate, what you ate and when you last slept (among other things). +ll of that is happening without you having to thin" a$out it at all (than" goodness A I&m flat out $alancing a cheGue $oo", let alone doing all that). It is a truly elegant design, $ut it is one that is wholly dependent on the assumption that the environment that %designed& it is still the same as when it was put together.

*= +AT 4A<ES ;O) +AT , O: DOES IT#

We are thin $y design. If we are eating the diet our digestive system is designed to use, one dominated $y foods that are compounds of glucose or can $e converted to glucose, the insulinPglucagon (for car$ohydrates and proteins) and ((2 (for fats) feed$ac" loops will "eep us thin. We will eat only when we are hungry and we will store minimal additional $ody fat. We come eGuipped with a fully functioning Foule(calorie) detector, the hypothalamus. It has no need for Foule(calorie) ta$les or calculators to determine how much food we need or how much fat we have stored on the $ody. It has $een designed $y millions of years of evolution to accurately and elegantly count and control our energy inta"e so that we maintain optimal $ody weight. .o, if we are so perfectly designed, how do we get fatM If you read all the reports of the experiments each of these researchers did in discovering the effects of each of the hormones they uncovered, it $ecomes very clear that o$esity and anorexia were very simply induced (or cured) in the animals they were studying. +ll they had to do was chop this $it off or inFect a $it more of that. The willpower of the animal seemed to have very little to do with whether it decided to eat or not. There was no need to send them off to the mouse gym or enrol them in The Biggest /oser. Their appetite and therefore their weight was all very simply controlled $y changing the hormone mix. +ssuming humans are running to the same $lueprint, and nothing in the research suggests we aren&t, there must $e something else $esides lac" of willpower at play in ma"ing us fat.

3or decades, governments and doctors ali"e have $een telling us that the %something& that is ma"ing us fat is Guite o$viously fat. When doctors first started loo"ing for explanations for why we were suddenly getting fat, the o$vious candidate for an increase in $ody fat was increasing consumption of foods containing fat. +fter all, that sounds intuitively logical, and fat consumption was increasing roughly in line with the increase in human $ody fat production. In ,?!? the average +merican was consuming Fust over , "g of fat every year. #y ;!!, this had almost tripled after a significant spi"e in the &?!s. The %fat ma"es you fat& message was first promoted $y *r +ncel 2eys. In ,?=?, 2eys Foined the 1ayo 3oundation, run $y the /niversity of 1innesota in 0ochester, 1innesota, where he created a new division of $iochemical research on human $eings, Human 6hysiology and #iochemistry. The following year he was invited to organise what was to $ecome the 5a$oratory of 6hysiological Hygiene at the university&s main campus in 1inneapolis. #y this time, World War II was engulfing )urope and +merica&s involvement was $ecoming more certain $y the day. The /. *epartment of *efense was one of the $iggest-paying customers of 2eys& new la$, and one of his first contracts was to run su$sistence tests for the *epartment. His tas" was to determine the least amount of food reGuired to "eep a

+i ure *=1: This graph is $ased on data from the /.*+ (/. *epartment of +griculture). +n o$vious cause of the o$esity epidemic is fat consumption, said the researchers, and graphs li"e this show we clearly are eating more fat A $ut is it really the causeM

com$at soldier alive and in fighting condition. #y ,? ,, 2eys was serving as special assistant to the .ecretary of WarL his primary role was to develop rations for com$at troops. 2eys and his team had scoured the local supermar"et to create what was essentially a lunch $ox full of high-Foule(calorie), long-life foods. The infamous 2-rations (%2& for 2eys) $ecame A and remain, al$eit heavily modified A a staple of the /. military. +s the end of the war approached, 2eys $egan to realise that starvation was going to $e a significant pro$lem in )urope when the fighting stopped. He o$tained funding and resources for the 1innesota .tarvation )xperiment, in which he and his team fed volunteers half the normal num$er of Foules(calories)

for adult males, while ensuring that they "ept up a normal exercise regime. The idea was to put the volunteers on a diet that simulated what life was li"e in the war-torn remains of )urope. 8n average, each man lost ;< per cent of his $ody weight, ,! per cent of muscle strength and <! per cent of endurance over the five months of the study. The starvation studies gave 2eys access to significant population and food data coming out of post-war )urope. 5oo"ing at this data, 2eys noticed that as food supplies reached starvation levels, the death rate from coronary heart disease dropped significantly. 2eys couldn&t explain that counterintuitive o$servation. .urely more people should $e dying of heart attac"s as they starved, not fewerM 2eys developed a theory to explain the data. He thought that a fullFoule(calorie) diet contained more fat and therefore more cholesterol than a starvation diet. If there is too much cholesterol in the $lood, it can accumulate and cause arterial $loc"ages (atherosclerosis), which can lead to heart attac" or stro"e. The elimination of fat in the starvation diet would therefore mean that patients would have less heart disease. 2eys& theory that there was a correlation $etween dietary fat and heart disease was Fust a theory, and it was $ased on only a few o$servations, so, $y then a very influential researcher, he o$tained funding to launch a long-range study aimed at determining the factors involved in %degeneration of the heart&. He recruited ;@C 1innesota $usinessmen and set up a meta$olic research unit at a local hospital. #y the time 2eys started his study in ,?<=, it was well "nown that the $uild-up of cholesterol ('ree" for solid $ile) was a maFor cause of some types of heart disease. (holesterol, a fatty su$stance manufactured $y our liver, provides material for the repair of cell walls and the manufacture of some hormones. It is critical to normal $rain and nerve function and is used as a transport mechanism to carry fatty acids in the $loodstream.

8ver time, cholesterol deposits $uild up on artery walls. When the cholesterol $uild-up entirely $loc"s an artery supplying $lood to the heart wall, a heart attac" can occur. *r 2eys& study of the 1innesota $usinessmen was a precursor to his more ela$orate .even (ountries .tudy, which launched in ,?<@ and ran for the following decade. The now famous study examined data on the diets of a selection of different countries and seemed to show that the higher the level of fat in a nation&s diet, the greater its rate of heart disease. 2eys explained the results $y suggesting that a diet rich in saturated fat, found in animal products such as meat, eggs and dairy products, produces higher levels of cholesterol in the $lood. This, in turn, increases the ris" of the artery-furring process that gives rise to heart disease. The o$vious outward symptom of all this fat consumption is weight gain. 3rom the mid-,?<!s, 2eys actively promoted his theory to an increasingly health-conscious pu$lic. With his wife, 1argaret, 2eys popularised the %1editerranean diet& with a series of $estselling $oo"s. The diet is $ased on mimic"ing the food inta"e of 1editerranean and +sian cultures that scored well on the .even (ountries .tudy. *r 2eys must have $een doing something right $ecause he lived to the ripe old age of ,!,, passing on peacefully in his sleep at the end of ;!! . 2eys is pro$a$ly almost single-handedly responsi$le for the five decades of product mar"eting directed towards low-fat foods that followed the pu$lication of his famous study. The case against saturated fat and cholesterol was, however, pro$a$ly not as open-and-shut as 2eys and his followers would have us $elieve. When *r 2eys pu$lished his study, he focused on Fust seven countries. #ut at that time, data from ;; countries existed, which may suggest 2eys was perhaps a little selective a$out the evidence he decided to include. In the study, 2eys produced a graph with the amount of fat in the food of the

seven countries plotted on one axis and the average $loodcholesterol levels for those countries plotted on the other axis. In *r 2eys& graph, the data points (fat in the diet versus cholesterol) fell on a straight line. 1athematically this meant that fat consumption and cholesterol were $eautifully correlated for those seven countries. /sing that single graph, 2eys drew the conclusion that dietary fat consumption caused high $lood cholesterol. That conclusion $ecame an easy-todigest (pardon the pun) message that half a century of lowcholesterol mar"eting has ingrained as modern health fact $eyond dispute. 3at ma"es you fat. If data points from the fifteen countries that *r 2eys failed to include are added to his graph, the correlation appears far less convincing and the conclusion that there is any relationship $etween dietary fat consumption and cholesterol or o$esity correspondingly more difficult to maintain. )ven within the data presented $y 2eys there were significant pro$lems. 3or instance, despite similar fat inta"es, heart disease deaths in 3inland were found to $e seven times higher than in 1exico. The 1editerranean island of (rete was an even more astounding a$erration. With almost ! per cent of the Foule(calorie) inta"e of (retan participants coming from fat, they experienced the lowest death rates of all countries studied. 6rofessor 2eys explained these a$errations $y theorising that, unli"e the saturated animal fat that was in +merican and 3innish diets, the maFority of the fat in the (retan diet came from olive oil and fish, which are rich in unsaturated fats. 2eys concluded that, although saturated fat can $e harmful to your health, unsaturated fats can have positive health $enefits. .u$seGuent studies have also found enormous variance in heart disease rates within countries, despite consistent $loodcholesterol levels. 2eys& message to avoid saturated fat and you would stop $eing fat certainly had a simple logic. #rilliant mar"eting $y 2eys

and those that followed on the %eat less fat& $andwagon ensured that for the last three decades of the last century we were all encouraged to purchase fat-free or fat-reduced foods at every turn. *etailed studies of food consumption ha$its conducted $y the /. *epartment of +griculture from ,?>, to ;!!! have confirmed that 2eys& and his followers& message got through. *uring those three decades, the percentage of the food energy in the average +merican&s diet that came from fat actually decreased (from =C.< per cent to =;.@ per cent). The strange thing was that not only did the su$stantial decrease in fat consumption not result in a reduction in the average waistline, $ut it was expanding faster than it ever had A in fact, it had dou$led. We had o$eyed *r 2eys& command to eat less fat and it seemed to $e ma"ing us fatter, not thinner. I was less than convinced. If I were inclined to $e mischievous with statistics, I could easily Fustify a message that not eating fat made you twice as fat. What I was a$out to discover was not so much that fat was good for me, $ut that, left to its own devices, my $ody could deal with fat in my diet. )ating fat put fatty acids in my arteries, that was for certain. #ut my $ody could tell when I had had enough fat and stop me eating more. I was a$out to discover that my $ody had no such control over fructose, and yet it Fust as effectively pumped fatty acids into my arteries. )ven worse than that, $ecause fructose was invisi$le to my appetite control, it allowed me to eat Fust as much fat as I normally would, and then eat as much fructose (which $ecame fat) as I could shove into my mouth. 7o wonder I was getting fatter no matter how much low-fat food I purchased. +s long ago as ,?>>, *r 'eorge 1ann descri$ed the dietPheart idea (eating fat gives you heart disease) as the %greatest scam in the history of medicine&. *r 1ann, a professor of 1edicine and #iochemistry at 4ander$ilt /niversity in Tennessee, concluded after studying the 1aasai people of 2enya during the early

&C!s that diet could not possi$ly influence cholesterol levels. 7ot unli"e most of my children, the 1aasai $elieve that vegeta$les are food for cows, not humans (they are cattle farmers). They each su$sist on ;5 of full-cream cow&s mil" per day and when they cele$rate they do so with an orgy of meat and $lood consumption, with each person eating more than ,"g of meat in a sitting. -et 1aasai tri$es have the lowest cholesterol readings ever measured, on average half that of an adult +merican. I "new from personal experience that going fat free made almost no visi$le difference to my waistline. 6erhaps I was less of a heart attac" waiting to happen, $ut $ased on *r 1ann&s wor", I dou$t it. I was still fatL it was Fust that food was less pleasant to eat. The %fat gives you heart disease& theory and the natural corollary (which 2eys claimed was o$vious), the %fat ma"es you fat& theory, didn&t gel with what I had discovered a$out our digestive system either. +ccording to everything I had read, eating fat should have "ic"ed in the ((2 feed$ac" loop, which would tell my hypothalamus I was full and stop me eating more than I needed. I shouldn&t $e a$le to get any fatter eating fat than I would eating car$ohydrates. .ure, fat might $e worse for cholesterol (I wasn&t convinced a$out that either), $ut I couldn&t see how it could $e responsi$le for o$esity. *r (leave had said sugar was clogging up our pancreas (perhaps not exactly his words) and that the cure was more $ran. I hadn&t seen anything in all my reading to this point to Fustify a theory that sugar was affecting the pancreas (or that $ran was li"ely to help in any way even if it was). .ugar was a food li"e any other and all the normal mechanisms should apply, shouldn&t theyM #ut *r (leave&s graphs seemed to show a strong relationship $etween rapidly rising sugar consumption and o$esity-related diseases. +s we "now, unli"e most car$ohydrates li"e grains, $reads and

pasta, which are almost entirely glucose $ased, sugar is only half glucose. The other half is fructose. I theorised that perhaps the answer lay in the degree to which we were adapted to dealing with large Guantities of fructose in our diet. It was time to see what the medical esta$lishment "new a$out the consumption of fructose and whether it might have an effect on our weight. It was luc"y I had $een $oning up on 'ree" and 5atin medical terms, $ecause if I was expecting to find anything written in plain )nglish I was a$out to $e very disappointed. It immediately $ecame apparent that I wasn&t the only person Guestioning the evidence and the conclusions $eing drawn from *r 2eys& wor". His detractors weren&t famous +mericans with a diet $oo" to sell, so it too" a little more digging to find their wor". +t around the same time that .urgeon-(aptain (leave and *r 2eys were wor"ing on their solutions to the o$esity pro$lem, 6rofessor :ohn -ud"in was ta"ing a different tac". #orn in the )ast )nd of 5ondon in ,?,!, :ohn -ud"in studied 6hysiology and #iochemistry at (am$ridge and, while studying for his 6h*, he developed an interest in nutrition. He later $ecame a doctor, serving in the +rmy 1edical (orps in West +frica during World War II. +fter the war, -ud"in was appointed 6rofessor of 6hysiology at the /niversity of 5ondon&s Nueen )li9a$eth (ollege (N)(), eventually esta$lishing the first university department in the /2 that offered undergraduate-level nutrition degrees. -ud"in $ecame the .chool&s 6rofessor of 7utrition, a Fo$ he retained until he retired in ,?>,. *uring the ,?<!s 6rofessor -ud"in $ecame increasingly distur$ed $y the o$vious inconsistencies in the evidence emerging from *r 2eys& research lin"ing animal fats to heart disease and o$esity. .o he $egan searching for another dietary factor. #ecause he was an expert in car$ohydrate meta$olism,

he initially focused (li"e *r (leave) on sugar consumption $ecause, li"e fat, its use was rapidly increasing. In la$oratory and human tests, he found that eating ta$le sugar increased the amount of 5*5 cholesterol (the %$ad& cholesterol) in the $lood. #ut not only that, he found that all circulating fats (T('s) generally increased. There is a growing $ody of evidence lin"ing T('s to the clogging of arteries, which may increase the ris" of a heart attac" or stro"e. In fact, some researchers now thin" that T(' levels in the $lood may actually $e more important than cholesterol levels in esta$lishing heart disease ris". 6rofessor -ud"in also noted increased uric acid levels. 0emem$er, $ecause of a lac" of insulin in a dia$etes patient, the $ody thin"s it&s starving and starts eating its own protein and fat to produce "etones, which are used for energy. The +t"ins diet (or any other high-protein diet) produces the same effect $y starving the $ody of car$ohydrates, forcing it to switch to protein and fat meta$olism as its primary source of energy. /ric acid is the $y-product of that process. 6rolonged excess uric acid production eventually leads to the high $lood acidity that does so much damage to the eyes, "idneys and other fragile organs in dia$etics. *octors "new that high uric acid levels were associated with a type of arthritis called gout, renal ("idney) failure, gallstones and an increased ris" of heart disease. They also "new that eating too much meat, particularly internal organs li"e the offal granddad used to eat, could cause uric acid levels to $e higher than normal. *r -ud"in&s discovery that eating sugar could also cause high uric acid levels came as a $it of a shoc". +nother unexpected increase detected $y *r -ud"in was in the hormone cortisol. (ortisol is produced $y the adrenal gland (the ma"er of adrenaline), and is often called the stress hormone $ecause it&s released $y the gland in response to stress. (ortisol gets everything wor"ing harder and faster

during times of stress (which was pro$a$ly particularly handy when $eing chased $y a woolly mammoth or sa$re-toothed tiger). It temporarily increases $lood pressure (for faster thin"ing) and $lood sugar (for extra energy), and suppresses the $ody&s immune response, so energy is focused on the more immediate concern of staying alive, rather than the endless hunt for nasty infections. (ortisol release is cyclical. -our $ody gives you a "ic"-start in the morning $y sGuirting Fust a little more than normal into the $lood and it tones it down when you are trying to sleep. 6retty much any time you are a$out to have a stressful experience (fear, pain, a meeting with your pu$lisher, that "ind of thing), cortisol levels increase. +nd also, *r -ud"in somewhat surprisingly discovered, when you eat sugar. That might go a long way to explaining the %sugar high& that every parent of young children will tell you is very real. The other surprising change in su$Fects fed large amounts of sugar was that their $lood $ecame stic"ierL in other words, it clotted more easily. This is worth remem$ering, especially in the context of the fact that most cases of heart disease over the past hundred years are of a form that is new, namely heart attac" or myocardial infarction A a massive $lood clot leading to o$struction of a coronary artery and conseGuent death of the heart muscle. 6rofessor -ud"in&s initial findings were pu$lished in ,?<>, the year $efore *r 2eys launched his famous .even (ountries .tudy. -ud"in and his team followed up that research during the &C!s with investigations of larger populations that showed that the rise in the incidence of heart disease consistently coincided with the rise in the consumption of sugar, $ut could not $e consistently associated with the consumption of fat, whether it was saturated or unsaturated. +s dramatic as those findings were, the real surprise came

when *r -ud"in su$stituted fructose for sugar in his experiments. 0emem$er that ta$le sugar (or sucrose) is a com$ination of two simpler sugars, glucose and fructose. -ud"in "new that the human $ody $ro"e sugar into these constituent parts as part of the digestive process and wanted to determine whether either part had more influence on his findings. %The effects of eating sucrose in the Guantities we eat are magnified with fructose. 3ructose is the dangerous part,& he said. *r -ud"in pu$lished a popular explanation of his concerns a$out sugar in ,?>;. His $oo" Sweet and Deadly came in for sustained attac" from *r 2eys, principally $ecause it suggested that it was sugar and not fat that was the cause of heart disease. The retiring #ritish academic was no match for the wellpu$licised +merican, and *r 2eys& theories won the day in the popular (and scientific) conscience. 1eanwhile, the /. *epartment of +griculture was doing some interesting things with rats. The /.*+ has a long and proud history in human nutrition research. In ,?<=, the tide of interest in human nutrition that was floating *r 2eys& $oat had also inspired the /.*+ to esta$lish the +gricultural 0esearch .ervice, with a mission to find solutions to agricultural pro$lems that affect everyday +mericans. + "ey facility for the service is the #eltsville Human 7utrition 0esearch (enter in 1aryland (#eltsville for short). *r -ud"in&s warning $ells on sugar (and in particular, fructose) had $een muffled $y the intervention of the 2eys media machine, $ut *r .heldon 0eiser, the lead researcher on car$ohydrate meta$olism at #eltsville, had $een reading -ud"in&s wor". He decided to start feeding some hapless rats fructose-rich diets. 3rom ,?>< until his retirement in ,??!, *r 0eiser pu$lished study after study that concluded without a shadow of a dou$t that it was the fructose half of sugar that

was doing all manner of damage in his furry su$Fects. 8n the high-fructose diet, the rats developed severe pro$lems with vital organs. 5iver, heart and testes exhi$ited extreme swelling, while the pancreas atrophied, invaria$ly leading to the death of the rats. Interestingly, the damage was much greater in male rats than in females. *r -ud"in had discovered a similar trend among the ra$$its used in his experiments, and had theorised that perhaps female reproductive hormones in some way reduced the negative impacts of the sugar. He went on to verify this in limited human trials, which showed that postmenopausal women were at Fust as high a ris" as men, $ut premenopausal women had much lower ris"s associated with the inta"e of sugar. )m$oldened $y almost a decade of dead rats, and drawing some criticism a$out the applica$ility of rat studies to human consumption patterns (no$ody in the /. had paid much attention to -ud"in&s wor"), *r 0eiser decided to conduct a limited human version of his experiments in ,?@ . The study&s official goal was to investigate the effect of fructose consumption on the health of ; men aged ;, to <>, consuming a diet marginally low in copper. Health surveys conducted $y the /.*+ during the &>!s had revealed that the average +merican had far too little copper in their diet, and experiments with rats had repeatedly shown that copper deficiency magnified the ill-effects of fructose, particularly in male rats. The diets used in the study were designed to represent typical +merican diets in $oth composition and si9e. The men were divided into two groups of ,;. 8ne group was fed a diet where ;! per cent of the Foules(calories) came from fructose and the others were fed the same diet except the fructose was replaced with corn starch. #oth diets were low in copper. The study had to $e terminated when four of the ,; men in the fructose group developed cardiac pro$lems, ranging from severe tachycardia (his heart rate tripled) to mild heart

attac"s, within the first ,, wee"s. This "ind of result is why it&s easier to get funding for rat studies. The rats don&t employ high-Guality legal teams so the ris" of $eing $an"rupted $y doing a fructose study is somewhat minimised. This was the only /. study I was a$le to find where they had actually tried purposefully to feed humans a fructose-$ased diet. *r -ud"in had done some similar studies using ordinary ta$le sugar fed to people in /2 hospitals, $ut they were much shorter in duration. It loo"ed li"e .urgeon-(aptain (leave might have $een on to something. 3irst *r -ud"in and then the /.*+ had systematically proven that, at least in rats (and no-one was game to try humans again), it was not a good idea to eat sugar in the Guantities found in the +merican diet in the &@!s. +nd the reason for that was clearly identified as $eing related to the fructose half of sugar and not the glucose half. The $ig Guestion for me at this point was whyM Why should fructose have all these nasty side effectsM What was the $ody doing with it that created all the pro$lemsM +nd why, given it&s $een a part of our diet since the dawn of (our) time, was it suddenly a pro$lemM It was time to immerse myself in the chemistry of fructose. *octors had "nown for a long time that dia$etic patients could manage their illness $y $eing careful with their diet. #y trial and error, doctors "new that some foods produced a sharp increase in $lood sugar and others did not. (ar$ohydrates were divided into simple and complex groups. *ia$etics were advised to avoid simple car$ohydrates li"e sugars, white rice and white $read, which were "nown to increase $lood sugar sharply, and see" out complex car$ohydrates li"e wholegrain $reads, oats, mueslis and $rown rice. In ,?>C, 6hyllis (rapo, a nutritionist at the /niversity of (alifornia in .an *iego, pu$lished a study that proved that while this advice was generally good, there was one simple

car$ohydrate that was an exception. 3ructose did not affect $lood-sugar levels in the same way that other simple car$ohydrates did. .he went on to show definitively in su$seGuent studies during the late &>!s and early &@!s that dia$etic patients could $e fed fructose without ris"ing increased $lood-sugar levels. #ased on this research, in ,?@ the +merican *ia$etic +ssociation recommended that dia$etic patients $e given foods that used fructose as the sweetener rather than sugar. (learly they hadn&t $een reading a$out *r 0eiser&s rats or they might have reconsidered the advice. It too" a while to sin" in, $ut $y ;!!; the +*+ had completely reversed its recommendation on fructose, saying that added fructose should $e completely avoided. They didn&t Fustify their change of heart other than to say that, notwithstanding its proven lac" of $lood-sugar response, %fructose may adversely affect plasma lipids&. That&s doctor-spea" for eating fructose may increase the amount of fat you have circulating in your $loodstream, something *r -ud"in had $een saying since at least the late &>!s. (learly something had given them a $ig enough scare to ma"e them completely reverse their recommendation on fructose. 6erhaps they had finally caught up on their reading and come across some of *r 0eiser&s unfortunate rats (and people).

-= .IOC&E4IST:; 1/1
The thing that was worrying me $y now was what happens to all that fructose that we&re eatingM I was a$out to discover that the answer (in a nutshell) is that it is turned into fat. +nd, unli"e fat, it $ypasses the control mechanisms that we have evolved to stop us eating too much of it. )ating fructose is li"e eating fat that your $ody can&t detect as $eing fat. While *r 0eiser was feeding rats too much fructose, new cellcloning techniGues and gene research were allowing $iochemists to figure out exactly how fructose is a$sor$ed $y the $ody and what happens to it after it hits your $loodstream. #y ;!!,, the research of many $iochemists over the preceding decade and a half had resulted in the consolidated view that I am a$out to outline. There may $e a drier and more incomprehensi$le area of science than $iochemistry, $ut so far I haven&t come across it. .tay with me though, $ecause as it turns out, the "ey to all the o$servations made $y doctors -ud"in, (leave, 0eiser and their colleagues is at the cellular level. The cells of our $ody cannot Fust help themselves to $lood sugars (glucose, galactose or fructose). They need to have a special protein within the cell itself in order to a$sor$ the sugar and then use it in a chemical process inside the cell. +s a family, these proteins are called glucose transporters, or '5/Ts for short. Than"fully $iochemists are a pragmatic lot and rather than name each of them after their favourite 'ree" or 5atin word, they Fust num$ered each of the '5/Ts. I found that the $est way to thin" of a '5/T is that it exposes an indent on the outside of a cell into which only one type of sugar molecule will fit. .ort of li"e a Figsaw pu99le loo"ing for a missing piece. When a molecule of the right shape comes

along, it loc"s into the molecule-shaped hole made $y the '5/T in the cell wall. The '5/T then pushes the sugar through the cell wall and waits for the next molecule to come along. .o far, $iochemists have identified ,= different mem$ers of the '5/T family. They are not entirely sure what all of them are for, $ut '5/Ts , to <, the important ones from our perspective, are well settled. '5/Ts ,, = and are for glucose only, '5/T< is only for fructose, and '5/T; is for $oth glucose and fructose. '5/T, is used $y almost all cells in the $ody to ta"e up the low levels of glucose reGuired to sustain respiration. It is present in large Guantities in foetuses and at much lower levels in adults, where it is concentrated in red $lood cells. Its concentration increases when there is less glucose in the $lood and decreases when there is more. '5/T, is the $asic %"eep every cell alive& protein, which ma"es sure our cells are getting enough glucose to "eep functioning. '5/T; is the protein used $y the liver to a$sor$ $oth glucose and fructose. It is also the glucose sensor used $y the islets of 5angerhans in the pancreas to determine how much insulin or glucagon to release into the $loodstream. +s we shall shortly see, fructose is a$sor$ed through the '5/T; proteins, $ut $ecause the pancreatic cells have none of the en9yme needed to use fructose, they are pushed straight $ac" out again. 3ructose molecules go whi99ing through the '5/T; proteins without eliciting any response at all and no insulin is produced. #esides the islets of 5angerhans, '5/T; is also found in the liver and the hypothalamus. '5/T; is insulin dependent, which means that the num$er of glucose molecules that it transports across the cell wall (and therefore detects) is regulated $y how much insulin is present in the $lood. The more insulin there is in the $lood, the more glucose '5/T;

transports and the more insulin is produced. /sing this simple mechanism, the level of insulin in the $lood should always parallel the level of $lood sugar in healthy humans. '5/T= is the specialist transporter located predominantly in our $rains and, to $e specific, in the neurons. 5i"e '5/T,, '5/T= is not dependent on the presence of insulin. It "eeps vacuuming glucose out of our $lood even if there is no insulin at all. It&s a handy design feature shared $y all animals, that '5/T, (for $reathing) and '5/T= (for thin"ing) "eep wor"ing even if there is some pro$lem with our energy inta"e and detection system. '5/T is the really important mem$er of the family for those of us interested in how the $ody uses and stores energy. '5/T is present in large Guantities in our muscle and fat tissues and, li"e '5/T;, it is insulin dependent. The presence of insulin stimulates muscle and fat cells to move all their '5/T proteins up to the cell $oundary, priming the cell to suc" as much glucose as it can out of the $lood as fast as possi$le. This is how insulin stimulates energy use $y muscles and fat storage $y fat cells. The more insulin there is in the $lood, the faster the glucose is vacuumed up $y the '5/T proteins in the muscles and fat cells. '5/T< is the protein associated with the a$sorption of fructose. -ou will find '5/T< in only one place in a healthy female $ody A the small intestine. In men, it&s also present in the testes for reasons that are not entirely clear to $iochemists at this stage. In the small intestine, '5/T< is present in significant Guantities. Its only purpose is to vacuum up any fructose we eat and transport it directly from the intestine into our $loodstream. .ince the existence of '5/T< and its role in fructose a$sorption was first confirmed in ,??;, a range of interesting rat tests (yes A everyone is still too scared to test fructose on humans J except at the local Fuice $ar) have

revealed some intriguing facts a$out the way we ingest fructose. It seems the amount of '5/T< present in the intestine is directly related to how much fructose rats (and $y extension, humans) eat. Within one day of starting a highfructose diet, the num$er of '5/T< proteins in the rats& intestines had increased fivefold and continued to increase gradually for as long as the fructose diet continued. The $ody actually manufactures more '5/T< proteins to ma"e sure we have plenty on hand Fust in case we encounter some more fructose. 5et&s Fust $ac" up a little here $ecause this is an important point. What the research is telling us is that firstly, we can&t a$sor$ fructose through our intestine at all unless we have '5/T< proteins there. .econdly, the more fructose we eat, the more '5/T< proteins we ma"e, which means the more fructose we can a$sor$ efficiently. +nd we&re not tal"ing a$out glacial reaction speeds here. The $ody reacts immediately and decisively. +s soon as fructose is introduced to our gut, the $ody significantly ramps up our a$ility to ensure it enters our $loodstream. It&s almost as if we are designed to detect and a$sor$ as much fructose as we can possi$ly get our hands on as fast as possi$le. If fructose is present in our food, we don&t want to waste one gram of it. +pparently age also ma"es a difference to the num$er of '5/T< proteins we have availa$le. 0ats and ra$$its have no significant Protein Trans7orts Sti!u5ated Location Pur7ose J 1y , '5/T, 'lucose Wor"s all the time )very cell 2eeps every cell alive

6ancreas, The amount *etects the 'lucose and hypothala '5/T; of insulin in presence of fructose mus and the $lood glucose liver '5/T= 'lucose Wor"s all the time #rain 2eeps the $rain alive 6owers the muscles and stores glucose as fat 'ets as much fructose into our $loodstream as possi$le

'5/T

'lucose

The amount 3at and of insulin in muscles the $lood

'5/T< 3ructose

The amount .mall of fructose intestine ingested

3igure C.,D The '5/T proteins and their uses.

Guantities of '5/T< until after they are weaned. Human children one to three years of age on normal diets (don&t worry, no-one was feeding children fructose to see what happened) also seem to lac" it in significant Guantities. The symptoms of a lac" of '5/T< are exactly the same as those of an ina$ility to a$sor$ lactose J a$dominal pain and chronic non-specific diarrhoea (often called toddler&s diarrhoea). + series of studies conducted in ,??C appeared to lin" the lac" of development of '5/T< with these symptoms in most toddlers. .o it seems toddlers have a $uilt-in resistance to fructose in the diet. The results of over-consumption might not $e too pretty on the outside, $ut on the inside of their little $odies, fructose is not getting into the $loodstream. #y the time you finish reading the

next section, you&ll wish you were still a toddler. '5/T< is not present in significant Guantities anywhere in our $ody except in the intestine. This ma"es it Guite different from the first four '5/Ts, which deal with glucose. 'lucose is suc"ed out of our $loodstream $y the first four '5/Ts and distri$uted all over our $ody. The only place after digestion that contains '5/T< (and therefore an a$ility to use fructose) is the testes. In a healthy $ody, no other cell has any use for all the fructose $eing vacuumed up $y the '5/T< in our intestine. )ven the testes have only a very limited capacity to a$sor$ it. The location and function of '5/T< explains *r (rapo&s o$servation in the &>!s that fructose did not cause insulin levels in the $lood to increase, $ut perhaps the +merican *ia$etics +ssociation (+*+) should have dug a little deeper $efore recommending that every dia$etic pig out on fructose. .ome interesting research pu$lished in ,??C $y the .loan2ettering (ancer (enter in 7ew -or" showed that very high levels of '5/T< were also found in the $reast tissue of women suffering from $reast cancer. 7ormally '5/T< is not found in $reast tissue at all. 7ot surprisingly, the presence of '5/T< in $reast tissue is now $eing studied as a potential early-detection test for $reast cancer. The fol"s conducting the 1olecular Imaging 6rogram at .tanford /niversity confirmed the via$ility of Fust such a test in ;!!@. 8$viously, there is a difference $etween '5/T< distri$ution in healthy $odies as opposed to the $odies of people suffering from some diseases. .o if, when we are healthy, none of our cells except those in the liver has any significant a$ility to use fructose, what on earth are our $odies doing with all that fructose that we are so efficiently a$sor$ing from our foodM To answer that Guestion it loo"ed li"e I needed to come to grips with what was going on in the liver, and to do that I needed to understand a $iochemical process called glycolysis (from the

'ree" gly' A sweetL lysis A letting loose). /nfortunately, 5atin and 'ree" seemed to $e the preferred naming conventions for $iochemists after a $rief $out with $eing logical in simply num$ering the '5/T proteins. .o far I have $een saying that glucose is used $y our cells to produce energy that "eeps us upright and $reathing. The role of glucose in "eeping us alive was o$served $y some of the very earliest $iochemistsL all of them wanted to "now how exactly that tric" was achieved. 8ne of the phrases I came across a lot when reading a$out the history of the discoveries in car$ohydrate meta$olism was %the process was turning out to $e much more complex than had $een imagined ,! years $efore&. It was a phrase I was $eginning to sympathise with wholeheartedly, the more I read in this area. 8ne of the pioneers of human meta$olic $iochemistry was an )nglish chap $y the name of +rthur Harden. #orn in 1anchester in ,@C<, in ,?,; he too" up a professorship in #iochemistry at the /niversity of 5ondon, where he stayed until his retirement in ,?=!, one year after he collected the 7o$el 6ri9e in (hemistry. The 7o$el 6ri9e was for a paper he wrote in ,?!C that descri$ed how phosphate is used $y yeast cells to convert glucose to ethanol and car$on dioxide. This process, "nown as fermentation (yep, the same one used in ma"ing $eer and wine), is the means $y which some chemicals seem to $e a$le to cause car$ohydrates first to decompose, and then to transform themselves into other su$stances altogether. In ,@?>, 'erman chemist )duard #uchner had proved that extracts of yeast that definitively contained no living organisms ($ecause he pulverised the yeast with a mortar and pestle $efore using it) were a$le to turn sugar into alcohol and car$on dioxide A something the wine industry had "nown at a practical level for millennia A $y adding phosphates. This proved that a chemical su$stance rather than a living organism in the yeast

was responsi$le for the fermentation. #uchner had called the su$stance 9ymase, $ut we "now these su$stances today as en9ymes. #uchner pic"ed up the ,?!> 7o$el 6ri9e in (hemistry for this discovery. In his fermentation experiments, Harden managed to separate out the 9ymase from the rest of the yeast mixture produced according to #uchner&s recipe. He proved that the 9ymase was in fact the thing that powered the fermenting. Without the 9ymase, the yeast was inert A nothing interesting happened no matter how much phosphate you added to it. If, however, phosphate and the en9yme were present, fermentation would proceed until all of the glucose was used up. The relevance of that o$servation wasn&t immediately o$vious, $ut it is credited with $eing the foundation stone of an important new $ranch of $iochemistry, intermediary meta$olism. This $ranch concentrates on the study of compounds that come into existence, often only very $riefly, during the course of many $iochemical reactions. Harden had found that an en9yme was critical to the chemical process called fermentation, which our $odies used to turn glucose into energy, $ut things were still a little misty $eyond that. In ,?=C, the same year Harden was "nighted for his wor", Herman 2alc"ar, a *anish $iochemist, confirmed the central role of an energy-carrying molecule in the fermentation process descri$ed $y Harden. 2alc"ar proved $y studying frog legs that phosphate compounds did produce energy. It&s a pity he wasn&t 3rench or I could have come up with all manner of amusing dou$le entendres at this point. He proved that he could get the muscles in frog legs to continue to contract using phosphates, even when they were cut off (literally) from their normal sources of energy. In ,? ,, 2alc"ar&s colla$orator, 3rit9 5ipmann, confirmed the existence of +T6 (adenosine triphosphate). 5ipmann was a

'erman $iochemist who received the 7o$el 6ri9e in 1edicine for his discovery in ,? < of an en9yme critical to the oxidation of fatty acids (the way our $ody converts fat to energy). 1ore important to our discussion at the moment, however, is his confirmation of the existence of +T6. +T6 is the energy highway of our $odyL it stores and transports energy. The glucose that is dragged into our cells through the '5/T receptors is converted into +T6 $y a chemical reaction involving phosphates and an en9yme. To release the energy, Fust add water and another en9yme. If an en9yme is present, water reacts with the +T6 to produce energy, another chemical called +*6 (adenosine diphosphate) and a phosphate. )very single day every one of us creates and destroys an amount of +T6 eGuivalent to our own $ody weight. The energy released $y that series of reactions is how we convert glucose into energy and what "eeps us powered up. That series of reactions is what $iochemists call glycolysis. +s Harden first proved, glycolysis does not happen unless the en9ymes are present. This means that controlling the en9ymes is a way to throttle the process, and it turns out this is exactly what the $ody does with its hormones. The hormones discussed earlier, in particular insulin and glucagon, activate or shut down these en9yme switches in our cells $y shuffling the en9yme molecules $etween the nucleus (where they are hidden from view) and the cell $oundary (where they can do their stuff). The exact chemistry of how +T6 is produced and used $y our cells had to wait until the &@!s and &?!s and is still su$Fect to ongoing study (the ,??> 7o$el 6ri9e in (hemistry went to fol"s studying +T6) A as I said at the start of this section and many have said $efore me, it always turns out to $e more complex than we thought ,! years ago. .ome of the more recent investigations have, however, shed some light on

differences $etween how glucose and fructose are treated in the process of glycolysis. These differences pretty solidly explain much of what doctors -ud"in and 0eiser saw happening to the rats they fed too much fructose in the &C!s and &>!s. 0emem$er that in order for the whole glycolysis process to "eep going the cells need a good supply of the right en9ymes. +s the good *r Harden found, no en9yme means no reaction and no energy. We have four en9ymes used for converting $lood sugars into energy. 8ne is a general-purpose en9yme that is availa$le in pretty much every cell in our $ody, and the other three are specialist en9ymes (one for each type of sugar) that are found only in our liver. Hexo"inase is the name of the general-purpose sugarconverting en9ymeL %hexo& $ecause all three sugars have molecules that loo" li"e hexagons. Hexo"inase is distri$uted throughout the $ody and theoretically could $e used to convert all three sugars into energy, $ut it doesn&t convert anything other than glucose. )ven though our cells could use hexo"inase to convert all that circulating fructose into energy, they don&t get the chance $ecause hexo"inase can only

+i ure -=$: How car$ohydrates end up $eing turned into energy.

$e used to convert whatever sugar actually gets inside the cell. 1ost of the healthy cells in our $ody do not possess the '5/T ('5/T; or '5/T<) proteins necessary to suc" fructose through the cell wall. +ll they have is ordinary old garden variety '5/T,, which only vacuums up glucose. '5/T, and hexo"inase provide our underlying %power on& state for all cells, and '5/T= does the same thing for the $rain. 3at cells also have plenty of hexo"inase $ut, instead of '5/T,, they have '5/T proteins, so they also only wor" on glucose. There&s a pec"ing order at the $lood glucose $uffet. #rain cells and ordinary cells get to eat first. Their '5/T protein wor"s whether there is insulin or not and they have an en9yme ready to convert the glucose they get into energy Fust to stay alive. Then, as insulin levels increase, fat and muscle cells get to dine $ecause insulin triggers their '5/T proteins. #ut neither '5/T,, '5/T= (the $rain) nor '5/T (fat and muscle) proteins are a$le to a$sor$ fructose. The fructose goes sailing merrily $y most of our cells A that is, until it gets to the liver. Things are different in the liver. 5iver cells are full of '5/T; proteins that can a$sor$ glucose and fructose. :ust li"e '5/T in the fat and muscle cells, '5/T; is sensitive to insulin. +s insulin levels rise, the '5/T; proteins suc" more and more glucose and fructose into liver cells. That&s where we find the three specialist en9ymes. The en9yme needed to use glucose is (not illogically) called gluco"inase (%ase& $eing the ending meaning en9yme). The one used for fructose is fructo"inase and, you guessed it, galacto"inase is for galactose. The primary function of gluco"inase is to convert excess $lood sugar into our temporary short-term $atteries (glycogen) and our longer-term energy stores (fatty acids). /nli"e hexo"inase, gluco"inase is not active all the time. +t normal pre-meal concentrations of $lood sugar, the liver is a net producer of glucose (using up the $atteries to "eep us humming along). It&s

only when $lood glucose and insulin start to rise after a meal that the liver starts to access the glucose in the $loodstream, using gluco"inase, to create short-term energy storage, the $ac"up energy it had $een using $efore you ate that doughnut. 'luco"inase needs insulin in order to function, and gluco"inase itself is less efficient than hexo"inase. These two facts together put the liver third in line at the $lood sugar $uffet.

#rain cells and normal cells will ta"e glucose if it&s there and use it immediately. 3at and muscle cells must wait until insulin "ic"s in $ut once it does they can compete eGually with the other cells. 5iver cells also have to wait for insulin $ut have a less powerful en9yme, which slows down their use of the glucose.

/nder normal conditions, the vast maFority of the glucose a$sor$ed $y the liver is converted to glycogen for storage, plus a little energy to "eep the whole mechanism wor"ing. If too much energy is created, a secondary process converts the excess into fatty acids, which are pumped out into our $loodstream. There is normally very little fatty acid production, $ecause there is a very important control point in the whole process. .o far, in an effort to "eep the process of glycolysis even remotely explaina$le, I&ve com$ined a lot of steps togetherL however, at this point it&s necessary to dive a little deeper. +round the middle of the progression from glucose to energy, *r 2alc"ar&s energy-transport molecule, +T6, is created. The en9yme used to create it is called (wait for it) phosphofructo"inase-, (632-,). 632-, is a gate"eeper that stops the liver ma"ing too much energy and fat. It creates +T6 (which eventually turns into energy if needed, with any leftovers $eing turned into fat), $ut if there is too much +T6 in

the cell, 632-, is deactivated. If +T6 is $eing used up Guic"ly, then there will $e relatively little of it in the cell and 632-, will $e switched on to ma"e some more. It&s a very simple and elegant feed$ac" mechanism that means that, in normal conditions, we are designed not to ma"e too much energy and therefore not to create excess circulating fatty acids out of the leftovers. '5/T; proteins in the liver are Fust as good at suc"ing fructose into the cells as they are at vacuuming up glucose. +t last, circulating fructose has found some cells that are happy to invite them inside. +nd once they get through the door, they find fructo"inase waiting with open arms. 3ructo"inase does not need insulin to start going to wor" on fructose. It starts converting it to +T6 immediately and rapidly. 4ery rapidly, in fact. 3ructose can $e a$sor$ed $y the liver twice as fast as glucose and it gets a significant head start as well, $ecause it doesn&t have to wait for insulin to fire it up. With fructose in the $lood, the liver can el$ow its way to the head of the $uffet line. The gut will process as much fructose as we put in our mouths, with no "nown limit. The liver has no competition for the fructose in the $lood. It&s the only maFor organ with the '5/T protein needed to drag it out of the $loodstream and the en9yme needed to convert it to energy. It doesn&t have to wait for insulin levels to rise $efore it can get started on the main course, and it can eat it up twice as fast as it can eat glucose. .ounds li"e a pretty efficient way to get energy A eating fructose is "ind of li"e throwing on the after$urners. There&s Fust one little pro$lemD it is a very small detail, $ut it might Fust $e the detail that lies $ehind a significant num$er of our modern health pro$lems, including the o$esity epidemic. When fructo"inase creates +T6, it $ypasses the step in the glycolysis process that is controlled $y 632-,. 0emem$er, the

632-, en9yme stops us getting fat on glucose. When too much +T6 is produced, 632-, switches off and stops the process. +s Harden found, no en9yme means no chemical reaction. 3ructose s"ips that critical regulatory step. It Fumps straight to +T6 with no regulation at all. If we have lots of fructose in our $lood, it automatically and rapidly overloads the +T6 production system of the liver. 8ur ever-efficient $odies don&t waste all that +T6L it Fust gets converted straight to fatty acids. .mall Guantities of fructose don&t have any serious effects. + little extra +T6 is created, which shuts down the glucose a$sorption until +T6 levels return to normal. #ut put a lot of fructose into that loop and it doesn&t matter how long the glucose system is shut down forL fructose will still "eep pumping up the +T6 volume and the fat production. That one little detail A that fructose $ypasses the glycolysis control mechanism in the liver A means that it directly creates vast amounts of circulating fatty acids (including 5*5 cholesterol).

Interesting research in ;!!= $y scientists from the *epartment of 1olecular 6hysiology and #iophysics at the 4ander$ilt /niversity in 7ashville, Tennessee, showed that fructose has exactly the same stimulatory effect on gluco"inase as insulin. #iochemists now $elieve that a small amount of fructose in the diet is necessary to get the glucose processing under way. .mall amounts of fructose appear to $e a sort of starter motor for our glucose digestion in the liver. The fructose acts to stimulate the gluco"inase activity in anticipation of the release of insulin $y the pancreas. .o we need a little fructose in our daily diet A pro$a$ly a$out the same amount as you would find in a couple of pieces of fruit. 3rom an evolutionary perspective, this pro$a$ly ma"es sense, since prior to a$out ,@=! that was Fust a$out the only way to get fructose into your tummy.

3ructose also s"ips the glucose-driven control mechanisms of

the pancreas. If we consume more fructose each day than what is found in one or two pieces of fruit, it is ignored $y the pancreas and no insulin is released in response to its consumption. This was the $ig discovery that inspired the +*+ to decree fructose as the preferred sweetener for dia$etics. #iochemistry has since caught up with o$servation and we now clearly understand why this is so. 5i"e the liver, the pancreas uses '5/T; transporters to a$sor$ $oth glucose and fructose. /nli"e the liver, the pancreas has almost no fructo"inase, which means that although the fructose is transported into the cell, it can&t $e used so it is washed straight $ac" out again. That, on its own, would $e nothing to worry a$out. It&s what&s going on in the liver that&s the dangerous part. 3ructose is $eing efficiently converted to fat faster than you can say phosphofructo"inase. Telling dia$etics (or anyone else) to eat pure fructose was, and is, an exceedingly dangerous thing to do. #ac" to the Guestion that started my hunt through the arcane world of molecular $iochemistry A what happens to all that fructoseM The answer appears to $e thisD it gets rapidly and totally converted to circulating fatty acids and manages to avoid all of our control mechanisms in the process. When we eat car$ohydrates, proteins and fat, insulin and ((2 tell us when to stop eating, and insulin and 632-, control the use of the glucose. There are no eGuivalent controls for fructose. When the only fructose in our diet was in ripe fruit, this didn&t matter much. We have enough fructose sensors in our pancreas to trigger an insulin response in the Guantities found in a few pieces of fruit. It is only when we over-consume fructose that the %loophole& in our appetite-control mechanism opens up. In a modern diet, where most food is now flavoured with fructose compounds (li"e sugar and high-fructose corn syrup), this is a recipe for o$esity and much worse.

+s far as our pancreas is concerned, fructose Foules(calories) are largely invisi$le. Insulin release is not triggered $y its consumption. )arlier I descri$ed the 'I diets, which $ecame popular in the last decade. -ou&ll remem$er that the theory $ehind a 'I diet (for people who aren&t dia$etic) is that, $ecause the food has a low 'I, insulin is not

+i ure -=%: The fructose loophole in our appetite-control system.

released and fat storage is inhi$ited. Insulin is, however, only used for converting glucose into fat. It is not reGuired to convert circulating fatty acids into fat. If we eat a high-fructose diet, the fructose will $e converted directly to fatty acids and, in turn, $ody fat. 'iven the choice, our fat cells would much rather store circulating fatty acids as fat than go to all the trou$le of converting glucose to $ody fat using insulin. It only ta"es ;.< Foules(calories) to convert ,!! Foules(calories) of

fatty acids into $ody fat. It ta"es ;= Foules(calories) (,! times as much energy) to convert ,!! Foules(calories) of protein or glucose into $ody fat. .o, given the choice, our $odies will store fatty acids every time, that $eing the more energyefficient course to follow. That&s a lot of $iochemical mum$o Fum$o to a$sor$ in one sitting, so let&s recap. We have one primary appetite-control centre in our $rain called the hypothalamus. It reacts to four maFor appetite hormones. Three of them (insulin, leptin and ((2) tell us when we have had enough to eat, and one of them (ghrelin) temporarily inhi$its the effect of the other three and tells us that we need to eat. )very piece of food we consume stimulates the release of one or more of the %enough to eat& hormones once we have had enough to eat. There is one su$stance that does not stimulate the release of any of the %enough to eat& hormones. That su$stance is fructose. 3ructose s"ips the fat-creation control mechanism in the liver (632-,) and is directly converted to fatty acids (and then $ody fat) without passing through either of our maFor appetite-control gateways (insulin or ((2). 3ructose is also invisi$le to our $uilt-in Foule(calorie) counter (the hypothalamus). We can eat as much fructose as we can shove down our throats and never feel full for long. )very gram of the fructose we eat is directly converted to fat. There is no mystery to the o$esity epidemic when you "now those simple facts. It is impossi$le not to get fat on a diet infused with fructose.

0= &ONE; WIT&O)T .EES

The message from the accumulation of all the research I had $een reading was clear A fructose $ypasses all of our appetitecontrol systems and Fumps a critical step in our meta$olism that would ordinarily stop our arteries filling up with circulating fat. )ating fat still puts fat in our arteries, $ut we have a $uilt-in control to stop us eating too much fat. 7o such control exists for fructose. I could see that eating fructose could $e really $ad news. #ut how much fructose were we actually eatingM .urgeon-(aptain (leave&s graph certainly suggested we were eating a lot more sugar than at the turn of the century, and sugar is half fructose. #ut his graph only went up to ,?<<. I decided to find out more a$out whether fructose was really a factor in the modern diet. 1ost of the rat studies I read a$out had used fairly large doses of fructose to produce the results they did. +fter reading many newspaper articles a$out medical %discoveries&, I had come to the conclusion you could induce cancer in a rat $y feeding it Fust a$out anything in a large enough dose. Were we really eating that much fructoseM +s we "now, fructose is what ma"es fruit sweet. It&s no coincidence that the most popular fruits today are the sweetesttasting ones. They are also the ones highest in fructose. .o fruit and vegeta$les are a source of fructose, $ut not a very rich source. )ven the sweetest fruit (the hum$le apple) contains less than @ per cent fructose $y weight. 6ut another way, the average apple contains a$out the same amount of fructose as ; teaspoons of sugar. The /. *epartment of +griculture has "ept detailed statistics on total /. fruit and vegeta$le consumption since ,?>!, and the limited statistics availa$le in +ustralia

show similar trends A an increase in consumption, driven largely $y an industry that has only really existed since the ,? !s, the pac"aged Fuice $usiness. In ,@C?, a 7ew :ersey dentist and communion steward at his local church, Thomas Welch, successfully applied 5ouis 6asteur&s principles of pasteurisation (discovered Fust seven years earlier) to

+i ure 0=1: The average fructose content $y weight of popular fresh fruits and vegeta$les, $ased on Guantities measured $y the /.*+.

grape Fuice. 6asteurisation involves heating liGuids Fust enough to "ill most micro-organisms $ut not so much as to sterilise them $y $oiling, which usually destroys the taste as well. /ntil that point the only way to enFoy grape Fuice was to $e there as it was stomped out of the grapes or wait a few years and enFoy the fermented variety that came in a $ottle with a cor". *r Welch had a strong motivation for his wor". His invention meant that he didn&t have to freshly sGuee9e the grapes every communion .unday. *r Welch&s son (harles (also a dentist)

decided there was more potential in the production of grape Fuice than supplying the local altar. +fter rave reviews from the Fuice-sipping pu$lic at the (hicago World&s 3air in ,@?=, (harles threw in his dental practice and concentrated on the Fuice $usiness full time. 3or some reason, the /. government thought their sailors might $e more effective warriors if they weren&t drun", so when the /. 7avy su$stituted grape Fuice for wine on all its vessels in ,?, , the grape Fuice industry came into its own. 6eople had tried pasteurising all sorts of other fruit and vegeta$le Fuices with no success, $ut $y ,?;>, the Welch :uice (ompany was a$le to extend the methods to tomatoes, and the first non-grape Fuice rolled off the production lines. 1eanwhile, in )vanston, Illinois, W' 6eacoc" applied the Welch pasteurisation methods to a range of vegeta$les, creating the 4ege-1in line of Fuices, $ut they were not exactly flying off the shelves until he decided in ,?== to com$ine eight of them into a drin" he called 4ege-1in @. 4ege-1in @ didn&t taste great $ut, at the suggestion of a local grocer, he changed the name to 4-@ :uice, added some sugar and increased the amount of tomato Fuice in the mix. .ales of the new 4-@ drin", which was almost ?! per cent tomato Fuice, really too" off in ,?=C. 1eanwhile, over in (alifornia, the methods used to produce tomato Fuice were $eing applied to a potentially vastly more lucrative fruit crop, the orange. #y the early ,? !s, large-scale commercial production of pac"aged orange Fuice was possi$le and the Fuicing industry has not loo"ed $ac". .ince then, vegeta$le- and fruit-Fuice consumption has risen steadily. 3rom a $ase of 9ero in ,? !, the average /. citi9en was consuming =5 of fruit Fuice every year $y ;!!;. The average +ustralian consumed a more moderate =<5 per person per year, $ut it had nevertheless $ecome a significant addition to the modern diet. +nd that was $efore the advent of the modern-day %Fuice $ar&, which has increased +ustralian fruit Fuice sales $y over C! per

cent from ;!!= to ;!!>. 4egeta$le Fuice consumption grew even more rapidly. 3rom a standing start in ,?==, +mericans were gulping down @,5 of vegeta$le (?! per cent tomato) Fuice per annum $y ;!!<. :uicing converts fruit and vegeta$les from a food source containing significant fi$re mass, flavoured with fructose, to one containing little other than fructose and water A oh, and some vitamin (.

+i ure 0=$: Total /. fruit and vegeta$le consumption ,?>!A;!!< A $ased on /.*+ data A most of which relates to accelerating consumption of Fuices.

While our use of fruit and vegeta$les has increased slightly overall, it has $een due largely to increased Fuice consumption against a $ac"ground of falling whole fruit and vegeta$le consumption. We are applying our intellectual and industrial muscle to ma"e sure we extract the sweetness from the food

and then throw the rest away. 1on"eys on the plains of +frica would do the same if they could, $ut there is nowhere to plug in their Fuicing machines. We have, in the last C! years or so, $ecome very good at getting Fust the $it we are really interested in and discarding the rest. Increasing Fuice consumption is certainly increasing the rate of fructose consumption, $ut it is $y no means the maFor source of this dangerous su$stance in the modern diet. 5ong ago, our ingenious fore$ears figured out an even more efficient way to extract sweetness from plants, store it and then add it to all of our food. Why hunt for ripe apples and $ananas to put in your Fuicer, when you could ma"e anything as sweet as you wantedM +$out ?!!! years ago, Fust as the )gyptians were thin"ing seriously a$out odd-shaped $uildings and the (hinese were putting in the groundwor" for the firewor"s that would $e needed for the -ear ;!!! cele$rations, some fol"s in 6apua 7ew 'uinea detected something that would ultimately affect every person on the planet. They noticed that one of the native grasses was very sweet-tasting. In fact, it was more than twice as sweet as the nearest fruit availa$le to those tri$espeople, the $anana. 1odern analysis reveals that the grass, which grows ; to C metres tall, contains ,< per cent fructose $y weight. The 6apuan highlanders didn&t ta"e the discovery much further than realising that suc"ing on a sugarcane stem was a nice way to pass the monsoon, $ut slowly, sugarcane gained popularity as a good thing to have growing around the village. We now "now that once refined and concentrated, sugar is more than six times as sweet as an apple, the sweetest commonly occurring fruit. 0efined sugar&s <! per cent fructose content, com$ined with our lust for sweetness, ensured that sugarcane $ecame one of our earliest successful experiments in cultivation. 8ver the next ;!!! years, its fame slowly spread from island to island, finally ma"ing its way to the outer arms

of the Hindu empires of Indonesia, from where it swiftly leapt to India. While there was always a ready mar"et for the sweet grass, it was hard to transport without it going $ad (it was, after all, Fust grass A imagine what your grass clippings would loo" li"e after a few months at sea), so you had to live in its native tropics to $enefit. +$out seven millennia ago, some fol"s in India figured out that crushing the stems of the giant grass produced a very sweet %Fuice&. Its sap is pure sucrose (ta$le sugar) dissolved in water. The sap was a delicacy used much li"e honey (and often in place of it) to sweeten foods. When the greatest 'ree" general of all time, +lexander the 'reat, conGuered the 6unFa$ in =;> #(), his troops $rought the secret of the reed that produced %honey without $ees& $ac" to their 1editerranean homeland. They called it sak'har. #y the year =!! our Indian friends had discovered that if they dried the sap, they were left with a very tasty crystal that could $e added to any food to ma"e it sweet. )ven more importantly, dried sugar crystals lasted much $etter than cane or sap on long sea voyages. 6rogrammed as we are for sweetness, cultivating sugarcane naturally $ecame a very high priority and crystallised sugar suddenly $ecame a valua$le and highly trada$le %spice&. #y < !, the 6ersians (modern-day Iranians) had learned the Indian secrets of ma"ing sak'har. 7ot unsurprisingly, the +ra$ians decided that sugar production was a s"ill that was worth copying when their armies conGuered 6ersia in C ,. The +ra$ian armies too" the secrets with them so when they invaded .icily in @!!, one of the first crops to $e planted was sugarcane. .ugar mills were set up and a $ris" trade in the white gold was esta$lished all across the +ra$ian lands. When the (hristian crusades rolled through the holy lands at the $eginning of the second millennium, one of the treasures they too" $ac" to )ngland was the secret of sugar.

In )ngland, for many centuries, sugar was an expensive commodity. 7evertheless, demand for sugar was irrepressi$le. #y ,;<? it was readily availa$le if you had the money (the eGuivalent of Q;@< per "ilo). .ugar certainly wasn&t cheap $ut, if you had the cash, there was plenty you could do with it. (ulinary discoveries flooded in from the +mericas in the , !!s and ,<!!s. (offee, tea and chocolate were all $itter on their own, $ut add a little sugar and, voilR, suddenly you have luxurious new treats. 8nly ,< per cent of soup recipes in coo"$oo"s from the ,<!!s included sweet ingredients, and those that did mostly added honey. #ut the incessant demand for sugar made it profita$le to $ring more and more of the product into the mar"et, which in turn drove the price down. #y the ,@!!s almost half of all pu$lished soup recipes were sweetened.

+i ure 0=%: )nglish retail price of sugar , !!A,?C! in ;!!> +ustralian dollars A no wonder it was descri$ed as %white gold& in the , !!s.

In , !!, sugar was still way too expensive for the average peasant on the street, $ut the price was coming down Guic"ly as )ngland&s empire expanded to include tropical lands where sugarcane grew in natural a$undance. #y the middle of the ,<th century there were plantations in 1adeira, the (anary Islands and .t Thomas, supplying )urope with sugar. #y the end of the ,Cth century, sugar farming and milling had spread over the greater part of tropical +merica, followed in the next century $y the development of sugar exports from the West Indies. The demand for sugar was one of the maFor reasons for the slave trade for two centuries or more A cutting down <metre-high cane fields reGuires a lot of very cheap la$our. #ritain too" :amaica and other parts of the West Indies from .pain in ,C<< and from then on $ecame heavily involved in the sugar industry. #y ,><! there were ,;! sugar refineries operating in #ritain. Their com$ined annual output was still only =! !!! tons $ut the enormous demand ensured sugar was extremely profita$le. 6rofita$le commodities attract the tax man li"e moths to a flame. )very government since the 0omans had ensured that sugar filled the coffers with gold (which is why, today, we have such excellent records of the growth of the sugar industry). In #ritain, for instance, annual sugar tax receipts in ,>@, totalled Q<! million in today&s terms, and grew tenfold to over half a $illion dollars in the three decades that followed. #y ,@> , the pu$lic&s demand for reasona$le sugar prices could no longer $e repressed and the #ritish government was forced to a$olish the sugar tax. 3or the first time ever, the ordinary citi9ens of the )mpire could afford to eat sugar (it was still the eGuivalent of Q;< a "ilo, so they still weren&t sprin"ling it on their cereal, $ut at least now they could use it on special occasions). 5ower prices and the resulting mass-mar"et demand meant that

industrial-scale production could accelerate. 1any of today&s ta"en-for-granted foods such as confectionery, ca"es and $iscuits, as well as sweetened drin"s, were invented and popularised towards the end of the nineteenth century around sugar as a maFor ingredient (which $y then cost %Fust& Q> a "ilo). 6russia (a region located approximately in modern-day 'ermany) was not terri$ly happy a$out the state of affairs in the sugarcane trade. It didn&t own any tropical territories to spea" of and this meant that if 6russians wanted sugar (and they did, of course), they had to $uy it from one of their )uropean cousins after paying a suita$le %tax&. This was intermittently complicated $y $eing at war with said cousins. The 6russians decided they needed an alternative to sugarcane that could $e grown in nice handy places li"e, say, northern )urope, rather than having to travel to irritatingly hot places, controlled $y enemies of the state, Fust to get some sugar in their coffee. 6russian scientists were immediately set the tas" of testing all availa$le northern )uropean plants to find a replacement for sugarcane. In ,> >, 3ran9 +chard succeeded in identifying the $eet species as the one with the maximum sugar content. #y the start of the nineteenth century, 'erman sugar $eet crops $egan delivering good enough yields to allow )uropean-grown plants to compete with imported sugarcane as a source of the %white gold&. 7elson&s victory at Trafalgar in ,@!< and the ensuing naval $loc"ade of )urope guaranteed that sugar $eet $ecame the source of sugar for continental )urope from then on. #y ,@C!, such was the demand for sugar that 'ermany changed from $eing a net importer of sugar to an exporter. In the /nited .tates, sugarcane cultivation $egan in the tropical climate of 7ew 8rleans in the eighteenth century. )arly attempts to create a sugar industry in the /nited .tates did not

fare well. 3rom the late ,@=!s, when the first factory was $uilt, until the ,@>!s, sugar factories closed down almost as Guic"ly as they opened. +nd attempts to create a home-grown sugar industry weren&t helped $y the destruction of the sugar industry in the 'ulf states during the /. (ivil War. 3inally, in ,@>;, a (alifornian factory was a$le profita$ly to produce sugar in significant Guantities. +fter that sha"y start, the /. sugar industry grew at $rea"nec" speed. +t the dawn of the twentieth century, more than =! factories were in operation in the /nited .tates. .ugar arrived in +ustralia with the first convicts in ,>@@. The 3irst 3leet pic"ed up some sugarcane on the way past .outh +frica and planted the first crop at 6ort 1acGuarie. +s with the rest of the world, actually producing sugar in commercial Guantities proved difficult until the first via$le mill got going at Hastings, 7ew .outh Wales, in ,@C>. #y ,@C@, there were nine mills producing C! tons of sugar a year in 7ew .outh Wales. The $y then separate colony of Nueensland produced =! tons of sugar that year. #y ,@@<, there were ,!; mills in 7ew .outh Wales and ,CC in Nueensland. Nueensland had the advantage of cheap (virtually free) indentured la$our from 6olynesia to wor" the plantations. #y ,?; , +ustralia was producing more sugar than it could consume and exporting commenced. #y the end of World War II, +ustralia was producing ?<! !!! tons per annum. #y ,?< , it was ,.= million tons and $y ,?@! this had more than dou$led again to = million tonnes. #y ;!!!, +ustralia was producing more than .C million tonnes (worth Q,.; $illion) of sugar a year. Today, @< per cent of +ustralia&s sugar crop is exported, ma"ing +ustralia the second-largest sugar exporter in the world, $ehind #ra9il. )very$ody really li"ed the sweet stuff. *emand for sugar grew more Guic"ly than even the exponential growth in world population. In the ,@=!s, when the world population had Fust passed , $illion, sugar production was a$out @!!g per year for

every person in the world. #y the mid-,?>!s, with the population standing at Fust over $illion, world sugar production stood at ;!"g for every man, woman and child on the planet. 6eople were $y then consuming ;< times as much sugar as their great-granddaddy had Fust , ! years earlier. The inFection of cane (and eventually $eet) sugar into the western diet introduced a significant new source of fructose for the first time in the evolutionary history of humans. +t the start of the nineteenth century, annual average fructose consumption was less than a "ilo a year, sourced almost entirely from eating fresh fruit, and honey for the occasional treat (honey was neither cheap nor plentiful). #y ,@@<, every adult over the age of ;! in the /nited .tates was consuming ,="g of added fructose in the form of ;<"g of sugar, a su$stance that their parents had never even seen, let alone tasted. #y ,?!? /. sugar consumption had almost dou$led again to nearly !"g per person per year, and $y the early ,?=!s, +mericans were eating almost <!"g of sugar per year. +nd that&s where our fructose consumption pro$a$ly would have stayed had it not $een for the invention of some interesting new ways to add fructose to our diet. 3rom ,?=! to ,?>!, sugar consumption plateaued at Fust under <!"g per year (except for some rationing caused $y World War II, which saw consumption fall). 8$viously we had added sugar to Fust a$out everything that we wanted sweetened. There seemed to $e a natural limit to how sweet we wanted our food to $e. 6rice was no longer the issue. +t less than Q, per "ilo, any$ody could afford to eat nothing $ut sugar if they wanted to. (learly (as any mother of an engorged two-year-old will tell you) you can eat only so many lollies, $iscuits and ca"es $efore you get sic". If you had wanted a cool drin" on a hot summer&s day in ,@@C in downtown +tlanta, 'eorgia, you wouldn&t have had many options. The introduction of prohi$ition earlier in the year

meant that $eer and anything harder was out. .o you might have $een tempted to wander into :aco$&s 6harmacy (the largest in town) and head for the soda fountain for a long glass of car$onated water, what we call soda water today. .oda water was considered to $e $eneficial to general well$eing and soda fountains had $ecome very popular. That summer, for the first time ever, you would also have $een a$le to $uy (for the grand sum of < cents A Q,.=! in ;!!> +ustralian dollars), a glass of *r 6em$erton&s 3rench Wine (oca, a nerve tonic, stimulant and headache remedy. The (oca was a syrupy sweet $rown liGuid that had a tangy taste reminiscent of caramel and vanilla, with a little "ic" from the crushed leaves of the coca plant (perhaps more famous today for its other product, nose candy) and caffeine-rich "ola nuts. +$out six months later, an enterprising soda Fer" decided to Fa99 up his soda water $y adding *r 6em$erton&s syrup to the glass. (oca-(ola was $orn. Ten litres of (oca-(ola syrup was made $y mixing up ,. "g of sugar with >.<5 of water and a series of secret flavouring ingredients that included caramel, vanilla, coca leaves and "ola nuts. Today, ,.; $illion serves of it are sold every year. (oca-(ola A today consisting essentially of sugar, flavouring and car$onated water A was one of the first flavoured %soft& drin" concoctions, $ut it was $y no means the only one. #y the turn of the twentieth century, there were over a hundred different $rands of car$onated soft drin" on sale in the /nited .tates, with the most popular flavour $eing ginger ale. Turning the flavoured syrup into the fi99y drin" we "now today was simply a matter of adding five parts soda water to one part syrup. It was a recipe that lent itself to very efficient distri$ution. Instead of shipping the end product around the country, pharmacies and ($y ,@@?) $ottlers could $e sent $arrels of syrup that they could mix with water for local sales. #ottled soft drin"s were immediately popular with the $uying pu$lic A now they could ta"e them home and enFoy their

favourite %soda& any time they wished A $ut it was not until ,?;@ that $ottle sales outstripped soda fountain sales. #y the end of World War II, the average +merican was drin"ing =@5 of car$onated soft drin" every year. That alone accounted for of the "g (? per cent) of sugar they were then consuming every year. Two decades later, in ,?C<, they were drin"ing twice as much soft drin" and it accounted for @ of the "g (,@ per cent) of sugar they were consuming every year. 5iGuid sugar was Guic"ly replacing confectionery as the primary source of sugar in the +merican diet. #y ,?@<, softdrin" consumption had dou$led again, $ut the availa$ility of new low-Foule(calorie) sugar su$stitutes meant that only threeGuarters of the drin"s sold were %full strength&. .oaring world sugar prices and a plummeting mar"et for corn during the ,?C!s and &>!s drove the /. corn industry to invest heavily in promising research focused on converting cornstarch-derived glucose into the much sweeter, and therefore more valua$le, fructose. In ,?C@, the first commercial shipment of high-fructose corn syrup (H3(.) capa$le of $eing used as a sugar su$stitute hit the mar"et. In Fust two decades it displaced cane sugar as +merica&s primary source of fructose. Today ; per cent of all corn grown in the /nited .tates goes into the manufacture of H3(.. This has occurred in no small measure $ecause the ma"ers of (o"e and 6epsi, who $etween them purchased almost ;! per cent of all sugar sold in the /nited .tates at the time, decided to switch from sugar to H3(. in the early ,?@!s. The relatively low cost of H3(. ena$led food companies to %super-si9e& food portions, particularly drin"s, at little cost, increasing profits and perceived value for customers. H3(. fast $ecame the primary sweetener for manufactured food products in the /nited .tates. #y ,?@<, +mericans were consuming ,C"g of sugar (or H3(.) from soft drin" every single year. Total sugar and H3(.

consumption was only slightly higher, at C"g, $ut full-strength soft drin" now represented =< per cent of the sugar the average +merican consumed in a year. #y the turn of the century, +mericans were consuming ;C"g of H3(. in soft drin"s, $ut $y now +merica had moved off the sweetness plateau and total sugar consumption had also increased. 7evertheless, soft drin"s still represented per cent of the C!"g of sugar consumed $y the average +merican in a year. In ,@>!, the only way anyone could eat any significant amount of fructose was either to $e the "ing of )ngland (or a close relative), or to come into the small fortune reGuired to $uy sugar or honey. +lternatively, you could $uy a lot of fruit and Fuice it yourself. Whichever way you cut it, money was reGuired. There was no cheap or easy way to eat fructose in any "ind of Guantity. #ut ,=! years later, the average +merican was eating =="g of fructose every

+i ure 0=(D Total per capita /. fructose consumption $y source A the amount of added fructose went from nothing in ,@>! to over =!"g per year $y the year ;!!!.

single year Fust from sugar, H3(. and fruit Fuices. +nd that was $efore you started counting consumption from honey and syrups (together a further "ilo per annum). .tatistics on +ustralian fructose consumption are harder to come across. We don&t have an eGuivalent of the /. *epartment of +griculture fastidiously compiling %food disappearance data&. #ut from the data we do have, our consumption is significantly lower than in the /nited .tates. In ,???, every person in +ustralia ate Fust under =@"g of sugar. This seems mostly to $e related to the fact that we drin" only half as much car$onated soft drin" as our +merican friends. #ut we are catching up fast. .oft-drin" consumption increased $y =! per cent in the &?!s alone. We prefer to support our cane farmers rather than our corn farmers, so very little H3(. is used in +ustralia. +dd the fructose from the sugar (,?"g) to the =.<"g we were getting from Fuices, and it means +ustralians were consuming a$out ;;.<"g of fructose $y the turn of the twenty-first century. It&s not as $ad as the =="g the +mericans were gu99ling, $ut it&s still an awful lot more than the less than 9ero "ilos of added fructose we were eating ,=! years $efore that. + lot of the people conducting experiments on rats had $een criticised for giving the animals unrealistically high doses of fructose. %8f course the rat would die. 5oo" how much fructose you gave it,& would $e the cry. %7o person actually eats that much fructose.& These figures tell a different story. )very man, woman and child in the /nited .tates (and +ustralia) is eating that much fructose and more. The /.*+ rats were actually on lower fructose diets than most of the people feeding them. This was getting really scary. If we were all really eating that

much fructose, and fructose really had the effects on us that the medical research suggested, we were in real trou$le. 'iven that the average +merican adult was eating =="g of fructose every year, and that since fructose su$verts our appetite control and creates fat immediately, =="g would $e directly converted to almost ,<"g of $ody fat every year, it was a significant miracle that every$ody in the country wasn&t clinically o$ese already. +ll the gyms, fitness cra9es and diets were wor"ing to "eep the inflation at a lower rate, $ut %pushing water uphill with a ra"e& was a phrase that sprang to mind when they were viewed in the context of the fructose tidal wave. +nd while no-one was having to install larger seats in our airplanes to accommodate most +ustralians, the data suggested we were heading in that direction.

2= PO::IDGE IN T&E A:TE:IES

I was clinically o$ese when I started trying to understand the o$scure world of medical research. I wanted to find out why I was fat and how I could reverse the process. Through many years of trial and error I had found out the hard way that nothing any diet guru said was ever li"ely to ma"e any difference. 1y research had spurred me on to discover what William #anting had found ,<! years $efore me A lowcar$ohydrate diets (li"e +t"ins) were different. They wor"ed, $ut were impossi$le to stic" to in the long term unless I was prepared to transplant myself to a society that Fust ate meat (li"e the +las"an Inuit $efore the western world showed them a %$etter way&). #ut the research had revealed a lot more to me than why I was fat. + lot of those rat experiments were telling me that $eing fat was the least of my worries. .ure, fructose was ma"ing me fat, $ut these rats were suffering far worse fates than $eing giggled at $y the other rats at the gym. They were dying of truly horri$le diseases. *iseases that sounded li"e those that I had $een reading a$out more and more in the newspaper. Things li"e heart disease, dia$etes, stro"e, liver cancer, pancreatic cancer and $reast cancer. I decided to do some digging on what research had $een done on the association $etween some of these diseases and fructose consumption. The o$vious place to start was o$esity. It&s the uneGuivocal sign that something is going wrong with our $ody. There is a lot of tal" a$out the o$esity epidemic in the media today, $ut rather than rely on the hype, I wanted to sort out exactly how fat we were all getting and how fast. 0esearchers measure the extent to which we are overweight using a standard measure called the $ody mass index, or #1I. 8ur #1I is a num$er calculated from our weight in "ilograms

divided $y the sGuare of our height in centimetres.

The #1I formula was invented in a$out ,@=< $y #elgian mathematician and astronomer 5am$ert Nuetelet. Nuetelet was also responsi$le for starting 3lorence 7ightingale on her one-woman crusade that changed the way sic" people are cared for. He felt very strongly that pro$a$ility should $e applied to all sciences where there was an element of o$servation. .ince a$solute certainty was impossi$le when loo"ing at large num$ers of stars, roc"s, animals or people, $eing a$le to apply pro$a$ilities rather than precise measurements would $e handy. His theory was that people&s measurements varied only so much. If you line up ,!! people you would $e extremely unli"ely to come across anyone who was ,! metres tall. The height of a person varied within a range of limits that could $e measured $y loo"ing at a sample of the population. 8nce he had the sample num$ers he could apply his new pro$a$ility theory to give an estimate of how many people in the whole population were what height. The same process could $e applied to other measurements, such as weight. In ,@;<, Nuetelet started pu$lishing papers on what he called social statisticsD studies on crime rates, $irth, death and marriage rates, and human physical appearance. He was the first to collect large amounts of data on these su$Fects and apply statistical methods to them. To ensure he had a standard $asis for comparison for the data he was collecting a$out human height and weight, he devised the Nuetelet index and pu$lished it in ,@=< in what was the first statistical population study of human appearance. The index allowed Nuetelet to compare directly the weight of two people of different heights and genders. The Nuetelet index is now called the $ody mass index, or #1I.

#1I provides a relia$le indicator of the amount of $ody fat for most people. +n adult is considered overweight when their #1I lies in the range ;< to ;?.?, and o$ese when it is =! or more. I am ,.@m (< feet ,, inches) tall. When I started loo"ing for answers, I weighed in at a hefty ,;!"g. +ccording to the #1I

graph (over the page), I was well into the o$ese 9one. +s I write this, I am @!"g, which means that I have Fust slipped into the top of the normal 9one. The #1I is not a definitive tool that should $e applied strictly. It was developed as a way of statistically comparing large populations of individuals, not as a method for individual diagnosis. There could $e all manner of reasons why a particular person is outside a given $and in the #1I chart $ut not actually over- or underweight. #ody composition, for example the amount of muscle versus fat, will affect the measure. 1uscle is denser than fat so elite athletes will record higher #1I num$ers than the rest of us. #ut $eing mista"en for an elite athlete has never $een one of my pro$lems.

+i ure 2=1: The #1I chart A simply locate the point where your height crosses with your weight to see which range your #1I lies in.

0ace can also ma"e a difference. (aucasians and people of +frican descent can rely on the #1I as $eing fairly accurate, $ut the World Health 8rgani9ation has recently recommended that for people with a .outh-)ast +sian $ody type, the cut-off $etween healthy and overweight should $e lowered from ;< to ;=. That $eing said, the #1I is a fairly relia$le indicator of population trends and a very solid indicator of how we measure up as a population. It also provides a relatively accurate way of comparing the population over time $ecause even if the #1I wasn&t explicitly calculated when the data was collected, most health surveys do record weight and height statistics, which allows #1Is to $e calculated long after the research has $een pu$lished and the participants have gone home (although you have to watch out for the studies where these were selfreported rather than measured A we are all taller and thinner when we fill in survey forms). #1I ranges are $ased on adult si9ings. #1I figures are different for children and are dependent on their age. +s a general rule of thum$, a two-year-old child is regarded as o$ese when their #1I hits ,@ (rather than =! for an adult). +nd that threshold increases gradually until an ,@-year-old has the same limit as an adult. If you loo" at #1I calculations over time you Guic"ly realise that the o$esity epidemic is very real and is a very recent phenomenon. The /nited .tates has $een "eeping comprehensive health data on their population for longer than most other nations, so a lot of the examples I use are $ased on their data. +s the rest of the world started to catch up, we got $etter at "eeping statistics, so where I can, I have supplemented the /. data with more modern examples from the rest of the world. In ,?,!, Fust over one in five /. adults was overweight and fewer than one in five of those people was o$ese (one in ;< for

the whole population). 5ess than a century later, two out of every three /. adults are overweight and half of those people are now o$ese (one-third of the whole population). In less than ,!! years, the chances of a given /. adult $eing overweight have gone from very unli"ely to highly pro$a$le, and the trend is accelerating. It too" half a century to dou$le the percentage of overweight people in the /. population. 3orty years later, it had almost dou$led again. If the o$esity epidemic continues at its current pace, four out of five of the /. 'eneration S ($orn ,?CCA,?><) will $e o$ese (not Fust overweight A o$ese) $y age >!, in around ;!=C. #y then, a person with a normal #1I will $e as rare as an eight-leaf clover. *on&t laugh too loud at the +mericans. In +ustralia, our statistics are Fust as shoc"ing. #y the year ;!!!, Fust over C! per cent of the +ustralian adult population was overweight or o$ese. In ;!!!, one

+i ure 2=$: The percentage of overweight and o$ese adults in the /nited .tates, as recorded in intermittent studies. In the space of less than a century, the num$er of overweight people has tripled, and the num$er of them that are o$ese is seven times as high.

in five adults in +ustralia was clinically o$ese. :ust two decades earlier, only one in , +ustralian adults was o$ese. We aren&t yet at the /. $enchmar" of one in three, $ut we are eating hard to get there. We are now statistically more li"ely to $e overweight than not. +ccording to the World Health 8rgani9ation, a $illion of the world&s C $illion people are now considered overweight and =! per cent of those people are o$ese. The vast maFority are concentrated in the /nited .tates and )urope, $ut the rest of the world is catching up fast. In )urope it&s almost one in two A ;!! million A adults that is measura$ly overweight. )ven in )uropean countries where o$esity is less prevalent, the percentage has increased steadily in recent times. In 3rance, with a population of Fust over C! million, <.? million people are o$ese today, whereas the figure Fust ,! years ago was only =.C million. In (hina, more than ;! per cent of the people in certain cities (the westernised ones) are now classified as seriously overweight. This acceleration in weight gain is not limited to adults. The percentage of young people in the /nited .tates who are overweight has more than tripled since ,?@!. +mong children and teens aged six to ,? years, ,C per cent (over ? million young people) are considered overweight. There are a$out , million overweight pre-teen children in the )uropean /nion and at least = million of them are o$ese, according to a recent study $y the International Tas" 3orce on 8$esity. In 6ortugal, for example, more than =! per cent of nine-to ,C-year-olds are o$ese, three times more than a decade ago. +pproximately < to > per cent of +ustralian children are currently estimated to $e o$ese.

5i"e you, I had heard all these num$ers (or something li"e them) $efore. #arely a news $ulletin goes $y without some politician $leating a$out how fat we are all getting or some nutritional genius telling us a$out the next great discovery that will stop us getting fat. -ou stop hearing the detail and the fact that we are all getting fatter $ecomes $ac"ground noise. #ut once I understood where the fat was coming from A fructose A I started paying attention. We were getting fatter, a lot fatter A and very, very Guic"ly. If o$esity was a disease li"e $ird flu, we&d $e $un"ered down with a shotgun and three years& supply of $a"ed $eans in the garage. #ut no$ody actually dies from o$esity itself. -ou never hear of anyone $eing pronounced dead from $eing fat. 7o, people die from other diseases that may or may not $e related to $eing fat, li"e cardiovascular disease (heart attac" and stro"e), "idney failure or various cancers. 8$esity is a symptom, not a disease. .ome diseases are directly related to increased $ody mass, such as osteoarthritis and fractures (due to increased pressure on Foints and $ones), hernia and sleep apnoea (the treatment for which is $ecoming a huge industry), $ut these are relatively insignificant when compared with the mass murderers of modern society. The $iggest "iller in +ustralia today is cardiovascular disease ((4*). It is almost completely attri$uta$le to $loc"ed arteries, or, more medically, atherosclerosis (from the 'ree" athera, meaning porridge A $ecause that&s what it loo"s li"e A and skleros, meaning hard, leading to the rather descriptive %arterial hardness caused $y porridge&. .ounds $etter in 'ree", doesn&t itM). These $loc"ages are formed from the exact fatty acids created in overa$undance $y the consumption of fructose. The percentage of the population suffering from these diseases has risen in direct parallel (with a <<-year time lag) with the acceleration in fructose consumption. In +ustralia, @,!!! people will die from a (4* this year, over

=! times as many as will die in a car accident and over =!! times as many as will die from +I*.. In the /nited .tates, around C<! !!! people will die from a (4* this year. 8ne and a half million +ustralians are estimated to $e living with a disa$ility associated with a (4*. The name of the particular (4* that threatens or ta"es your life depends largely on which maFor organ is near$y the %porridge& $loc"ing your artery. The organ system needing treatment also determines which type of specialist operates on you (if you ma"e it to the hospital). 8ne (4* alone, ischaemic heart disease (IH*), is responsi$le for C= per cent of the (4* deaths in +ustralia today. IH* is also often referred to as coronary heart disease, or (H*. IH* is a reduced $lood supply to the heart, usually caused $y atherosclerosis $loc"ing the coronary arteries that supply the heart. It usually ta"es a$out <! to C! years to accumulate a lifethreatening $loc"age, which is why very few people under the age of ! suffer heart attac"s. + symptom of IH* is increased $lood pressure, or hypertension. 8ne of the "nown effects of insulin is that it causes the arteries to dilate in healthy people, which normally causes a lowering of $lood pressure. When a person&s $lood is filled with excess fatty acids, however, they $ecome insulin resistant, resulting in arteries not dilating in response to insulin. 1any researchers now $elieve that this failure to dilate may $e the cause of a significant percentage of hypertension cases. +nother symptom is angina, caused $y the heart having to cope with a reduced $lood supply. +ngina is a warning sign that the artery is dangerously $loc"ed. )nough $lood can get through the narrow opening for normal daily needs, $ut when more $lood is needed in a hurry (usually $ecause of exercise or stress) and not enough can get through, the temporary chest pains called angina ensue. + more definitive symptom is myocardial infarction (1I). 1I is the classic sudden-death heart attac" we see all the time on T4 A clutching the chest, our hero falls to the street and is

pronounced dead $y the not-Guite-on-time am$ulance crew. This year, one Guarter of all +ustralians with heart disease will experience their first-ever symptom (a fatal 1I) within the hour $efore they die. +n 1I is generally caused $y the porridge (which has a hard s"in) rupturing and sGuirting fatty acids into the $lood at the site of the rupture. This usually induces a $lood clot that either $loc"s the artery totally or causes the heart muscle to die. )ither way, the end result is a heart attac". It is very difficult to o$tain accurate historical data on the rates of heart attac", mostly $ecause 1I wasn&t even recognised as a medical pro$lem until ,?,; (due to its rarity A $ut more on that shortly). +nd what caused it wasn&t nailed down with any certainty until the ,?;!s. In some very rare instances, though, researchers have $een very luc"y. When accurate records are "ept a$out people&s $irths and deaths, it is possi$le to construct a complete cradle-to-grave analysis of a whole set of lives lived. When the data is old enough, researchers can proceed with some certainty a$out causes of death $ecause every$ody they are studying is now dead. 8ne such study was completed in the late &?!s $y +ustralian researchers see"ing to determine if there was a relationship $etween low $irth weights and death $y heart disease. They found there wasn&t, $ut in the process they used the excellent death registry created $y William Henry +rcher to compile an extensive data$ase of causes of death in the early +ustralian colonies.

When William Henry +rcher, a statistician $y training, was demoted from his position of managing actuary at the (atholic, 5aw and 'eneral 5ife +ssurance (ompany of 5ondon in ,@<;, he decided to throw in the Fo$ and move his family to the new colony at 6ort 6hillip #ay, +ustralia. His rare statistical training stood him in good stead with the governor and, in ,@<=, he was appointed to the newly created position of 0egistrar of #irths, *eaths and 1arriages for Her 1aFesty&s (olony of 4ictoria. +rcher is credited with creating one of the most detailed and accurate data$ases of $irths, deaths and marriages in the world.

+rcher&s data$ase was used $y the researchers in conFunction with the records of what is now the 0oyal Women&s Hospital in 1el$ourne to create a complete dataset for the lives of people $orn at that hospital $etween ,@<> and ,?!! who survived $eyond the age of ! (almost =!!! people). The age-adFusted dataset reveals that prior to ,?=! less than ; per cent of people had died from symptoms that today would $e diagnosed as an IH*-induced 1I (heart attac"). 3rom ,?=! to ,? ? a$out four times as many (@ per cent) died from the condition. 3rom ,?<! to ,?<?, the figure Fumped to ;> per cent, more than ,! times as much as it had $een Fust two decades earlier. +nd << years after the introduction of sugar use in commercial Guantities, almost =! per cent of deaths were attri$uta$le to heart attac"s caused $y the $loc"age of the arteries with fats. )xactly the same fats that we now "now are produced as a direct result of the consumption of fructose. There are many pro$lems with relying too much on a study done in this way with such a comparatively small and old dataset, $ut the results do match up with similar wor" done in the /nited .tates. The /. studies suggest that 1I was almost nonexistent as a cause of death in ,?!! and caused no more than =!!! deaths per year $y ,?=!. *r 6aul *udley White, who introduced the electrocardiograph machine to +merica, said

during a ,?<C +merican Heart +ssociation televised fundraiserD %I $egan my practice as a cardiologist in ,?;, and I never saw an 1I patient until ,?;@.& #y ,?C!, there were at least half a million 1I deaths per year in the /nited .tates. The other maFor variant of (4* that "ills thousands of people every year is stro"e (cere$ral infarction). + stro"e is a disruption of the $lood supply to the $rain. :ust li"e atherosclerosis of the arteries leading to the heart, when the arteries leading to the $rain fill with porridge, $lood supply is reduced. .ometimes the atherosclerosis ruptures and produces a clot that completely $loc"s $lood supply to part of the $rain. #rain cells can survive a$out four minutes without the oxygen that the $lood supply $rings. +fter that, $rain-cell death near the site of the $loc"age $egins. *epending on how long treatment is in coming or whether the $lood supply is completely $loc"ed, stro"e is more surviva$le than 1I. 8nly one in three stro"e sufferers dies as a direct result of the stro"e (compared with ?! per cent of 1I sufferers). However, they do not generally escape without some $rain damage as a resultL only ,! per cent return to normal. +$out ,< per cent of all hospital $eds and one-Guarter of all nursing-home $eds are filled with survivors of stro"e at any given time. /nli"e the heart, there are many entry points for $lood supply to the $rain, and stro"es tend to have local effects that then slowly spread. +round ,; !!! +ustralians will die this year from stro"es. :ust as with heart attac"s, not all stro"es are caused $y atherosclerosis, $ut they account for the maFority $y far A more than @! per cent. +therosclerosis is o$viously not confined to arteries that supply the $rain and the heart. It can and does occur anywhere in the $ody (especially the legs), $ut a $loc"age in most other locations, while serious, is not normally as deadly, with %only& ;<!! +ustralians expected to die in ;!!@ as a result of those types of $loc"ages. That&s still more than the national road toll,

$ut it pales into insignificance against the => !!! dying from heart attac" and stro"e. 1odern statistics reveal that the num$er of people dying from a (4* pea"ed in a$out ,?C@ A at almost C< per cent of the total num$er of deaths that year A and has $een declining since then to the current =! per cent. The decline is uniform across all age groups, $oth sexes and in all first-world countries. 3ollowers of the anti-fat message of *r +ncel 2eys have $een Guic" to claim the credit for the decline. + closer loo" at the data reveals that the primary cause is Fust plain old-fashioned economics rather than a reduction in the amount of fat we eat. *on&t get me wrong, there is nothing wrong with eating less fat (and in doing so, you will definitely reduce the amount of circulating fatty acids in your system), it&s Fust that your $ody is already capa$le of controlling how much fat you eat and it is relatively unimportant as a source of fatty acids if you also continue to eat fructose. The decline in deaths is actually attri$uta$le to a lot of money and the $etter medicine that it $uys. In ,?; , six +merican doctors (one of them $eing *r 6aul *udley White A the chap who was not to see an 1I until ,?;@) formed the +merican Heart +ssociation (+H+), a small scientific society aimed at promoting pu$lic interest in heart disease. With 1I causing less than ,! per cent of deaths at the time, the pu$lic was un$elieva$ly ignorant a$out the disease, to paraphrase *r White. The +H+ remained relatively o$scure for ;< years, relying on dues from its (mostly medical) mem$ers. Its annual $udget never exceeded Q<! !!! during that time. In ,? @, that all changed very suddenly when the +H+ successfully managed to lo$$y the /. government to esta$lish the 7ational Heart Institute (7HI). + significant factor in its success was the fact that, $y then, one in three +merican deaths was caused $y a (4*. (4*s were clearly at epidemic proportions and urgent action was needed. +t the same time, the +H+ transformed

itself into a voluntary health agency and $ecame a maFor recipient of 7HI-controlled funds to develop expertise in (4* research. The +H+ had transformed itself from an o$scure scientific society to a maFor distri$utor of research grants for heart disease research, all courtesy of an epidemic that was clearly spiralling out of control. Today the +H+ employs ;<!! full-time staff and .< million volunteers, and $oasts a mem$ership of over =! !!!. It is the second-largest not-forprofit health agency in the world. The +H+ raises over Q !! million every year and spends over Q,!! million a year funding or supplementing government funding for medical research on heart disease, as well as its own internal research and education programs. In ,?C@, two decades after the 7HI was esta$lished and the +H+ transformed, things were not going so well. #y then, two out of every three +merican deaths were caused $y a (4* and the story was similar in most of the developed world. (4*s were o$viously an extreme priority for government and private health spending ali"e. The +H+ and the 7HI had spent ;! years pouring money into research and seriously multiplying the num$er of cardiologists, and eventually cardiac surgeons, $y creating vast num$ers of academic stipends to encourage the teaching of cardiology. The only result $y then was a dou$ling in the num$er of deaths due to (4*, $ut the spending was a$out to pay off. .ince ,?C@, the num$er of deaths due to (4* has more than halved. This num$er of deaths is still significant, $ut it means we have now put ourselves $ac" in the position we were in when the +H+ and the 7HI started out A %only& one in three deaths are due to a (4*. In ,?C , the age of intervention in the treatment of arterial disease dawned with the first successful use of a $alloon-tipped catheter to treat atherosclerosis in a leg artery. #efore this, the primary treatment for (4* was to $e put into a hospital $ed until you died (rather li"e type I dia$etes $efore the discovery

of insulin). The new catheter treatment involved inserting a thin tu$e into the artery and threading it to the point of the $loc"age. The $alloon was then inflated against the $loc"ed area to create a wider passage for $lood flow. It wasn&t tried on a heart artery until ,?>>, $ut it was so successful that less than a decade later =!! !!! such operations were $eing performed every year in the /nited .tates. The first $alloon catheter operation was performed in +ustralia in ,?@!. That year, ,, in total were performed. #y ,?@C, technology had developed to the point where the first stent was implantedD a metal or synthetic mesh cylinder inserted after the $alloon catheter has widened the artery, to prevent it from narrowing again. #y the turn of the century, ;! !!! +ustralian $alloon catheter operations were $eing performed every year.

In ,?C>, 0ene 3avalaro, an +rgentine cardiac surgeon wor"ing at the (leveland (linic, in 8hio, was pioneering the other significant advance in heart disease treatment, a surgical techniGue where$y a $loc"age was $ypassed altogether using a grafted artery (usually) from the patient&s leg. #y ,?@!, almost !!! +ustralian $ypass operations were $eing performed annually. +nd $y the turn of the century, that num$er had increased almost fivefold to nearly ,@ !!! per year. In ;!!>, around <!! !!! $ypass surgeries were performed in the /nited .tates.

The drug companies were not going to miss out on the $iggest pu$lic health spending $onan9a in history. They started research immediately and $y the late &@!s were a$le to release a raft of new drugs targeting cholesterol and $lood pressure. (onsumption of many of these drugs increased eightfold in the decade that followed and continues to clim$ rapidly. The development of the surgical techniGues and drugs has $een a worldwide phenomenon, with all first-world nations

implementing these maFor interventionist techniGues shortly after their first successful trials. It is important to note that prevalence (the num$er of people with a disease in the population) of (4*s has not decreased. In +ustralia, it continues to increase at a rate of a$out ; per cent per annum, a$out twice the rate of population growth. +nd $lood cholesterol levels remain Fust as high as they were in ,?@!, when such things first started $eing measuredL a$out <! per cent of the population continues to have high $lood cholesterol. We haven&t cured anythingL we are Fust $etter at ma"ing sure fewer people die from it. The medical profession has shown us the difference $etween an untreated (4* and a treated (4*. If it&s not treated, it accounts for two in every three deaths. If vast amounts of money are thrown at the pro$lem, we can get that down to one in every three deaths. I suspect we have reached the limits of technology to solve the pro$lem and we are a$out to face another acceleration in the death rates, $ecause nothing has $een done a$out the maFor underlying cause. When you $rea" the figures down $y gender, women seem to have an advantage. 6re-menopausal women are half as li"ely as men to suffer from a (4*. +fter menopause they catch up, and if they (and the men) lived to $e ?!, they would $oth have the same chance of death due to a (4*. This suggests to me that there is something protective a$out $eing a woman in so far as the effect that fructose has on the production of circulating fatty acids. 1any of the rat researchers noticed the same thing. 1ale rats fared much worse in the fructose feeding than female rats of $reeding age. 3emales $eyond $reeding age lost their protection and suffered Fust as much as their male counterparts. /p to the age of =<, there are fewer overweight women than men and they are less li"ely to suffer a (4* when they are

+i ure 2=%: ;!!< +ustralian figures for the percentage of women and men in each age category who are o$ese A women have an advantage $efore menopause, $ut then well and truly ma"e up for it afterwards. The stats drop off after C< $ecause the really o$ese people are dying $y then.

pre-menopausal. #ut ! years later, they are in Fust as much trou$le as the men. It appears that there is something a$out the interaction of female reproductive hormones and fructose meta$olism that favours immediate $ody-fat creation rather than increased circulating cholesterol levels. 0esearchers at the 1ayo (linic )ndocrine 0esearch /nit in 0ochester, 1innesota, have pu$lished the results of limited trials they performed in ,??<, which showed that oestrogen helps fat cells vacuum fatty acids out of the $loodstream. This means that, if you happen to have oestrogen in your $lood ($ad luc", gentlemen), the fatty acids created $y fructose will $e more efficiently turned into $ody fat rather than hanging around in the $loodstream and ma"ing $owls of porridge in the arteries. While this may $e very $ad news for women see"ing to fit into this year&s $i"ini, it is pro$a$ly good news for their chances of

$eing "illed $y a (4* (or any of the other diseases we are a$out to discuss). 1ore recent research, conducted in ;!!; $y the *ivision of 'eriatric 1edicine at the /niversity of (olorado, found that oestrogen also seemed to ma"e insulin wor" more efficiently in clearing the $lood of glucose. To prove this they inFected postmenopausal women with oestrogen and measured the $efore and after differences in how efficiently the insulin did its wor". This interaction $etween fructose (or at least the fatty acids it produces) and female reproductive hormones has also $een put forward $y some researchers as a possi$le reason for the recent rapid decline in the age of female sexual maturity, with girls hitting pu$erty much younger than their mothers and grandmothers did. It is very early days for research in this area, and certainly too early to ma"e any definitive conclusions, $ut I am watching it with interest. (4*s are not a high-pu$licity set of diseases. )ven though they "ill huge num$ers of people, the victims are mostly elderly. In the last five decades or so, we have $ecome inured to the concept of people dying of heart attac"s or eventually from stro"es. +fter all, we&ve all got to go somehow and that&s how most people seem to die. +dvances in medical treatment have meant that there is no o$vious impact of the escalation of these diseases (yet), such as there suddenly $eing no way to live past C!. +nd it doesn&t affect the lifestyles of the young and newsworthy. -ou can have a (4* your whole life and the first you will $e aware of it is when you suffer the first fatal symptom. The $uild-up of arterial porridge is a slowaccumulation disease with a very decisive outcome, $ut often no degradation of lifestyle $efore that point.

3= 4O:E <ILLE:S
(ardiovascular diseases are not the only new diseases our love affair with fructose has created. Type II dia$etes was rarer than (4*s in ,?!! and, compared with (4*s, still doesn&t "ill a large num$er of people today. In ;!!@, =<!! +ustralians were expected to die $ecause of dia$etes (twice as many as would $e "illed on our roads) and another @<!! from (4*s where dia$etes has $een a contri$uting factor. #ut there are two things a$out dia$etes that ma"e it much more newsworthy than (4*s. It affects younger people and, while it doesn&t necessarily "ill them, it significantly affects their lifestyle. /nli"e (4*s, as long as it is treated, dia$etes ta"es a long time to "ill the patient. + dia$etic will usually only die after a lifetime of altered or truncated living, complicated $y some non-fatal $ut very nasty side effects. +round one in =<! people in +ustralia suffers from type I dia$etes, and that num$er (as a percentage of the population) has not changed significantly over time. Whatever is wrongly identifying the islets of 5angerhans as viruses and destroying them in type I dia$etics has not changed significantly in the century or so that statistics on such things have $een "ept. Type II dia$etes is a different $east altogether. The outcome is the same, $ut the cause is very well documented and in many cases preventa$le. The num$er of people with type II dia$etes is accelerating rapidly. Type II dia$etes was once called late-onset dia$etes $ecause it normally only affected old people. #ut as the num$er of fat people in the population has increased and the population of fat people has $ecome younger, it is now $ecoming common in people in their ;!s and increasingly occurring in teenagers and even children. The disease is caused $y the $ody $ecoming immune to the

effects of insulin. Insulin is still $eing manufactured (often in huge Guantities) $ut the $ody $ecomes resistant to it, reGuiring more and more insulin to remove the amount of glucose $uilding up in the $lood. .tudies on rats, hamsters and dogs, as well as some limited human trials conducted during the last =! years, have proved that fructose consumption results in insulin resistance even when maintained for only short periods of time. The rapid increase in circulating fat caused $y the fructose meta$olism inhi$its insulin&s a$ility to instruct cells that reGuire energy to ta"e the glucose out of the $loodstream. )ventually, either the $ody cannot manufacture enough insulin to remove the glucose, or the islets of 5angerhans wear out from overuse and their capacity to produce insulin significantly reduces. The result is the same as for type I dia$etesD the $ody starves in a sea of food. Insulin resistance is a preliminary phase of type II dia$etes. When a person is insulin resistant, their $lood-sugar levels remain high for longer than would $e expected after eating a meal. This is a sign that the $ody is struggling to dispose of the glucose. The $ody has $ecome resistant to the effects of insulin. If insulin resistance is left untreated, it eventually develops into full-$lown dia$etes, where no matter how much insulin is produced, the $lood-sugar levels remain permanently too high. The prevalence of type II dia$etes is now increasing so rapidly that the (enters for *isease (ontrol and 6revention and the World Health 8rgani9ation characterise it as an epidemic. The International *ia$etes 3ederation estimated that in ;!!= a$out ,? million people worldwide, or <., per cent of the adult population, had dia$etes, and that this will almost dou$le to === million $y ;!;<. The num$er of people with confirmed insulin resistance was estimated at =, million in ;!!= and is expected to increase to >; million $y ;!;<. In less than two decades, almost , $illion people worldwide will $e affected $y

a potentially life-threatening disease that was virtually unheard of less than =! years ago. What&s worse is that these figures are li"ely to $e underestimates (they have already $een revised upwards $y

+i ure 3=1: The num$er of +ustralians with type II dia$etes has exploded in the last ;< years. The disease is now at epidemic proportions.

,, per cent since the predictions were first made in ;!!,). In some cultures, the future is already here. 6olynesians, +$original +ustralians and 7ative +mericans seem particularly suscepti$le to the effects of prolonged insulin resistance and prevalence rates are soaring. With type II dia$etes now affecting up to half of some populations of these indigenous peoples, they are now five times as li"ely to die from dia$etes as (aucasians. In 7ew Bealand, for example, one in five 1aori deaths is as a direct result of dia$etes, compared with one in ;!

in the (aucasian population. 8ne of the things the /.*+&s .heldon 0eiser and his team noticed during their experiments in feeding rats too much fructose during the late &>!s was that the rats on ;> per cent fructose diets developed insulin resistance after a relatively short time (two to four wee"s). The results were confirmed in ,?@? $y *r +W Thor$urn and his colleagues at the .t 4incent&s Institute in .ydney, using a four-wee" diet that consisted of =< per cent fructose. .ince then, numerous experiments with rats, ra$$its and dogs have proved definitively that a high-fructose diet increases an animal&s insulin resistance, whereas a highglucose diet does not. 3urther research pu$lished $y *r Thor$urn in ;!!; confirmed that it was the huge increase in circulating fatty acids induced $y the fructose that caused the insulin resistance. 6revious research had shown that increased fatty-acid levels interfered with the $ody&s a$ility to manufacture glycogen (the short-term glucose store maintained $y the liver). *r Thor$urn&s su$seGuent research showed that it also stopped muscles using the glucose for energy. In someone who is insulin resistant, high $lood glucose triggers the production of more insulin in an attempt to lower the $lood glucose. )ventually, in the early stages of type II dia$etes, enough insulin is produced to $rea" through the resistance caused $y the fatty acids and lower the glucose levels. If this pattern of overproduction is maintained for years on end, eventually either the $ody cannot ma"e enough insulin to lower the $lood glucose levels or the islets of 5angerhans $ecome permanently damaged. There are some lines of modern research that suggest that the presence of fatty acids may itself directly damage the islets, $ut at this stage that is speculation. 3rom our perspective, it doesn&t matter whether the effect is direct or indirectD the result is the same. It is still not clear exactly how the fatty acids interfere with the action of insulin, $ut it is $eyond dou$t that the massive increase in fatty acid

production, induced $y eating fructose, does cause insulin resistance and eventually leads to type II dia$etes. It seems the results are now in from our own little fructose-feeding experiment. If you feed millions of humans massive Guantities of fructose for the first ;! to =! years of their lives, you can create a type II dia$etes epidemic.

Type II dia$etes affects men much more than it does premenopausal women. The oestrogen research descri$ed in the previous chapter pro$a$ly goes a long way to explaining why. 8estrogen helps clear the fatty acids that cause insulin resistance, and it also appears that it helps insulin do its wor" even more directly $y accelerating the a$sorption of glucose. If you have oestrogen in your veins, it will ta"e a lot more fructose to give you type II dia$etes than if you don&t.

+ccumulation of fat in the arteries starts happening from the very first extra gram of fructose (or fat) consumed. 3ifty to C! years of continuous fructose feeding leads to a high li"elihood of a heart attac" or stro"e. The rapid increase in fructose consumption we have all $een part of in the last =! years has pro$a$ly accelerated that process, meaning that heart attac"s and stro"es may start to occur in younger and younger people. Type II dia$etes is different. It appears that we can tolerate a certain level of fat in the $lood caused $y fructose and not develop the disease A we can overproduce insulin at a certain level without shutting down the islets of 5angerhans. Thirty years after fructose consumption $egan increasing due to the introduction of soft drin"s to our diet in the early &<!s, Type II dia$etes started a mirror-image clim$. If the type II dia$etes curve is in fact a mirror of the fructose curve, =! years delayed, there is much worse news to come on the dia$etes front. 8ver the last =! years alone, type II dia$etes has changed from

$eing seen as a relatively mild and rare ailment associated with ageing and the elderly to one of the maFor contemporary causes of premature death in most countries. In virtually every developed society, type II dia$etes is the leading cause of $lindness, "idney failure and lower lim$ amputation (=!!! dia$etes-related amputations were expected to $e performed in +ustralia in ;!!@) and is a significant ris" factor for death from heart disease. Worldwide, there is a death due to type II dia$etes every ,! seconds, and an amputation every =! seconds. +nd there are predictions that the disease will singlehandedly wipe out whole races of indigenous peoples in the 6acific within ,!! years. *ia$etes is not as suddenly fatal as (4*s. It generally de$ilitates over an extended period $efore it "ills. :ust as with type I dia$etes, too much sugar in the $lood, over a decade or so, causes permanent damage to the fine $lood vessels in the "idneys, eyes, arms and legs, often resulting in $lindness, "idney damage and amputations. 6eople with dia$etes tend to live with a significantly reduced and eroding Guality of life. /nli"e with (4*s, the good news is that, if caught early, insulin resistance and even type II dia$etes can $e reversed $efore permanent damage is done. +nimal experiments have shown that very shortly after fructose feeding ceases, the fatty acids in the $lood reduce and insulin resistance su$sides. If insulin overproduction ($ecause of resistance) remains untreated for prolonged periods, eventually permanent damage is done to the islets of 5angerhans and this cannot $e reversed. When this occurs, the person has effectively turned themselves into a type I dia$etic and can no longer produce any, or sufficient, insulin for their needs. 3atal dia$etes-induced "idney failure occurs in ,< per cent of sufferers, and it seems there&s even worse news for males with excess long-term fructose consumption. *r 0eiser&s rat studies noted enlarged testes, enlarged male $reasts, decreased li$ido,

impotence and decreased sperm production among the plethora of rather nasty outcomes for his furry male su$Fects. These results have $een confirmed recently $y the advent of yet another significant new chronic disease related to fructose consumption. #esides type II dia$etes, insulin resistance also results in the development of non-alcoholic fatty liver disease (7+35*). 7+35* is an accumulation of fatty acids in liver cells that causes enlargement of the organ. In extreme cases it can cause the cells to $urstL the scar tissue that forms around the $urst cells is called cirrhosis. If enough of the liver&s normal mass is replaced $y scar tissue, cirrhosis is ultimately fatal (over =< !!! +mericans and ,<!! +ustralians died of cirrhosis in ;!!>, of which it is estimated ,@ per cent are thought to $e due to 7+35*). .tudies are now $eginning to confirm *r 0eiser&s o$servations, that a significant percentage of males with fructose-induced cirrhosis of the liver will experience testicular atrophy (the testes diminish in si9e and cease to function), impotence (no wonder there&s such a demand for pills that assist in this department) and enlarged male $reasts. 0esearch conducted colla$oratively in ;!!> $y teams in Italy and #ritain have confirmed that >! per cent of type II dia$etes patients will suffer from 7+35* and that patients with a (4* are very li"ely to have the disease even when they don&t exhi$it any of the other commonly accepted ris" factors for (4* (eating lots of fat, smo"ing, $eing overweight, etc.). #ecause of the relative newness of type II dia$etes and insulin resistance as maFor diseases, there has $een very little study of 7+35*, $ut early wor" suggests that it is $ecoming alarmingly common, particularly in children. It is estimated that up to ; per cent of the /. population now suffers from 7+35*.

The group of diseases and symptoms associated with heart attac"s, stro"e, type II dia$etes and 7+35* are called meta$olic syndrome. It is easy to see how fructose consumption can result in this syndrome A all of the conditions that fall under its um$rella relate directly to a single sourceD increased circulating fatty acids. +nd we "now that fructose is converted into fatty acids.

#ut there is another set of maFor "illers that some researchers $elieve are also connected to fructose, or at least to the fatty acids they produce. The set of diseases that "ills Fust a$out every$ody that (4*s and dia$etes don&t get are the cancers. *r -ud"in noticed that there was a high correlation $etween o$esity and the li"elihood that a person would end up suffering from some types of cancer. He cautioned strongly against drawing too many conclusions from statistics (o$viously a $eliever in the line %lies, damned lies and statistics&) $ut he felt it was worth noting that there were strong correlations $etween o$esity and colorectal, $reast, "idney and prostate cancers. (ancer is a large and diverse group of diseases potentially affecting every part of the human $ody. + cancer occurs when the mechanism that controls cell reproduction $ecomes defective and cells multiply out of control. When this happens, the cancerous cells can invade and damage the tissue around them. (ancer is never good, $ut it can $e very, very $ad if it occurs in or near a vital organ. (ancers are named for the systems that they affect. There are over ;!! types of cancer, $ut Fust five of them account for almost ?! per cent of all new cases. They are (in order of mortality rate)D lung cancer, melanoma, colorectal ($owel) cancer, $reast cancer and prostate cancer. We have a very solid idea a$out what causes two of those. Too much sunshine causes melanoma. +nd too much smo"ing causes lung cancer. The other three are cancers that *r -ud"in noticed correlated with

sugar inta"e. 8ver ,!,!!! +ustralians were expected to $e diagnosed with cancer in ;!!@ (excluding non-melanoma s"in cancers, which account for a further => !!! cases), and a$out =@ !!! people will die from cancer. The $iggest "iller is lung cancer, $ut the rate of death per ,!! !!! people has declined significantly in the last two decades. The next $iggest "illers are $reast and colorectal cancers. They are the second and third most common cancers (respectively) worldwide, with two-thirds of all colorectal and $reast cancers occurring in the more developed nations. There is a huge variation in rates of colorectal and $reast cancer from country to country, $ut it is always the case that if one is high, then so is the other. The lowest rates are in +frica and +sia (except :apan) and the highest in )urope, 7orth +merica and +ustralasia. #oth cancers are definitively related to the western diet. .tudies of people moving from less developed countries to the /nited .tates have shown that there is a rapid increase in ris" for colorectal and $reast cancer in those migrants, and the rates for second-generation migrants can $e dou$le that of firstgeneration migrants. (ountries that have had a rapid westernisation

+i ure 3=$D The num$er of cigarettes smo"ed per person per day in the /nited .tates compared with the num$er of lung cancer deaths per ,!! !!! men over the last century.

of their diet, such as :apan, have seen a rapid increase in the incidence of $oth cancers. +s soon as the diet lin" was noticed, the usual suspects were rolled out, with the 2eys adherents declaring that increased fat consumption was o$viously the cause. This was modified later to $e increased meat consumption after correlations with fat proved inconclusive, and then later still to insufficient fruit and vegeta$le (fi$re) consumption. This last o$servation may not $e too far from the mar". The mountain of money that found its way into (4* research in the &>!s and &@!s has recently had some side $enefits for cancer research. + clear association has $een esta$lished $etween insulin resistance and (4* as a result of the Insulin 0esistance +therosclerosis .tudy (funded $y the successor to the 7ational Heart Institute, the 7ational Heart, 5ung and #lood Institute) conducted in the /nited .tates in the early

&?!s. In-depth analysis in ;!!= of the response to Guestionnaires from that study $y researchers from the *epartment of )pidemiology (medical statistics) at the universities of .outh (arolina, 1innesota and Wa"e 3orest confirmed the su$sidiary conclusion from the original study, that fi$re increases insulin sensitivity. This means that fi$re has the same protective effect with regard to insulin use as oestrogen. 1ay$e .urgeon-(aptain (leave was on to something with his $ags of $ran after allM #oth fi$re and oestrogen appear to enhance the $ody&s a$ility to use insulin to overcome the effect of circulating fatty acids and remove them and glucose from the $loodstream. The o$servation that insulin resistance is related to increases in colorectal and $reast cancers has $een followed up with studies aimed at finding out why that is the case. + few of the studies are now starting to clic" together to form an overall theory. In ,?=,, a 'erman cell $iologist called 8tto War$urg pic"ed up the 7o$el 6ri9e in 1edicine for a little theory he had managed to prove in ,?; . His theory concerned the way in which cancer cells derive energy from the $loodstream. He managed to prove that a cancerous cell uses glucose to produce energy directly and without oxygen. #ut it can only use glucose (rather than fat or protein) to do this. + normal cell reGuires the presence of oxygen to produce energy, $ut it can do so from glucose, fatty acids or proteins. War$urg theorised that this difference in cell $iology was the cause of cancer and that all cancer was in fact due to defective cells that could not use oxygen to produce energy. 1ore modern research $ased on studies of the genome have suggested that this in fact may $e the cancerous cells adapting to a lac" of oxygen inside a solid tumour, rather than a cause of cancer. Whether it is the cause or not, it is clear that cancerous cells consume more glucose than normal cells. .tudy after study in the &?!s and early years of this century have shown that high $lood-glucose levels are

positively associated with cancer growth. In other words, the presence of high $lood-glucose levels assists greatly in accelerating the growth of cancers. This is not to say that the glucose caused the cancer. There are li"ely to $e as many causes as there are types of cancer. It is, however, clear that, whatever the cause, having a consistently high $lood-glucose level accelerates the growth of cancerous cells. High fatty-acid levels "eep glucose levels high $ecause the more fatty acids there are in the $lood, the harder insulin has to wor" to remove them. 8estrogen and fi$re are now "nown to $e a$le to help insulin out $y ma"ing insulin more efficient (we&re still not sure how) and clearing the $lood of glucose and fatty acids more Guic"ly. 6ulling all of this together, we have a universal theory for what has $een o$served in a multitude of studies in the last three decades. 3ructose increases circulating fatty acids, particularly 5*5 cholesterol. Increased fatty acids lead directly to heart disease and stro"e. Increased fatty-acid levels also reduce the effectiveness of insulin in clearing the $lood of glucose. Increased $lood glucose leads to type II dia$etes and feeds cancer. 8estrogen reduces (to a degree) the effects of fatty acids and allows insulin to wor" well despite their presence and to eliminate them from the $loodstream. This results in premenopausal women having lower incidences of heart disease, stro"e, dia$etes and cancer. 3i$re has a similar effect to that of oestrogen (so there is hope for men after all) in rendering insulin more effective and therefore lowering the ris" of all of those diseases. If you must eat fructose, then either have plenty of oestrogen on hand or eat a lot of fi$re (hang on A fructose plus fi$re J that sounds li"e whole fruit). #ecause it has an o$vious precursor ($enign polyps in the $owel), colorectal cancer is almost completely avoida$le as long as regular $owel chec"s are performed. This means the

death rate for that cancer has decreased significantly in the last two decades. 6rostate cancer is unfortunately incura$le and there is very little evidence that any of the interventions tried so far significantly affect the rate of mortality. (omparing fructose consumption in the /nited .tates ($ecause it has the $est statistics) and prostate cancer reveals some alarming facts. There has $een a sharp downturn in mortality attri$uta$le to prostate cancer since ,??!. +nd while the medical esta$lishment would love to ta"e the credit for it, study after study has failed to identify any treatment to which the trend can $e attri$uted. 6lacing the trend on a graph as I have done $elow might help to provide an answer. The incidence of death from prostate cancer appears to $e trac"ing (with a C!-year delay) the consumption of fructose in the /. population. If that is in fact what is happening (and it certainly loo"s li"e it), then the current downturn in mortality relates

+i ure 3=%: 6rostate cancer rates appear to $e trac"ing fructose consumption. The dashed line is a prediction calculated $y me $ased on

mortality continuing to trac" fructose consumption.

to the rationing of sugar that occurred during World War II, and the pea" in the &?!s was a conseGuence of the sugar $inge $etween the depression and World War II. If the apparent trend continues, we should shortly expect to see a significant upswing in mortality rates as the $a$y $oomers reach prostate cancer age. It isn&t a maFor pro$lem in +ustralia yet, $ut a very new cancer on the hit list of "illers is the one directly associated with the organ that produces insulin. (ancer of the pancreas stri"es approximately five out of every ,!! !!! people every year in the /nited .tates and is one of the deadliest forms of cancer. With an estimated =; ,@! +mericans diagnosed with cancer of the pancreas in ;!!@, and with =, @!! deaths, mortality approaches ?? per cent. This adds up to pancreatic cancer having the num$er-one fatality rate of all cancers and shooting to num$er four on the hit list of cancer "illers in the /nited .tates. Two recently pu$lished large-scale studies have demonstrated a strong lin" $etween a diet high in fructose and the li"elihood of developing pancreatic cancer. In ;!!;, *r *ominiGue 1ichaud of the /. 7ational (ancer Institute, and (harles 3uchs of the #righam and Women&s Hospital and the *ana-3ar$er (ancer Institute in #oston, identified ,@! cases of pancreatic cancer from among @@ @!; women who were monitored for ,@ years as part of the 7urses& Health .tudy. This is a longitudinal health characteristics survey that started in ,?>C with a group of ,;, >!! registered nurses aged $etween =! and <<. Women who were overweight and sedentary and had a high fructose inta"e were shown to $e almost three times as li"ely to develop pancreatic cancer. The researchers speculated that glucose resistance may $e to $lame and that insulin may even act as a growth factor for pancreatic cancer.

+ ;!!C study pu$lished $y the 2arolins"a Institute in .weden has confirmed the results of the /. 7urses& Health .tudy. The .wedish study $egan in ,??> when scientists ran a dietary survey of almost @! !!! healthy people, who were su$seGuently monitored until :une ;!!<. +ccording to the cancer registry, ,=, people from this group had developed cancer of the pancreas. The researchers have $een a$le to demonstrate that the ris" of developing pancreatic cancer is related to the amount of sugar in the diet. 1ost at ris" were those who dran" large Guantities of soft drin"s. The people who said that they dran" such products twice a day or more were ?! per cent more li"ely to develop pancreatic cancer than those who never dran" them. 6eople who added sugar to food or drin"s at least five times a day were at a >! per cent greater ris" than those who did not. 6eople who ate fruit Fams at least once a day also ran a higher ris" A they developed the disease <! per cent more often than those who never ate them. The evidence lin"ing sugar and cancer is starting to accumulate. .tudy after study associating sugar consumption and particular cancers is seeing the light of day. +fter decades loo"ing for associations $etween fat or meat and cancers, researchers are producing consistent evidence that $ac"s up *r -ud"in&s educated guess $ac" in ,?>; A sugar consumption is closely associated with cancer. I am ta"ing that one step further and suggesting that the particular mechanism of that association is the fructose-induced fatty-acid accumulation that promotes a high-glucose environment. That environment is the perfect feeding ground for the growth of cancerous cells. 7o chapter on the evil created $y fructose would $e complete without a Guic" loo" at the most o$vious fructose-created condition of all. )very dentist will tell you not to eat sugar (and definitely not in liGuid form) if you want to "eep your teeth past the age of =<. The $acterial infection that causes tooth decay is the most common infection in humans. #ut no$ody

ever died of tooth decay. That and the fact that Fust a$out every$ody has it has minimised its significance. 0esearchers have "nown since the &C!s that tooth decay is caused $y Fust one (Stre&to'o''us mutans, or .1) of the ;!! to =!! species of $acteria that inha$it our mouths. In hundreds of very well-controlled studies, scientists were a$le to determine that feeding rats sucrose (ta$le sugar) encouraged .1 to produce decay, $ut feeding them pure glucose or fructose on their own did not. 1icro$iological studies conducted throughout the &>!s and early &@!s showed that .1 needed $oth the glucose and the fructose present in sucrose. If $oth sugars were present, there was a perfect environment for .1 to do its destructive wor". .ucrose doesn&t exist in any Guantity in our natural environment (unless you are in the ha$it of suc"ing on sugarcane), so the discovery that sucrose was necessary for tooth decay went a long way towards explaining why dental cavities were not a significant medical pro$lem $efore ,@<!. It also appears that .1 prefers a constant supply of sucrose rather than $ig lumps at intervals. /nli"e all the other conditions caused $y sugar, tooth decay is not so much dependent on the Guantity consumed, $ut rather the freGuency of consumption. (onstant snac"ing on sugar and sugar-laden drin"s provides the perfect environment for .1, $ut a large amount of sugar at a mealtime doesn&t help it much at all, especially if you are in the ha$it of cleaning your teeth after a meal. .1 li"es a sludge of sucrose to $e present on the teeth at all times. The costs associated with treating the symptoms of the activity of .1 have grown exponentially in the past five decades (strangely coincident with the growth of the soft-drin" industry). 'overnments, desperate to avoid the popular demand for them to pay the $ill for a disease that affects everyone, have increasingly turned to the Guic"-fix solution of mass medication with fluoride.

We spend a lot of money fixing and treating (with varying degrees of success) the damage done $y sugar. The +ustralian Institute of Health and Welfare (a federal government department) has developed a sophisticated data-collection and analysis methodology for health-system cost measurement. +ccording to +IHW num$ers, in ;!!,, +ustralia spent Q<.< $illion on (4*s, Fust short of Q, $illion treating type II dia$etes, another Q;.? $illion on cancers, Q=. $illion on oral health (no wonder the government is "een on fluoride) and Q,.< $illion on osteoarthritis. In addition to the Q, .= $illion of annual direct costs, we spent at least that amount in lost productivity and other employment-related indirect costs to the economy. If you&re li"e me, $illions, trillions and ga9illions are largely irrelevant without some $asis for comparison. In the same year, we spent only Q $illion treating inFuries and Q=.> $illion on mental disorders (mostly +l9heimer&s and dementia treatment in nursing homes). The amount directly spent on fructose- and sugar-induced disease in ;!!, was Fust a little $it less than +ustralia spent on defence in ;!!<, even after paying for some less than cheap ongoing military deployments in IraG, Timor and +fghanistan. *rug companies love type II dia$etes in particular. In +ustralia, ;< cents in every health dollar spent on dia$etes goes directly into their poc"ets. In the /nited .tates in ;!!,, Q=.< $illion was spent on drugs aimed at managing type II dia$etes and it is easily the fastest-growing pharmaceutical mar"et. The drugs do not cure the diseaseL they simply slow its progression (so the patient or, in +ustralia, the government has to $uy the drugs over a longer period). The drugs generally either stimulate the pancreas to produce more insulin or increase insulin sensitivity. The real irony is that, of all the diseases I loo"ed at, type II dia$etes is the one that can $e cured simply $y not eating fructose (as long as it has not progressed to the point of destroying the islets of 5angerhans).

*rug companies prefer to promote a slightly different message. Their message is that you can manage your insulin resistance $y stimulating the pancreas to produce more insulin. 1uch li"e fluoridation, it is an attac" on the symptom rather than the cause. (holesterol-lowering drugs are in the same category. If you have high cholesterol, try a little experiment. .top eating fructose for two wee"s and see what happens to the fatty-acid levels in your $lood. -ou (and your '6) will $e ama9ed. *oing this won&t reverse your accumulated atherosclerosis, $ut it will lower your 5*5 cholesterol and $lood triglyceride readings, and the reason is simpleD you will $e removing the ingredient from your diet that most directly produces them.

PA:T $ W&AT CAN ;O) DO#

1/= W&AT A.O)T E@E:CISE#
-ou would have to loo" pretty hard to find a pu$lic-health message today that did not encourage you to exercise %as part of a healthy lifestyle&. )xercise is now so tightly $ound up with weight loss in the minds of governments, educators and the pu$lic that to challenge the suggestion appears as foolhardy as arguing that the s"y is not really $lue. #ut this %truth& is in reality a very recent phenomenon. The common $elief that exercise causes weight loss can $e traced to one very influential nutritionist. 3rench-$orn hero of the resistance in World War II, :ean 1ayer moved to the /nited .tates Fust after the war. He wor"ed at the /7 3ood and +griculture 8rgani9ation in Washington, *(, while earning a doctorate in 6hysiological (hemistry at -ale. He Foined Harvard&s newly founded *epartment of 7utrition after earning his doctorate and $ecame a prolific and highprofile pu$lisher of papers and $oo"s on hunger, nutrition and the then newly emerging pu$lic-health pro$lem of o$esity. In ,?<? the -ew 0ork Times credited 1ayer with destroying the theory that exercise had nothing to do with losing weight. /ntil the late &<!s doctors had uniformly (well, as close as they ever get, anyway) $elieved that exercising more simply made you more hungry. 1any studies had shown that patients lost more weight if they lay in $ed than if they pursued vigorous exercise. It was an accepted tenant of medical practice that prescri$ing

exercise to treat o$esity was a"in to prescri$ing $eer to treat alcoholism. #anting had discovered this a century $eforehand with his rowing, $ut it too" the doctors a while to catch up. *r 1ayer&s populist writings on the su$Fect changed all this. He pu$lished paper after paper that showed that o$ese people were less physically active. He drew the conclusion that $eing more physically active would ma"e you less fat. His wor" showed definitively that fat people do exercise less than thin people, $ut are they fat $ecause they exercise less, or do they exercise less $ecause they are fatM 1ayer went wholeheartedly for the first explanation and his impecca$le credentials and swash$uc"ling war-hero charisma, coated with a li$eral dash of 3rench accent, pushed the theory into the +merican and then the world consciousness. *octors didn&t go down without a fight. +s late as ,?C<, they were still writing to the -ew 0ork Times in response to articles pu$lished $y 1ayer, decrying his exercise theories as nonsensical. #ut 1ayer, li"e 2eys, was on a mission to convince the pu$lic of his perspective, and convince them he eventually did. +ncel 2eys convinced us that fat ma"es us fat (and gives us heart attac"s) and :ean 1ayer convinced us that the cure to $eing fat is exercise. #oth managed to carry their messages in the face of strident medical opposition and $oth messages are core components of nutritional thin"ing today. There are lots of good reasons to exercise. The 1ayo (linic says there are seven $enefits to exercise. 8nly one of them is weight loss. The others are improving your moodL com$ating heart disease $y improving $lood circulationL strengthening your heart and lungsL helping you get a $etter night&s sleepL putting the spar" $ac" in your sex lifeL and Fust for fun. -ou could do it $ecause it gives you an endorphin rush A that was certainly my primary motivation at university. -ou could do it $ecause it gives you %head-space&. While you exercise, your mind can wander and $e free to get away from the pressures of

the day. -ou could do it for %you& (getting away from the "ids) time. 7o-one is going to criticise you for devoting a half-hour to solitary exercise a day. -ou could do it Fust to feel well. There is no dou$t that exercise is crucial for overall health. 1y point is that exercise alone won&t allow you to lose significant amounts of weight, if you continue to consume large amounts of fructose. The interesting thing that I discovered is that I felt a lot more li"e exercising after I lost my weight than $efore. When I was o$ese I was lethargic and apathetic. )xercise was the last thing I felt li"e doing. 7ow, I actually feel li"e getting out and doing something after a $ig meal. I&m not ta"ing up Fogging any time soon $ut the thought of a $it of activity no longer fills me with dread. I firmly $elieve that *r 1ayer chose the wrong option. 3at people do less exercise $ecause they are fatL they are not fat $ecause they do less exercise. )xercise aside, the reason for the rampant explosion in mortality from diseases that no$ody had heard a$out a century ago is, according to the experts, willpower. +ll of a sudden in the last ,!! years of our ,=! !!!-year history as a separate species, the human race as a whole has gone insane and lost all control over appetite. The experts tell us we are fat $ecause we refuse to exercise enough and $ecause we eat too much fat. )very other mammal on the planet is getting $y Fust fine (except for the ones we adopt as pets). There are no fat lions wandering the plains of +frica. There are no o$ese mon"eys $ending tree $ranches in the rainforests of Indonesia. The lions are not insisting that their prey have the fat trimmed off $efore a meal. +nd neither they nor the mon"eys are spotted too freGuently at the gym or out for a Fog. They eat when they are hungry and stop when they are full, Fust li"e our fore$ears did. We, the people of the twenty-first century, are the only mammals who have suddenly decided to wipe ourselves out with o$esity.

We say we&re trying not to $e fat. 1ost of us are $uying the ?> per cent fat-free foods. 1any of us $elong to at least one gym, even if we don&t attend all that often. We&re trying hard to cut down on fat and lower our cholesterol, $ut it seems that even with all that effort we are the generation that Fust can&t stop getting fatter and sic"er. 'overnments and medical experts, despairing at our lemming-li"e race towards o$livion, exhort us to stop $eing so lac"ing in willpower and ta"e up Fogging and eat more low-fat food. We are not fat $ecause we suddenly lac" willpower or $ecause we don&t exercise enough or $ecause we eat ham$urgers at 1c*onald&s. 8f course, not exercising, or eating too much, will ma"e us gain weight. It&s a simple case of mathematicsD if you consume more energy than you expend you will gain weight. We don&t get fat from sitting next to fat people on the $us. We get fat from putting too much food in our mouths relative to the energy we need. That is $eyond dispute. The Guestion is why all of a sudden we want to eat more Foules(calories) than we need. The diet gurus tell us that it is $ecause we have all those shiny new fast-food restaurants tempting us from every street corner, $ut this is not the first time in history that there has $een plenty to eat (whether it is coo"ed Guic"ly or not) and modern +mericans and +ustralians are not the first people to $e exposed to a high-fat diet. 0emem$er, the Inuit lived on nothing $ut whale fat for thousands of years. 3ood energy is measured in "iloFoules or calories A the older Imperial system. 8ne calorie is the same as .,@< "iloFoules ("F). +nother common energy measure, although not commonly applied to people or food, is the watt. + watt measures electrical energy consumed per hour. Thin"ing of energy this way helped me understand what people were going on a$out when they tal"ed a$out $urning Foules or calories. +t last I had something to compare it with. + C!-watt light $ul$ uses C!

watts of energy every hour. 8ne watt is eGuivalent to three and half (=.C) food "iloFoules per hour. (!.@C calorie per hour) The C!-watt $ul$ would need to %eat& Fust over ;!! "iloFoules (<; calories) every hour to light the room. -ou need a$out !! "iloFoules (,!! calories) per hour Fust to "eep your $ody alive, so in light-$ul$ terms, an adult human is a ,;!-watt appliance. The average can of soft drin" contains a$out C<! "iloFoules(,<< calories). In other words, the can contains enough energy to light a room for three hours, or run a human for ?! minutes. The energy contained in petrol is also measured in Foules(calories). 8ne litre of petrol contains a$out =;!!! "iloFoules (@!!! calories) (a$out the same as a litre of olive oil), so if your car is getting ,C"m per litre, it is $urning ;!!! "iloFoules (<!! calories) every "ilometre it travels. The "ill or $e "illed nature of evolution has ensured that a mammal that&s survived as long as we have in the evolutionary chain is pretty miserly with its energy consumption. +nimals that waste energy need to eat more food. 7eeding more food in nature With the ener y fro! J ;ou cou5d , 8ne can of soft drin" 5ight a room for three hours .tay alive for ?! minutes #oil ;5 of water *rive a car ;<!m 0ide a $icycle @"m
3igure ,!.,D We get good mileage from our food. If *etroit could

manufacture a car as fuel efficient as the human $ody, it would get ,;@!"m from every litre of petrol.

means more chance of missing a meal. 1iss enough meals and you don&t survive long enough to reproduce. 7ature&s a tough place and energy wasters went $y the wayside many millennia ago. 8ur enormously efficient energy use means that all we need to travel @"m on a $icycle is the energy contained in the ,! teaspoons of sugar in that can of soft drin". To do the same thing in a car, we would need the energy contained in ,"g of sugar (;!! teaspoons). 6ut in this fashion, riding a $icycle @"m and not drin"ing a can of soft drin" $oth have approximately the same energy effect. I "now which I would rather do.

Don9t consu!e

or

Do e6ercise

(an of soft drin" (hocolate $ar 3ast-food $urger

C<!"F ,;=!"F ;,<!"F

0ide a $icycle @"m .wim laps for an hour 0un C"m

3igure ,!.;D .ome actions that have eGuivalent energy effects.

-ou could wor" out how many Foules were in a piece of food $y $urning it completely and measuring the heat given off. If you $othered to do that you would come to the conclusion that our food is made up of four $asic components, and that each of

these components has a fixed Foule value. 3ourteen per cent of our energy needs are supplied $y proteins, at the rate of ,>"F per gram. 6roteins are found in meats and some nuts and vegeta$les. 3ifty-three per cent of our energy is supplied $y car$ohydrates, again at the rate of ,>"F per gram (car$ohydrates are pretty much everything we eat that is not meat or fat). Thirty-three per cent of our energy comes from fat found in meats and vegeta$le oils. 3at is a more efficient energy store than protein or car$ohydrate, $ecause it doesn&t need to contain water to hold it all together. 8ne gram of fat yields almost twice as much energy (=@"F) as either protein or car$ohydrate. The only other maFor source of energy (well, more maFor for some of us than others) is alcohol. 8ne gram of alcohol stores ;?"F of food energy. 3i$re is a "ind of car$ohydrate that we can&t digest $ecause we literally don&t have the stomach for it. (ows and other grass eaters have evolved a capacity to digest fi$re using an extra stomach. .ince we haven&t gone to so much $other, fi$re doesn&t yield any energy in our diet. .alads, fruits, whole grains and vegeta$les are high in fi$re, which is why their Foule values are so low compared with their mass.

8ur super food converter turns every edi$le part of food (which is everything except the fi$re) into energy. +nything we don&t immediately need for energy is stored as $ody fat or glycogen for later use. 8ur extraordinarily efficient energy use means that increasing the amount of physical exercise we do is significantly less effective at reducing fat storage than consuming less energy in the first place.

The amount of energy we need to live o$viously depends on what we are doing, $ut an average young adult male is li"ely to

need a$out ,!,!!! "iloFoules (;<!! calories) per day, and an eGuivalent female pro$a$ly needs a$out @!!! "iloFoules (;!!! calories) per day. (hildren, sedentary and older people reGuire less energy and physically active people need more. If we are eating around a$out the average for our age and gender, around >! per cent of the energy we consume is reGuired Fust to "eep us alive. This is called our $ase meta$olic rate (#10). +n adult&s $rain alone consumes ;< per cent of our energy inta"e and a child&s $rain uses < per cent of all the energy they consume. The remainder of the #10 is used to "eep our heart $eating, our lungs $reathing, our $ody temperature sta$le and so on. + further ,! per cent of what we eat is consumed in digesting the food and converting it to energy. That leaves us with ;! per cent for everything else, li"e wal"ing to the $us, ma"ing the $ed and any other exercise we choose to do. If you are an exercise nut then you will need more than that ;! per cent and you&ll get it either from your stored $ody fat or from rewarding yourself with a can of soft drin" and a chocolate $ar after a wor"out. When I was in university, I suffered from an extreme ina$ility to $e $othered going to lectures. (onfronted with the need to satisfy people (such as my parents) who were suffering under the impression I was attending an educational institution, and having no desire to actually attend a lecture, I eventually drifted towards the very well-eGuipped gymnasium. The gymnasium had lots of interesting gadgets that you could use and appear to $e doing something. Weightlifting in general appeared to $e a form of exercise that didn&t reGuire running (not my forte A this was $efore everyone went treadmill cra9y). Having more hours than were decent availa$le to me, I eventually $egan using the eGuipment properly. The inevita$le endorphin rush "ic"ed in and I found myself actually addicted to wor"ing out. .pending three to four hours a day at the gym for four years had a fa$ulous effect on my physiGue. I slimmed

down and was no longer the pudgy teenager who had entered that august institution. I could eat whatever I li"ed, "nowing that I would head for the gym and $urn it off. The effect lasted exactly long enough for me to fool my wife-to-$e into marrying me. +s soon as I stopped exercising li"e a maniac, the weight I had lost (and much more) piled $ac" on and it seemed there was nothing I could do a$out it. 8ver the years I would sporadically do a $it of exercise, $ut nothing ever "noc"ed more than a "ilo off and it certainly didn&t seem to $e worth the effort. What I didn&t realise was that I had nature wor"ing against me on two fronts. 3irstly, my $ody was Fust too efficient. I had never done the maths to see exactly how much exercise was needed Fust to $urn off that extra can of soft drin" and chocolate $ar I had got in the ha$it of gulping down, let alone actually eat into the fat stores. The reason for that was that the information isn&t laid out li"e that anywhere. It&s actually Guite tric"y to wor" through the data and come to those conclusions. #ut there&s nothing controversial or in dispute a$out any of it. It&s Fust that it seems someone forgot to pu$lish the user guide for the human $ody. I can see the policy reason $ehind avoiding that "ind of exposure. The last thing any$ody in authority wants is for us all to have another reason not to exercise. #ut it would $e handy to "now anyway. The second pro$lem was that the "ind of food I was eating was actually ma"ing it harder for me to lose weight, no matter how much exercise I did. +n example pro$a$ly $est illustrates this. + glass of whole mil" contains a$out @g of fat, @g of protein and ,,g of sugar in the form of lactose. 5actose is half galactose and half glucose. 'alactose is converted to glucose in the process of a$sorption $y my $ody, so the car$ohydrate in mil" is all glucose as far as my pancreas is concerned. 1y

hypothalamus accurately counts Foules and controls the consumption of mil" $y monitoring the car$ohydrates (using insulin and leptin), fat and protein (using ((2). 1y hypothalamus %sees& every single one of the C!!"FTs in the glass of mil". +ll of the normal hormone responses are triggered and I feel appropriately full for having consumed those Foules. 3or decades, Fust a$out anyone in authority had $een telling me that drin"ing whole mil" was a $ad thing to do $ecause of all the saturated fat it contained. Instead, I should $e drin"ing something much healthier li"e, say, a nice glass of apple Fuice. + similar Guantity of apple Fuice contains no fat (that&s good, according to the health gurus A so it would no dou$t $e proudly la$elled ,!! per cent fat free), no protein, , g of fructose, Cg of glucose and g of sucrose (; g of sugars in total). The g of sucrose is $ro"en into its component fructose and glucose $y our $odies, adding ;g each to the totals of fructose and glucose in the drin". .o the drin" effectively contains ,Cg of fructose and @g of glucose. The glucose is counted $y our pancreas Fust as with the mil". The ,Cg of fructose, however, is completely ignored $y the pancreas. The fructose is converted directly to a$out >g A four-ninths of ,C (the four $eing the Foules per gram of car$ohydrate, and the ninths $eing the Foules per gram of fat) A of circulating fatty acid. This is a$out the same amount of fat as with the mil", $ut this time no ((2 response is triggered $ecause the fat was introduced through the liver, not the intestine. 7o glucose is created as a result of the fructose ingestion and no insulin response is stimulated. 8f the !!"F in the Fuice, my hypothalamus only %sees& the ,= "F provided $y the glucose. The ;C@"F provided $y the fructose slips through completely undetected. To feel as full as I would after consuming the same Guantity of mil", I would need to drin" five times as much apple Fuice (a$out a litre). If I actually did that, I would directly create =<g of circulating fatty acids

or, put another way, four times as much as I would $y drin"ing the glass of mil". The fructose in the apple Fuice delivers $ig helpings of fatty acids while sidestepping the insulin- and ((2-driven appetite controls. 7ot too many people drin" a litre of apple Fuice in one sitting, $ut than"s to the mar"eting efforts of the fast-food and softdrin" giants, people freGuently consume a large soft drin" or sha"e with a meal. + standard large soft drin" in an +ustralian fast-food restaurant is C!!ml. That Guantity of soft drin" contains C@g of sugar. The sugar is half fructose. The = g of fructose is efficiently converted to ,<g of $ody fat and our $odies only count half the "iloFoules (<@!). The other <@! "iloFoules are completely ignored, giving our $ody permission to eat <@! more "iloFoules than we would otherwise eat in that meal. + large orange Fuice at the same restaurant might $e smaller (only ;<ml) $ut contains a$out the same amount of fructose. If you drin" fructose with a meal, the fructose gives your $ody permission to consume many more "iloFoules without feeling full. To eat = g of fructose in nature you would have to eat four large apples. Who could do that and still fit in a $urger and friesM If you consume those fructose Foules in the form of orange Fuice or soft drin" with a meal, you will still $e a$le to eat a large meal and not feel full, $ut the total num$er of Foules you eat will $e significantly higher. +ll of those extra Foules end up adhered to your waist and other less than desira$le places. #ut wait, there&s more. The presence of the fatty acids (created from fructose) in the $loodstream dulls the effect of insulin, eventually ma"ing us insulin resistant. This means we have to ma"e even more insulin to respond to the Foules we are detecting. 8ver time, as we $ecome more and more insulin resistant, we can eat more and more without feeling full. 3ructose pulls a real two-card tric" on our digestive system. Its Foules snea" past undetected, giving us permission to eat more. The undetected fructose gets

converted directly to fatty acids and then those fatty acids degrade our a$ility to tell when we are full, giving us permission to eat even more. In the ,?C!s, %meal deal& pac"aging started to dominate the /. and eventually the +ustralian fast-food industry. It is done to generate greater profita$ility $y ensuring we $uy a drin" whether we are thirsty or not. It also ensures that when we sit down to our

+i ure 1/=%: In the three decades $etween ,?>! and ;!!!, the average +merican increased their daily "iloFoule inta"e $y ;< per cent and their softdrin" and Fuice inta"e $y C= per cent. In the C! years $efore that, their "iloFoule inta"e had $arely changed at all. 7otice how it ta"es a$out five years for each new pea" in soft-drin" consumption to flow through into increased demand for more "iloFoules. The delay is caused $y fructose wor"ing its insulin resistance magic on appetite.

ham$urgers and fries, the sugar in the soft drin" (and the Fuices) permits us to eat more than we should, as well as ma"ing us fatter A I struggle to $elieve this is a happy

coincidence for fast-food purveyors. Total "iloFoule inta"e for the average +merican in the early ,?>!s was a$out the same as for their grandparents in ,?,!. However, the steadily rising wave of sugar consumption accelerated $y soft drin"s and Fuices ensured that $y the turn of the twenty-first century, +mericans were consuming ;< per cent more "iloFoules per day than they had $een Fust three decades earlier. That extra ;!!! "iloFoules per day translates to each of them accumulating an added "ilogram of $ody fat every two to three wee"s (assuming they do nothing else to com$at the weight gain). The average +ustralian&s daily "iloFoule inta"e is accelerating at a rate only slightly $ehind that of the average +merican. We are all eating hundreds of "iloFoules more per day than our parents were and then are terri$ly surprised when we "eep getting fatter. The average +merican adult consumed no added dietary fructose ($esides that found in fruit) in ,@<!. :ust ,<! years later they were consuming almost =;"g per year, the eGuivalent of two cans of soft drin" (or glasses of fruit Fuice) and one chocolate $ar every day. The =;"g of fructose they consume every year is converted directly to , "g of $ody fat and completely $ypasses their appetite-control mechanism. They still eat Fust as much as they otherwise would, and add , "g of $ody fat every year (again, assuming they do nothing else to com$at it). The average +ustralian is not far $ehind, so it&s no wonder that we constantly struggle to avoid gaining weight. )xercising and dieting help us lower that weight gain $ut it will always $e a losing $attle for as long as we continue to consume fructose. To $urn off that extra , "g (and Fust maintain our starting weight for the year) we would need to run >"m every single day of the year (yep, even on the wee"end). .taying thin in an environment where almost all food is now flavoured with fructose is li"e trying to row a canoe with a $ar$ed-wire paddle. )xercise is good for you for all sorts of reasons, $ut

losing weight shouldn&t $e one of the motivations. )xercising at a level that would even $egin to undo the weight you put on from consuming fructose is almost impossi$le (if you still want to do anything else in your life). + far saner approach is simply not to consume the fructose in the first place. 3ructose is a powerful catalyst for weight gain that no reasona$le amount of exercise can possi$ly com$at (unless you happen to $e a $ored uni student and don&t care too much a$out (4*s, dia$etes and cancer). I lost !"g doing no particular "ind of exercise A something I am sure would dismay the producers of The Biggest /oser. While my way definitely ma"es for $oring television, it&s hardly surprising given how extraordinarily efficient we are at using and preserving energy. 3or exercise to wor" as claimed, we would have to $e the most energy-inefficient creatures ever evolved. )xercise is certainly good for you. It "eeps you toned and all your maFor muscle systems in good wor"ing order. We are designed to wal" and run when we need to. We are, however, the only animal that feels the need to perform unnecessary exercise. We are uniGue in our desire to exercise purely for the purpose of losing weight. #ut it is a spectacularly inefficient means of achieving that goal (even if it does ma"e for good television to watch people trying). *on&t exercise if your dominant purpose is to lose weightD let a lac" of fructose do that instead. If you want to go for a wal" or "ic" a $all, then go right ahead. If you don&t feel li"e it, then don&t do it. 7ow, much more than I ever did $efore, I sometimes feel li"e exercising Fust to feel healthy or to play a sport. In fact, lethargy was one of the first things that disappeared when I stopped eating fructose. That $eing said, once you do correct your appetite control $y removing fructose, you will find any exercise you do feel li"e doing to $e incrementally more effective than previously. The reason is that you will not $e fighting the %invisi$le& fructose

"iloFoules that effectively ensured that for every step you too" forward, you too" two steps $ac". If you were previously consuming ,;!! "iloFoules per day in added fructose (a large Fuice and a couple of $iscuits), then that was ,;!! "iloFoules your $ody didn&t see. Those %free& "iloFoules were directly converted to ==g of $ody fat, meaning you would have to swim laps for an hour every single day Fust not to gain weight. If you eliminate fructose from your diet, your $ody will accurately count every "iloFoule. +ny unusual exercise that you do will $e financed from your fat treasury. -ou will feel hungry more Guic"ly after you have done the exercise, $ut if you simply eat when and what you normally would, you will not eat any more than you usually do, and you will have lost the fat forever.

11= A :ECIPE +O: COLD T):<E;

I am struggling to remem$er a day in my adult life when I didn&t consider myself on a diet. /sually there was nothing formal a$out it. I would hear a$out this or that diet $eing raved a$out on the telly or mentioned in scholarly tones on the evening news, and then I would pic" and choose which $its of it sounded sensi$le and "inda sorta $e on it (or something vaguely resem$ling it). I would always try to $uy low-fat things $ecause everyone said you should. +nd in $etween $outs of not $eing a$le to stand the aftertaste, I would generally choose diet soft drin"s. #ut much as dieting seems all pervasive now (Fust try to get through a day without seeing at least one advertisement or discussion a$out some "ind of diet), dieting as a phenomenon is a relatively new fad. Weight Watchers, one of the first organised groups of dieters, was founded as recently as ,?C=, Fust three years $efore I was $orn. The 1editerranean diet, the first mass-mar"et diet (invented $y *r +ncel 2eys A the fat hater), was similarly only first popularised in the ,?C!s. The num$er of overweight +mericans only $ro"e through the ! per cent level in a$out ,?C! (it too" until ,?>! in +ustralia). (learly, $efore ! per cent of us were overweight, there wasn&t the mass-mar"et appeal for dieting. In the four decades since the start of Weight Watchers, millions of diets have $een foisted upon an eager and ever more desperate pu$lic, with no o$vious $enefit except to ensure that the owners of women&s maga9ines enFoyed happy retirements. 7ow almost twice as many people are overweight and cutting "iloFoules, fats, car$s, and Fust a$out everything else the fads have demanded. When my wife 5i99ie announced our impending twinship, I was Fust as trapped in the dieting-with-no-visi$le-results treadmill as I

had ever $een. 3ree access to the $iggest medical li$rary in the world (the we$), however, allowed me to read my way to a conclusion that, now that I see it, seems $lindingly o$vious. 3ructose was "illing me and everyone else as surely as if arsenic were $eing poured into the water supply. 1y research had convinced me $eyond all dou$t that I had to stop eating fructose. I had to ensure vigilantly that as little of it crossed my lips as was possi$le. I had started out loo"ing for a way not to $e fat. I was now worried that $eing fat was the least of my concerns. I had to stop poisoning myself. If that stopped me $eing fat (or at least made it easier not to $e) then all the $etter. 1y first disappointment was discovering that food la$ellers aren&t reGuired $y law to include information a$out whether fructose is in the food we $uy, and if so, how much. +ll the la$els say is %sugars& under the heading %car$ohydrates&. -ou can get massive detail on every "ind of fatD saturated, monounsaturated, polyunsaturated, trans fats (than"s, I suspect, to *r 2eys& significant influence of health policy ma"ers). #ut all you get on sugars is %sugars&. That la$el includes all compounds that end in %ose&, so lactose, glucose, sucrose, fructose, maltose, etc. are all lumped in together. Ta"e a loo" at a carton of whole (unflavoured) cow&s mil" and you will see it contains .>g (or , teaspoon) per ,!!ml of %sugars&. .o a litre of plain whole mil" contains ,! teaspoons of sugarO #ut $efore you start tipping all your mil" down the sin", it&s $est to remem$er which sugar it is A lactose. 1il" does not contain any fructose, notwithstanding that its nutrition la$el would lead you to expect that it might contain Guite a lot. There is no way to tell from the la$el that mil" contains no fructose. When you loo" at flavoured mil", it gets even more complex. + litre of chocolate mil" typically contains a$out ,!!g of sugar.

It&s mil", so we "now $y a process of elimination that > of those grams comes from the lactose. The rest is what ma"es it sweetD ordinary old ta$le sugar (sucrose). The sucrose is of course half glucose and half fructose. The litre of chocolate mil" therefore contains ;C.<g of fructose. It would $e easier if it were Fust la$elled that way, $ut I found that I got pretty efficient at doing those sorts of calculations after a while. The good news is that we come eGuipped with a $uilt-in fructose detector that allows us to sense the presence of fructose $efore we swallow it. I don&t recommend conducting taste tests $efore $uying (unless you fancy close contact with the consta$ulary), $ut it is a very handy way to tell whether you should $e eating something. I found that I simply needed to $e aware of what the detector was telling me and react in the opposite way to the way I had to date. If food tastes sweet, it pro$a$ly contains fructose. The sweeter food tastes, the more fructose it pro$a$ly contains. I wouldn&t have "nown the exact num$ers, $ut I could have detected the presence of fructose in chocolate mil" $y the difference in taste $etween it and the plain mil". 1y $uilt-in fructose detector would already have told me the answer arrived at with so much la$el analysis and science earlier. 1il" is not sweetL therefore, it doesn&t contain fructose. .ince any amount of added fructose is an unaccepta$le amount, you really don&t need to do the maths. I have never $een very good at reading la$els and I don&t advocate it as a pastime unless you really do have nothing $etter to do. +fter several years of navigating around fructose in everyday food, I&ve developed some simple rules to live $y. 3ollow these rules and I guarantee you will successfully avoid ?? per cent of the fructose in your current diet. If you follow these rules, all the weight-loss eGuipment you will need is already $uilt into the $ody you wal" around in. -ou will have no need of "iloFoule-counting guides, food scales, 'I ta$les, car$ ta$les or fat ta$les. 1ost importantly, you will not feel li"e

you are on a diet and after a while food tastes $etter anyway. This will dramatically increase your chances of stic"ing to this new way of eating, and it will $e more li"ely to $ecome simply a lifetime ha$it. If you achieve that, you will pro$a$ly never gain weight again and you will li"ely have no need of any other diet again. -ou will disappoint millions of %health entrepreneurs& and destroy thousands of $usiness plans, $ut you will $e the lean, mean machine you were designed to $e from the $eginning. Here are the rulesD 0ule ,D 0ule ;D 0ule =D 0ule D 0ule <D Don9t drin" su ar Don9t snac" on su ar Party foods are for 7arties .e carefu5 at 1rea"fast There is no such thin as ood su ar

They sound familiar, don&t theyM They are a lot li"e what every &<!s and &C!s mother told their children a$out food, $ut which we all seem to have forgotten (with a$le assistance from some pretty s"ilful mar"eting campaigns).

:u5e 1: Don9t drin" su ar

In the modern world there are very few drin"s that aren&t sweetened with sugar and therefore fructose. If you are thirsty, drin" water or mil". If water and mil" don&t appeal, you aren&t really thirsty (if that doesn&t sound li"e your mother, nothing does). +ll full-strength soft drin"s are a$out C per cent fructose

$y weight. That translates to a$out ,!g of $ody fat for the average =><ml can of soft drin". The most popular fruit Fuices are even worse than soft drin" (this is pro$a$ly why they are the most popular). 3ruit Fuices often taste sweeter than soft drin"s, $ut the fruit Fuice industry has very cleverly convinced us that they are, in fact, %natural&, and therefore healthy. +n average apple Fuice is a$out > per cent fructose $y weight. This means that a drin" of Fuice the si9e of a soft-drin" can directly creates a$out ,;g of $ody fat. These figures are for unsweetened Fuices A often manufacturers (particularly those targeting children) add even more sugar to overcome the tart taste of citric acid in citrus Fuices, or Fust to ma"e it sweeter. -ou will $e a$le to detect whether sugar has $een added $y ta"ing a close loo" at the ingredients list. #ut at the end of the day, it doesn&t really matter whether you&re Fust drin"ing the fructose from the fruit or getting a little $it more from the added sugar. It&s all fructose and it&s all $ad for you, whether it&s %natural& or added. In redientsD Water, mango (,?U) and $anana (,>U) purees, cane sugar, flavour, vitamin ( (ascor$ic acid).
3igure ,,.,D The ingredients list from a popular $ottle of fruit nectar. In +ustralia, ingredients are listed in descending order. This ,5 drin" contains ,=;g of sugar, some of which is clearly added cane sugar.

There is a silver lining for those unimpressed $y my recommendation of a water and mil" fluids diet. 1ost alcoholic drin"s do not contain significant amounts of fructose, it $eing one of the sugars fermented to create the alcohol. #eer contains lots of maltose $ut is fructose free. 1ost wines are largely fructose free, except for dessert wines, some sweet spar"ling wines and %coolers&. 1ost hard liGuor is also fructose free, as long as you don&t add mixers ($esides water) to them. The only mixer that doesn&t contain fructose is soda water (tonic water is surprisingly high in sugar). 5iGueurs contain vast amounts of

sugar and must $e avoided. This was $ad news to meL I had a $it of a coffee liGueur ha$it $efore swearing off fructose. If you can&t face up to water, try switching to spar"ling mineral water (without flavouring) or plain old soda water. *iet soft drin"s, of course, do not contain fructose and are perfectly accepta$le su$stitutes as long as you are happy that the potential health effects of the su$stitutes are no worse for you than the fructose (see (hapter ,= on sugar su$stitutes). 8f course, coffee and tea ($eing pretty much hot water with $itter flavouring) are fine to drin" as long as you don&t add sugar. 6re-pac"aged iced-tea and iced-coffee drin"s are $oth very high in fructose. It&s important to point out that $anning fruit Fuice doesn&t mean cutting whole fruit out of your diet. 0ipe fruit does contain fructoseL that is, after all, where the name fructose comes from (fru'tus is the 5atin word for fruit). + fresh apple contains a$out the same fructose percentage $y weight as apple Fuice. The reality, however, is that the car$ohydrate $ul" and fi$re contained in an apple ma"es it very difficult to eat the num$er of apples reGuired to consume the same amount of fructose that is in the apple Fuice. We can all easily drin" a C!!ml glass of apple Fuice and eat a normal meal with it. 4ery few of us would $e a$le to eat the eGuivalent four large apples and then eat a normal meal. What9s o"ay Water What9s not 3lavoured waters (including children&s cordials)

(offee and tea (without Iced tea or coffee (if they sugar) contain added sugar)

1il" *iet soft drin"s #eer, most wines and %neat& hard liGuor

3lavoured mil" .oft drin"s *essert wines, sweet liGueurs and alcohol with a mixer (except water or soda water)

3igure ,,.;D .ome common drin"s and suggested fructose-free su$stitutes. -ou should really only drin" to Guench your thirst or get that 3riday-night glow A you can still do $oth and $e fructose free.

When fructose is consumed in whole fruit, the fructose in the fruit $ypasses our appetite-control mechanisms Fust as effectively as the fructose in the apple Fuice or soft drin". What slows us down is our stomach $eing physically full and our digestive system having to process the ,@g of fi$re (C! to >! per cent of an adult daily allowance) that the whole apple gives us. The practical reality is that most of us could not, and would not, eat more than one or two pieces (,!!A;!!g) of fruit in a sitting, and the stomach-filling effect of so doing stops us from eating ,!!A;!!g of something else as well. 0esearchers now "now that fi$re acts to increase the effect of insulin in clearing the $lood of the fatty acids created $y fructose. The apple you consume still contains fructoseL the difference is that there is less of it, and the damage is mainly limited to fat storage. #ecause of the fi$re contained in the apple, you are not left with circulating fatty acids to add to your ris" of a (4*, dia$etes or cancer. )ssentially, the fi$re converts the effect of fructose to $eing close to the same as eating too much of anything else A it ma"es you fatter if you eat too much of it and don&t use the energy. 0emem$er, our $odies have a limited capacity to process fructose and use it for energy Fust as if it were glucose. The

fructose in those few pieces of fruit can $e processed $y our $ody. It is only when we start introducing added fructose (without fi$re) that we start to cross into dangerous territory (you could call for *r (leave&s $ags of $ran, I guess). If you are li"e most of us and fruit represents an occasional supplement rather than a large portion of your diet, then there is a$solutely nothing wrong, and Guite a lot right, with continuing to eat whole fruit. :ust remem$er, fruit Fuice is not an accepta$le su$stitute for whole fruit. %*on&t drin" sugar& is a pretty straightforward rule. 5iGuid fructose delivered via Fuices and soft drin"s is the most dangerous, simply $ecause relatively large Guantities of fructose can $e ingested with no other elements (such as fi$re, other car$ohydrates, proteins or fat) to trigger your appetite control. 0ealising you need to stop drin"ing sugar is easy. 3or me, doing it was a little harder. I was on a one (at least) soft drin" a day ha$it. If I saw a soft-drin" machine outside the supermar"et, I was tempted to pop a coin in the slot and get a nice cold can. I live in a tropical climate so all those pictures of ice-cold cans of drin" were very tempting. The machines always sold cold water as well, $ut I couldn&t $ring myself to pay the same, or more, for so-called spring water. 1y preferred alcohol was gin and tonic or coffee liGueur. When I actually sat down and thought a$out it, cutting out fructose in drin"s was going to $e tric"y. The first thing I did was start $uying in $ul". I would $uy diet soft drin"s in ; -can cartons and fill the fridge at home. This was financially as well as medically smart as they were freGuently on special, which meant I was paying a$out a Guarter as much, or even less. Whenever I felt tempted to $uy a soft drin" I told myself I could have one at home, and if I couldn&t wait, I chose a diet version from the machine. The taste wasn&t Guite as good as the full-strength stuff $ut it still felt li"e I was getting a treat (which seemed to $e my primary

motivation). I worried a little a$out what the artificial sweeteners might $e doing to me, $ut I was more worried a$out what I knew fructose was doing to me. +fter a month or so, I was really getting to hate the aftertaste that comes with artificial sweeteners. *rin"ing soft drin" was turning from a pleasura$le reward into something I could easily dispense with. I decided to switch to unflavoured car$onated mineral water. It was cold, refreshing and didn&t have the aftertaste, so I enFoyed it more. #y then I had forgotten what the real stuff tasted li"e anyway, and the draw to drin" it was nowhere near as strong as it had $een. -ou might $e a$le to go cold tur"ey on liGuid fructose, $ut I needed to step down through artificial sweeteners. .ince then, I haven&t loo"ed $ac". I found that soda water was often cheaper than mineral water so eventually I switched to that. 7ow I rarely drin" anything other than mil" or plain old tap water. 7o willpower is reGuired to "eep me from the sweet stuffL it Fust no longer appeals, and the thought of what it will do to me is enough to "eep me from the remotest temptation. I still struggle to Fustify paying for tap water in a $ottle, $ut if I&m out and thirsty then that&s what I do. 8n the alcohol front, I switched to diet tonic in my 'VT and then eventually decided I preferred the taste of wine. It was much easier to switch at that level, $ut then again I had never $een a regular drin"er of anything $ut $eer and I didn&t need to change that at all. 5ow-car$ohydrate $eers have recently $ecome popular. 3rom a fructose perspective, the amount of car$ohydrate in $eer (which is maltose) is irrelevant. #ut if you li"e the taste and li"e paying more for $eer, then go right ahead and drin" low-car$ $eer.

:u5e $: Don9t snac" on su ar

It seems so harmless, doesn&t itM -ou&re standing there waiting

for the Fug to $oil and the Far of assorted cream $iscuits catches your eye. .urely Fust one or two won&t hurt, you thin" to yourself. I was caught $y the casual snac" several times a day on Fust a little $it of sugar. I wasn&t hungry, I Fust felt li"e a little treat. What I "now now is that each cream $iscuit contains a$out three teaspoons (, g) of sugar. )at two of those and you are pumping Cg of undetected fatty acids directly into your arteries. Thin"ing a$out it that way helped me pause $efore reaching for the Far. /nfortunately, there is no diet-drin" eGuivalent for $iscuits. They are still well and truly stuc" in the low-fat ages. %*iet $iscuits& generally have even more sugar than their normal counterparts. The manufacturers have to get some taste in there somehow, and $ecause they reduce the fat content, they compensate $y loading the $iscuits up with more sugar. #ecause I couldn&t do my diet soft-drin" su$stitution tric" with $iscuits, I Fust had to go cold tur"ey on them. This was pro$a$ly the hardest thing I had to do in my Guest to $ecome fructose free. 8f course, Fust one $iscuit will not do any permanent damage, $ut I found I needed to ma"e a clear $oundary for myself. It was much easier simply to say I was never going to have sweet $iscuits at all rather than say sometimes I could and sometimes I couldn&t. Whenever I did relax the rule a little, I found that $y the end of the wee" I&d eaten a whole pac"et of $iscuits, no pro$lem at all. 3our cream $iscuits a day (two in the morning and two for afternoon tea) deliver ,>!! "iloFoules and ;@g of fructose. This means that $esides dumping ,;.<g of fat into my arteries, the little snac" delivers <! invisi$le "iloFoules in Fust one dayO I would have eaten ,>!! "iloFoules, $ut my hypothalamus would have counted only ,=!!. + "ilogram of $ody fat contains =@,!!! "iloFoules, so if I snac"ed this way for a$out three months, I would gain ,"g without my $ody ever ta"ing account of having eaten it at all.

If I was capa$le of having one snac" a year, then this would not have $een a pro$lem for me. The trou$le was that I got in the ha$it of having a $i""ie whenever I made a cuppa and the simple maths shows that is a short trac" to $ig pro$lems (without even contemplating the fact that, since I lac" oestrogen and wasn&t eating fi$re with the snac", a fair $it of that "ilo of fat would still $e sitting in my arteries). The thought of all this was too ugly for me, hence 0ule ;D don&t snac" on sugar. I did come up with an alternative that wor"ed very well for me. I removed the Far of $iscuits and replaced it with a Far of nutsD sometimes macadamias, sometimes cashews, sometimes almonds A whatever ta"es my fancy at the time. I can Guite happily snac" on the nuts instead of a $iscuit. They still contain a lot of "iloFoules, $ut the difference is they are all $eing counted. If I snac" heavily, I&m Fust plain not hungry at mealtime and either don&t eat as much or don&t eat at all. The flipside to this rule is that, if you want to gain weight, you need to "eep eating when you feel full. .o if for whatever reason you want to gain weight, you will have to consciously resist the urge to stop eating when you feel you have had enough. 3or the rest of us this Fust means that when your $ody says you have had enough, stop eating, no matter how much is left on your plate or how irritating it is to throw away a halfeaten meal. The only way you would $e a$le to get through a fructose-free !!!-"iloFoule meal (which contains roughly two to three times the "iloFoules you need in a meal) would $e actively to fight the urge to stop eating. 0emem$er this when you are ordering and life will $e less frustrating (and expensive).

S!a55 #urger 3rench fries .oft drin" Total "iloFoules ;!!! ,!>! ;! = ?!

4ediu! ;!!! ,< ! C;! ,C!

Lar e ;!!! ,?!! ? ! @ !

3igure ,,.=D 2iloFoules in a typical fast-food %meal deal&. It&s surprising to many how easy it is to come $y a !!!-"iloFoule meal. + medium $urger meal deal will do it.

:u5e %: Party food is for 7arties

Thin" a$out the "ind of food you might encounter at a $irthday party. + good party would have sweets, cupca"es, ice-cream, Fellies, Fam tarts, doughnuts, chocolates and, of course, $irthday ca"e. )very single one of these foods is very high in fructose and should not $e part of your daily diet. I wasn&t in the ha$it of eating these foods every day (and I dou$t you are either) $ut it is easy to slip into the ha$it of having ice-cream after your main meal or rewarding yourself with a few pieces of chocolate when you sit down for the evening. This rule as"s you to cut out those treats. -ou will notice as you go fructose free that desserts you $arely noticed as sweet at all $ecome sic"eningly sweet. I couldn&t find any definitive research on this adaptation of the palate to sweetness, $ut it definitely happened with me. It&s at the point now that a plain old $anana tastes almost un$eara$ly sweet to me.

This is the rule that reGuires the most cooperation and understanding from your friends and family. /nless every$ody you "now is also going fructose free, you are going to $e offered these little treats. 6erhaps it&s a slice of chocolate ca"e to cele$rate a $irthday at wor". 6erhaps it&s every$ody else in your house having a $owl of ice-cream after dinner. 6erhaps it&s attending a dinner party and $eing offered a dessert that your hostess spent all afternoon slaving over. 5ittle though they may $e, it&s the constant repetition of those sweet treats that does the damage. )at Fust <!g (a$out four sGuares) of chocolate every night for a year and you will consume . "g of fructose. That . "g will translate directly to almost ;"g of extra $ody fat. #ut sometimes you Fust shouldn&t say no. /nless you never want to $e as"ed to a dinner party again, I wouldn&t $e reFecting the dessert your friend slaved over all afternoon if I were you. This rule doesn&t reGuire you to $e rudeL it simply reGuires you to "eep party foods out of your daily diet as much as you can. 8ne thing I found helped a little is to tell people what you are doing and why. They&ll usually understand and not offer you sweet food (this was especially effective for me, $ecause every$ody agreed I could stand to lose a chun" of weight and anything they could do to assist was performed at speed). I&m not saying you shouldn&t eat these foods at parties, $ut even if you do, you&re unli"ely to do too much damage (unless you go to a lot more parties than I do).

:u5e (: .e carefu5 at 1rea"fast

8ne of the things that really caught me $y surprise as a source of fructose was $rea"fast cereal. #efore you snigger too much, of course I "new that the o$vious ones made with things li"e chocolate had a ton of sugar. The ones I was surprised $y were

those that were heavily promoted as $eing healthy, high in fi$re, low in fat and generally fa$ulous for your $ody. -ou "now the type of thing A wheat fla"es mixed with fi$re stic"s (whatever they are), some sultanas and various and sundry $its of dried fruit. I had $een in the ha$it of eating a large $owl of a muesli-li"e mix of high-fi$re $its and pieces with Fust a twinge of sweetness provided $y the sultanas. I was go$smac"ed to discover that my favourite healthy cereal was actually ;C per cent sugar $y weightO #ut I needn&t worry, $ecause a little asteris" next to the sugar entry on the nutrition la$el informed me that it was mostly fructose (from the sultanas). That meant my average ,!!g $owl of healthy cereal was ladling invisi$le fat into my stomach at an extraordinary rate every morning. I decided to investigate the matter thoroughly and found that there were very few $rea"fast cereals that had less sugar than the average apple. If you want to eliminate fructose (and I assume you wouldn&t have read this far if you didn&t) then $rea"fast is going to present the greatest challenge for you. In other meals, sweet food is generally o$vious. :ust don&t have dessert and a sweet drin" and you will have done pretty much all you need to for most meals. ."ip morning and afternoon tea (at least the nontea or -coffee part of them) and you will $e almost fructose free. #rea"fast is tric"ier $ecause for most of us, $rea"fast cereals are the prepac"aged, easy option and we are stuc" with whatever the manufacturer chose to include. I didn&t much li"e the loo" of the low-fructose options in the cereal aisle. I had eaten those wheat $iscuits as a child, $ut usually only after adding half a cup of sugar to the mix. I did eat porridge in the winter, $ut only after adding honey. I decided to a$andon cereal altogether and switch to toast. + few wee"s without the fi$re inspired me to veer towards some of the newer high-fi$re multigrains. I now eat a high-fi$re multigrain $read li$erally smeared with 4egemite, Fust a$out the only spread without any

sugar. I realise that "ind of $read is not for everyone, so I&ve laid out in the ta$le on page ,C; some of the other options I occasionally consider when pure wholegrain $read for $rea"fast gets a $it tedious. 8$viously all of the figures assume that you will not $e adding sugar to your cereals (or your $acon and eggs). *oes this mean you shouldn&t eat $rea"fast cerealsM 7ot really, as long as you are careful a$out which ones. 0ead the la$el. If the level of %sugars& is less than ,!g per hundred (whether they are la$elled

+i ure 11=(: 6opular +ustralian $rea"fast cereals graphed $y fat (vertical) and sugar (hori9ontal) compared with an apple. The usual suspects are almost as high in sugar as a chocolate $ar. The shoc" is how high some of the %healthy& cereals are.

+ood #acon )ggs 0olled oats -east extract spread 1ultigrain $read 6anca"e mix (,) Weet-#ix White $read Wholemeal $read (orn fla"es 6eanut $utter 0ice $u$$les

A77ro6i!ate A fructose 1y 'ei ht !U !U ,U ,U ,U ;U ;U ;U ;U U U <U

Anythin 1e5o' this 7oint contains !ore fructose than !ost fruit= #ran fla"es 0aisin toast #ran stic"s 3i$re and fruit mix (,) 7ut corn fla"es High-energy cereal .ultanas and $ran .ugary colourful cereal 6anca"e mix (;) 3i$re and fruit mix (;) 1aple syrup .traw$erry Fam 1armalade >U ?U ,!U ,=U ,CU ,CU ,>U ;,U ;;U ;=U ;@U =!U ==U

Honey

,U

3igure ,,.<D .ome $rea"fast foods and the approximate amount of fructose they contain ($y weight). These percentages vary slightly across different $rands of similar products. In some instances they vary significantly, so it&s worth chec"ing the la$el. Try to avoid anything $elow the middle shaded line.

as natural or not) and they also contain ;.<g per hundred or more of fi$re, then they are no worse for you than eating an eGuivalent amount of fresh apples. .tomach distension will stop you eating too much and the neutralising effect of the fi$re will stop the fructose doing too much damage. 8f course you could save yourself Guite a $it of money $y Fust eating whole apples instead (a "ilo of apples costs a$out half as much as a large $ox of fancy high-fi$re cereal).

:u5e *: There is no such thin as ood su ar

Watch out for mar"eting tric"s. 1ar"eters "now that the smart fol" among us are already wary of %added sugar&. -ou&ve pro$a$ly already noticed foods la$elled %no added sugar&, a favourite among Fuice vendors, or %contains only natural sugars&, one the $rea"fast-cereal people li"e to use. 3ood manufacturers will happily tell you that $ecause the food was already incredi$ly sweet, meaning they didn&t have to add any sugar, it is somehow $etter for you. .ometimes they will say that $ecause the food was sweetened with honey it is somehow $etter for you than using sugar. .trictly spea"ing, honey is $etter than cane sugar. Honey contains ! per cent fructose compared with the <! per cent in sugar, $ut neither is going to

do your waistline or your arteries any favours at all. %7atural sugar& can often $e directly translated to %contains high levels of fructose&. 3ruit Fuices are all natural sugar A that&s a huge part of their mar"eting message A $ut as we&ve discussed, they contain high levels of fructose. To the point that if I was dying of thirst and given a choice $etween a soft drin" and any Fuice, I would have to choose the soft drin", $ecause it pro$a$ly has ,! to ;! per cent less fructose than the Fuice. (ereals pac"ed with sultanas and raisins are often up to ,< per cent (;CA=!g of %sugars& per ,!!g) fructose $y weight and are full of %natural sugar&L it&s no wonder they don&t need much added sugar.

+i ure 11=-: High-fructose foods ($y weight). It&s not all down to %evil& processed food manufacturers. -es, there are the expected party foods, $ut some of the highest-fructose products are what a mar"eter would call %natural&. Ta"e a loo" where honey, dates, figs and dried apricots appear. 8n this chart, an apple (the highest-fructose whole fruit) would appear Fust to the left of the reduced-fat chocolate mil".

%0educed fat& can also often $e directly translated to %high

fructose&. The food industry "nows that consumers peppered with a constant $arrage of %fat is $ad& messages want to see la$els li"e this on their food. #ut, as mentioned earlier, the reality is that reducing fat in food recipes often means increasing sugar. :ust for fun, next time you are at the supermar"et compare the sugar content of a low-fat food item with its full-strength cousin. It will often contain more sugar. Here&s a few to get you startedD Product 6eanut $utter +u55Bfat 8ersion Lo'Bfat 8ersion 7ercenta e su ar 7ercenta e su ar @U ,=U ,,U ,>U ;>U

(hocolate mil" ,!U 4anilla yoghurt ,<U 4anilla icecream ; U

3igure ,,.>D Here are a few everyday examples from the supermar"et shelves. 7ote that the low-fat version invaria$ly contains more sugar.

I found that the fat-free la$elling tactic is also a favourite with manufacturers of confectionery in particular, who freGuently proclaim that their Felly sweets and marshmallows are %?? per cent fat free& or similar. That sort of advertising ma"es a$out as much sense as a soft-drin" manufacturer proclaiming their products to $e fat free (perhaps their focus groups told them that we wouldn&t fall for that one). .weets are almost pure sugar. The only ones that aren&t are those that also include chocolate (which is one-third fat). The mar"eters& hope is that the %?? per cent fat free& la$el will convince you that you can

consume foods that contain >< per cent or more sugar without any concerns at all. I developed a neat little rule of thum$ to help me Guic"ly tell how $ad something was li"ely to $e for me. )very g of sugar I saw on the la$el translated to a$out ,g of $ody fat (on me) that wouldn&t $e detected $y my appetite-control system. %5ow 'I& is another mar"eting term that I saw Guite a $it of on the la$els in the supermar"et. +s we saw in (hapter =, a low'I food is one that has a low glycaemic index or insulin response. The theory is that, if you eat low-'I foods, energy is released more slowly and you will not have the pea"s and troughs associated with foods high in glucose. Theoretically, this means you should stay satisfied for longer and $e less li"ely to want to eat again a short time after your last meal. While the glycaemic index of foods is li"ely to $e critically important in diets designed to treat insulin resistance or type II dia$etes, it is very li"ely that it is irrelevant in the Guestion of weight control for those of us without those conditions, since it ignores the effect of leptin in moderating medium- to long-term appetite. 1y experience was that most foods la$elled as %low 'I& were $ad for me for entirely different reasons. The 'I num$er is prone to easy manipulation $y clever mar"eters. 3ood that has a large percentage of fat usually has a lower 'I rating, regardless of the amount of glucose in the product. This is also true of protein, $ut to a lesser extent, since proteins often end up $eing converted to glucose $y our $odies anyway. .ince fructose is largely invisi$le to our pancreas it also has a low glycaemic index. -ou can ingest large amounts of fructose and have almost no insulin response, hence a low 'I. .ome low-'I foods are genuinely good for you, such as the highfi$re multigrain $read ( @ out of ,!!) that I switched to when I found out my cereal was over one-Guarter sugar. #ut a lot of manufacturers are using the fructose loophole to gain a

mar"eting advantage. +n o$vious example of this is a ha9elnut spread that is << per cent sugar and =! per cent fat, $ut which o$tains a low-'I rating ( C out of ,!!). +lmost any chocolate$ased product will $e low 'I $ecause of the high amounts of fat and fructose, $ut most manufacturers aren&t courageous enough (yet) to la$el a $ar of chocolate %low 'I&. I discovered that I should treat low-'I foods with extreme caution. If you&re not dia$etic, it is pro$a$ly safer simply to disregard the low 'I la$el altogether and employ your $uilt-in fructose detector. 7ot all low-'I food is $ad, $ut the sweet ones most definitely are.

1$= SO IS T&IS A DIET#

When I started avoiding fructose I immediately started losing weight. It was almost completely effortless. .ure, initially I struggled with my soft-drin" addiction and occasionally found myself ta"ing Fust one (or two) $iscuits when offered. #ut with the coping strategies laid out in the previous chapter it didn&t ta"e long $efore I forgot the feeling of a sugar rush. I didn&t change anything else a$out my life. I didn&t start exercising more or watching what I ate in any other way. The interesting thing was that, within a few wee"s, I Fust wasn&t that hungry anymore. I used to happily down three pieces of pi99a and still want moreL now I found myself eating three and having to stop $ecause I felt painfully full. It had $een a long time since I felt full li"e that. I was definitely eating less $ut it didn&t reGuire any great feat of willpower. When I did eat, I really enFoyed it. I could still eat things I loved sometimes, li"e pi99a and sausage rolls and pies. I stopped caring a$out low fat. That doesn&t mean I actively sought out fatty food, it Fust means I didn&t worry a$out the fat content any more than I worried a$out the water content. I Fust ate whatever too" my fancy. I only had one rule A no fructose. Interestingly, Fust as *r -ud"in had discovered, when I told myself I could eat all the fat I wanted, I initially $inged, $ut after a while I found myself wanting it less and less. The weight didn&t fly off A this is no $ride&s two-wee" diet. In fact, it&s not a diet at all. It&s Fust removing a single su$stance from the food you eat (it helped me to thin" of fructose li"e slow-acting arsenic). 0ather li"e %going on the $ant&, I lost a$out half a "ilo a wee". It too" almost two years, $ut I lost !"g A and then stopped. I haven&t changed anything to this day, $ut I no longer lose weight. I still avoid fructose, $ut o$viously my $ody has reached some sort of eGuili$rium. I

don&t watch what I eat. 1y $ody does it all for me. When I feel hungry I eat whatever I li"e (except fructose). When I am full I stop. 3or the first time in my life I can rely on the fact that my $ody "nows what it is doing and trust the feed$ac" it gives me. If you do as I did and find your eGuili$rium weight is still a little higher than you would li"e it, and your idea of fun is not wor"ing out at the gym four hours a day, then there is one thing you might try. +s I&ve mentioned, I found in all my trial and error that low-car$ohydrate diets do actually wor", so you might li"e to reduce your car$ohydrate inta"e for a while. The only catch is that when you stop doing it and revert to normal car$ohydrate inta"e, do not fall off the fructose $andwagon or you will gain $ac" all the weight and more.

5ow-car$ diets are effective (at least in the short term), $ut if you thin" a$out it for a moment or two it will $e o$vious why they wor" initially and also why no-one can ever seem to stay on one for very long. The vast maFority of our food supply is glucose (car$ohydrate) $ased. If you decide that you will not eat most of the foods around you, you are li"ely to struggle to find sufficient "iloFoules in the remainder of the foods availa$le to you. If you stic" to the diet it will $e a daily fight to find anything you are allowed to eat, $ecause every vendor of food assumes that you, li"e the rest of us, want at least half (and prefera$ly three-Guarters) of your food to contain car$ohydrates. -ou will li"ely eat fewer "iloFoules than you reGuire out of sheer lac" of choice and you will li"ely lose a lot of weight initially. The daily struggle to find food you are actually a$le to eat will eventually get to you and you will a$andon the diet. Where most people go wrong is that in stopping the diet they revert to eating fructose and again mess up their appetite-control system. With no appetite control, they veer $ac" on to the path of continuous weight gain.

(ar$ohydrates (except for fructose) are not $ad for you. -ou need glucose from car$ohydrates to live. If you don&t get the

glucose from car$ohydrates, your $ody will switch to 6lan # and get the glucose from protein, and this is how these diets wor". 6lan # is less energy efficient than 6lan +, $ut o"ay to use in an emergency. 5ow-car$ diets do wor"L they are Fust hard to stay with. /se them if you want to lose weight Guic"ly or give yourself a nudge off a plateau. *on&t worry too much a$out the details. -our $ody really can&t tell the difference $etween (anadian ya" $utter and plain old $utter. :ust stop eating car$ohydrates. -our $ody will scream that it is starving (no matter how much protein you eat) for the first ; hours. +t this point you are $urning through your glycogen stores and your $ody is har$ouring the hope that you have Fust forgotten to eat. +fter this, your car$ohydrate-signalling system $egins to shut down and you will no longer feel hungry. )at proteins, salads and vegeta$les until you can stand it no more (I suspect a$out two wee"s), then revert to normal. The only car$ohydrate you have to avoid when eating normally is fructose, and than"fully you can rely on your perfectly functional fructose detection device. If food tastes sweet, don&t eat it. If it doesn&t, go right ahead A your $ody will tell you when to stop. The rules I wor"ed out to help me avoid fructose meant I could eat as much fat as my $ody would allow A $ut I do have one word of warning a$out that. +s I read far and wide on the $adness of fructose, I consistently came across studies on one type of fat that could $e very $ad for you A trans fat. Trans fat is a type of unsaturated fat and it, li"e fructose, has $een added to our diets in significant Guantities in the last ! years. Trans fatty acid molecules are made $y adding hydrogen molecules to unsaturated fats li"e vegeta$le oils to ma"e them more saturated. This gives the product a longer shelf life and a higher $oiling point (which ma"es it good for use in frying fast food). 4ast amounts of trans fats are added to our diets in this way. 1argarines that have not $een altered to reduce trans fats can contain up to ,< per cent trans fat (as a ratio of total fat).

4egeta$le oils used for deep frying in the fast-food industry can contain up to < per cent trans fat. + small amount of fat in nature is trans fat, too (; to < per cent of animal fat is trans fat). Trans fat loo"s Fust li"e normal fat to our appetite-control centres. /nli"e fructose, the amount of trans fat you can consume is controlled $y your appetite-control mechanisms, $ut it is so dangerous that even the small amount your $ody lets you eat should $e avoided. Trans fats have a proven effect on increasing 5*5 ($ad) cholesterol and, conseGuently, the ris" of heart disease. .o, while a fructose-free diet means you can eat as much fat as your $ody allows, you should avoid foods high in trans fats such as margarines and some frying oils, unless they specifically say that they have $een modified to reduce trans fats. 5oo" for la$els that promote trans fats in the ; to < per cent range or less on these types of foods. (ompletely removing added fructose from your diet will restore your appetite to normal within wee"s, if not days. /ntil your appetite control returns to normal (so you can tell when you are full), fruit consumption should $e "ept to the couple of pieces a day recommended $y most nutritionists. 8ther than that, it is simply a case of reading la$els. +s a rule of thum$, you can halve the num$er of grams under %sugars& per ,!!g for most foods to approximate the percentage of fructose in the food. -ou will $e distressed to find that all processed foods contain some sugar, $ut while there is no a$solutely safe level of fructose consumption, if you stay under the amount contained in a couple of pieces of fruit per day (<A,!g) you will pro$a$ly remain within the limits of your digestive system. 8ne of the $est things you will find a$out removing fructose from your life will $e that the less you have of it, the less you want it. 8nce your appetite-control mechanisms are wor"ing properly again, you simply won&t want to eat or drin" sweets or to snac" $etween meals. -ou will find foods you previously ate

without thought to $e too sic"ly-sweet to enFoy. -ou will still reach for the chocolate, $ut a com$ination of the very sweet taste and the "nowledge of exactly how many grams of $ody fat each piece is adding to your waistline (a$out ,g for every g of sugar on the nutrition la$el) will have you refusing any more than one piece (which you pro$a$ly won&t enFoy much anyway). 6eople will compliment you on your admira$le restraint $ut you will "now that no great wor" of willpower is reGuiredL you Fust don&t really want it anymore. If you simply do not eat or drin" food that tastes sweet you will $e in ,!! per cent compliance with the no-fructose rules. -ou can eat anything else you li"e (avoiding trans fats where possi$le), Fust don&t eat sweet-tasting food. This rule is very hard to stic" to for the first few wee"s. This shouldn&t come as a $ig surpriseL you have spent your life to this point o$eying your evolutionary design and see"ing out sweet food. #y implementing these rules you will effectively $e going %cold tur"ey& on sweet foods. This is the very hardest part of your new way of eating. If you can get through those initial couple of wee"s, everything thereafter will $e dramatically easier. #ut you must get through the withdrawal period. Have strength. 8nce fructose is removed from your diet, you will $e stopped from eating too much $y your now relia$le and accurate food meter. -ou won&t feel hungry $etween meals and you will avoid what is pro$a$ly for most of us the second-largest source of fructose in our diet, the occasional sweet $etween-meals snac". If you do this every day the weight will slowly and effortlessly peel away. -ou didn&t get fat overnight and you won&t lose it overnight either, $ut $y avoiding sweet drin"s and snac"s you will $arely notice the change in diet. Implementing the rules I&ve wor"ed out through trial and error allows you to lose weight without really doing anything (except avoiding fructose). -ou will not feel li"e you are on a diet at all.

1%= ALTE:NATIVES TO +:)CTOSE

8ne of the things that made it easier for me to give up fructose was $eing a$le to switch from full-strength soft drin"s to artificially sweetened ones. Than"s to the miracle of modern chemistry it was still possi$le to get my hit of sweetness without swallowing fructose. It seems I&m not the only one enFoying a gulp of artificially sweetened drin". +rtificial sweeteners are the $oom industry of the new millennium, and their existence has significantly throttled $ac" the upward acceleration of our lust for fructose. If they didn&t exist we would now $e consuming almost twice as much fructose as we currently do. There are four main artificial sweeteners. 1anufacturers prefer to call them non-"iloFoule sweeteners or high-intensity sweeteners, so as to distinguish them from other manufactured sweeteners such as ta$le sugar and H3(.. These chemicals taste hundreds of times sweeter to us than sugar, so while they contain the same num$er of "iloFoules per gram as any other car$ohydrate, their dieting power

+i ure 1%=1: +rtificial sweetener consumption has s"yroc"eted. The average +merican would $e eating ;,"g per annum more sugar (,!.<"g more fructose) if it hadn&t.

comes from the fact that much less is reGuired to o$tain the same sweet taste. 3or example, saccharin is <<! times sweeter than sugar, it is chemically sta$le when mixed with other foods and has a good shelf life. #ecause the human digestive system has no receptor proteins for it, it passes straight through our $odies. It therefore effectively contains no Foules. .accharin, the oldest high-intensity sweetener, was accidentally discovered in ,@>@ $y scientists wor"ing on coal tar derivatives at the :ohns Hop"ins /niversity in the /nited .tates. Ira 0emsen and his 'erman student, (onstantin 3ahl$erg, noticed that residue on their fingers from experiments with $en9oic sulfinide tasted initially intensely sweet and then $itter. The

story goes that Ira was eating a $read roll after a hard day in the la$ and noticed it $eing very sweet. +fter a $it of trial and error, he wor"ed out that the sweet taste was coming from chemical residues on his fingers from the experiments he had $een doing that morning. Ira and (onstantin wrote up their discovery in ,@>?, $ut it seems (onstantin was the more commercially savvy of the two, $ecause he arranged some funding from 'ermany and raced off to the patents office (much to Ira&s annoyance). (onstantin christened his new product saccharin, which was a little more mar"eta$le than $en9oic sulfinide. It was immediately a $oon in the treatment of type I dia$etics (the only type of dia$etic there was at that time), since they could consume foods sweetened with saccharin without raising their $lood-sugar levels. This "ept them safer from the ravages of (then) untreata$le high $lood sugar. .accharin was commercialised in the ,@@!s $ut didn&t enFoy any mass-mar"et success until the fat epidemic inspired the dieting industry in the early ,?C!s. .ince ,?!>, there have $een concerns a$out the safety of saccharin for human consumption. It was investigated $y the /.*+ for causing digestive pro$lems and was $anned as a food additive Fust prior to World War I. *uring the war, a sugar shortage forced the government to lift the $an so the incessant demand for sugar could $e satisfied (it would $e a $rave government that stood $etween the people and their sweet treats). .accharin&s unpleasant metallic aftertaste limited its potential mar"et to people who really had no choice (dia$etics and a country suffering from a war-induced sugar shortage). In ,?=>, a partial solution was discovered. (yclamate was also accidentally discovered in a la$ loo"ing at something else entirely. /niversity of Illinois graduate student 1ichael .veda was wor"ing on creating an anti-fever medication when he put his cigarette down on a $ench where some

cyclohexanesulfamic acid had $een spilled. When he pic"ed the cigarette up, he noticed a sweet taste. 1ichael also raced off to the patents office to protect the discovery of what he christened cyclamate. 3ood additive testing was a $it tougher $y then and it too" a lot of money to do the necessary testing. 1ichael sold his patent to +$$ot 5a$oratories, who did the testing that finally (in ,?<@) permitted cyclamate to $e approved as safe for use in food. (yclamate is much less sweet than saccharin, at only <! times as sweet as sugar. It also has an unpleasant aftertaste, $ut less so than saccharin and, to some extent, when they are mixed together they mas" each other&s aftertaste. .accharin mixed with cyclamate (,! parts cyclamate to one part saccharin) was mar"eted as a sugar su$stitute in restaurants under the $rand .weet&7 5ow and was used in the first no-Foule soft drin", T+#, released $y (oca-(ola in ,?C=.

The widespread use of saccharin mixed with cyclamate in the ,?C!s inspired more detailed animal studies (many funded $y the sugar industry), which started to raise concerns a$out $oth chemicals possi$ly causing cancer. In ,?C?, a rat study showed conclusively that the common ,!D, mixture of cyclamate and saccharin definitively caused $ladder cancer in rats. The /nited .tates immediately $anned cyclamate as a food additive. In ,?>>, a (anadian study showed that high doses of saccharin (the eGuivalent of @!! cans of T+# a day) caused $ladder cancer in ,> of the ;!! rats in the study. The (anadian government immediately $anned saccharin as a food additive. #ut the /nited .tates had a $igger pro$lemD $y then the /. pu$lic was consuming ;;<!!! tonnes of saccharin (mostly in diet soft drin"s) a year. When it $ecame pu$lic that the /. government was considering a $an, the howls of pu$lic protest (largely funded $y the saccharin industry) were loud and long. 6eople didn&t want to lose their diet drin"s. In the end, the /nited .tates compromised $y reGuiring products containing saccharin to carry a warning a$out possi$ly causing cancer, $ut a $an was not implemented. To this day, cyclamate is $anned in the /nited .tates $ut not (anada, and saccharin is $anned in (anada $ut not the /nited .tates. .weet&7 5ow is sold on $oth sides of the $order with different inert fillers instead of the respectively $anned ingredient. #oth cyclamate and saccharin are approved for use in +ustralia.

(yclamate and saccharin had the mar"et to themselves until ,?@,, when aspartame received /. 3*+ approval. +spartylphenylalanine,-methyl ester, once again, was an accidental discovery. In ,?C<, :ames .chlatter, a chemist wor"ing for '* .earle V (o, was loo"ing for an anti-ulcer drug when he lic"ed his finger. The sugar industry ensured that some well-funded researchers lined up their rats for aspartame when its turn came to $e tested. The usual dou$ts were raised a$out aspartame causing cancer, in particular $rain cancer, or possi$ly $rain damage. 1any years of lo$$ying ensured that aspartame remained on the $anned list until ,?@,. .oon after 0onald 0eagan $ecame the /. president in ,?@!, '* .earle&s ()8,

*onald 0umsfeld (yes, that one), reapplied successfully for certification for use in dry goods. +ustralia Guic"ly followed suit and approved aspartame in ,?@,. The /. 3*+ commissioner who approved aspartame was +rthur Hayes. Hayes resigned from the 3*+ in 7ovem$er ,?@=, shortly after extending aspartame&s approval for use in soft drin"s, and immediately too" up a position as a senior medical advisor to '* .earle&s pu$lic relations firm. *onald 0umsfeld engineered the sale of '* .earle to 1onsanto in ,?@<. The aspartame patent expired in ,??;, opening up 1onsanto to significant competition. 1onsanto sold the struggling aspartame $usiness to its present owners, 1erisant (a company created $y 1onsanto managers to $uy the $usiness), in ;!!!. #esides aspartame, 1erisant has a su$stantial saccharin $usiness $randed )Gual, which competes with .weet&7 5ow. +spartame tastes similar to sugar and has the same num$er of "iloFoules. It is, however, ;!! times sweeter, so where a softdrin" manufacturer would use <<g of sugar in a can, they can replace it (and its ?;! "iloFoules) with Fust one-Guarter of a gram of aspartame, which provides Fust four "iloFoules. /nli"e cyclamate and saccharin, aspartame is actually digested $y the $ody rather than simply passing straight through. +nd this is the source of many of the medical concerns with it. #esides the ac"nowledged danger to phenyl"etonurics (people who suffer from a rare genetic ina$ility to process phenylalanine A there is a warning on every product containing aspartame for these people), studies have shown all manner of adverse effects, ranging from $rain tumours to $rain lesions and lymphoma. 1any of these studies have come in for criticism concerning their methods, motivations and results. There is $ig money at sta"e in the artificial sweetener industry and deep poc"ets on $oth sides of the argument. 0ather li"e the controversial studies in the &C!s and &>!s that showed smo"ing caused lung cancer,

there is always another study availa$le to contradict. Two recently pu$lished large-scale studies have failed to show any adverse effects from aspartame consumed at the levels that is currently commonplace. +spartame is mar"eted as 7utrasweet and is the sweetener that I ingested large Guantities of while getting unhoo"ed from sugar soft drin"s. I don&t drin" them anymore $ecause after a$out four wee"s I no longer craved sugar and I was getting sic" of the metallic aftertaste of aspartame. I don&t "now whether it is any worse for me than fructose and I dou$t anyone else does either, given it has only $een commercially availa$le for ;< years, $ut I too" the calculated ris" that a short exposure to it might not "ill me. I hope I am rightL only time will tell. 3or now, I&ll stic" to water and mil" if I&m thirsty. The last of the $ig four is sucralose. 8nce again the story is of accidental discovery, $ut this time the researchers were loo"ing for a sweetener and they were doing it on the payroll of the $iggest sugar distri$utor in the world, Tate and 5yle. The Tate and 5yle scientists were wor"ing with *r -ud"in&s sugar research team at Nueen )li9a$eth (ollege, 5ondon, in the late &C!s when they discovered that trichlorogalactosucrose (chlorinated sugar A hence the mar"eting spin that it is made from sugar) tasted C!! times sweeter than sugar. .ucralose is mar"eted as .plenda and was approved for use in food in +ustralia in ,??= and the /nited .tates in ,??@. 5i"e aspartame, sucralose has the same num$er of "iloFoules as sugar and is digested $y our $odies. However, $eing three times as sweet as aspartame, even less of it needs to $e used to o$tain the same effect. .ucralose is a type of organochloride, a class of chemicals "nown to cause adverse effects in humans in relatively small concentrations. +s a result it has undergone a $arrage of testing li"e no other sweetener $efore. +ll approving countries have satisfied themselves that in the concentrations we are li"ely to consume, sucralose is safe (sounds reassuring,

doesn&t itM). The studies showed that when you fed mice the eGuivalent of ;!!! cans of diet soft drin" per day you could cause *7+ damage. If they dou$led the dose, they could cause $rain damage. High doses are used in studies li"e this to simulate lifetime consumption Guantities for us, $ut such an approximation is fraught with difficulties in applying the results. 8ne of the things I found interesting a$out all these rat studies was how intensively the sugar industry and its various lo$$y groups have targeted the tas" of proving artificial sweeteners are dangerous. 1uch more conclusive animal and human studies have shown how destructive sugar is, $ut there has never $een a suggestion that sugar should $e $anned. This is not to say I am in any way reassured a$out the sweetener studies. +rtificial sweeteners have simply not $een in our diet long enough to tell. 7o amount of rat studies will reassure me that industrial chemicals that have $een in our food supply for less than a few decades are definitely safe. 5ong-term trials have not $een done and many in the medical community Guestion whether they are safe for continuous human consumption. It too" almost ,!! years of mass consumption $efore researchers started Guestioning whether sugar was dangerous. (an we really "now if sucralose or aspartame are safe after Fust a few decadesM

.ucralose is the golden child of the Q,.< $illion sweetener industry. Its sales are accelerating at an exponential pace and it now commands over C; per cent of the artificial sweetener mar"et. + honey pot li"e the artificial sweetener mar"et is continuously attracts new players and we can expect to see a lot more chemicals approved for use in the near future. +litame (;!!! times sweeter than sugar) is already approved for use in +ustralia and is pending in the /nited .tates. 7eotame (,=!!! times sweeter than sugar) is pending approval in $oth the /nited .tates and +ustralia .

.ome of the $ad press a$out dead and deformed rats has convinced a few consumers to $e wary of artificial sweeteners. (onscious of this, some manufacturers are now promoting foods as sugar free that are sweet $ut do not contain sugar or any of the high-intensity sweeteners. These products usually contain polyols (sugar alcohols). The more popular polyols are sor$itol, maltitol, mannitol and xylitol. .or$itol is created from glucose. The change to the chemical structure of glucose means that sor$itol is incompletely ta"en up $y the glucose transport proteins in our gut. +s a result, a gram of sor$itol delivers only ,, "iloFoules, rather than the ,> "iloFoules contained in a gram of glucose. The other C "iloFoules per gram are ignored $y our $ody and pass straight through. #ecause of this, if you eat more than a$out <!g of sor$itol you will experience the same symptoms as people who are lactose intolerantD diarrhoea and $loating. .or$itol retains the same sweetness as glucose (it&s a$out C! per cent as sweet as sugar), so it often needs to $e mixed with a high-intensity sweetener to ma"e it taste the same as sugar. The really $ad news is that sor$itol is completely and rapidly converted to fructose $y our liver. The same is true for all of the other polyols. 3rom a meta$olic perspective, eating polyolsweetened food is exactly the same as eating sugar (except I guess slightly less of it actually gets into your system). That

$eing the case, you might as well eat the sugar as eat food that has $een altered to reduce its Foules using polyols. 6eople worried a$out sugar consumption often propose honey as the natural alternative. Honey is relatively expensive, $ut the fact that it is natural is often promoted as giving it a halo of goodness. Honey is ! per cent fructoseL that&s why it&s so sweet. 3rom a chemical perspective, there is no practical difference $etween eating a teaspoon of honey and a teaspoon of sugar. .ome people have said to me, %#ut it&s natural, so we must $e evolved to deal with it.& 8f course honey is natural, $ut it is extraordinarily difficult to get any Guantity of it if you have to deal with the $ees directly (try it, I dare you). 8nce it is farmed and conveniently placed in $ottles on the supermar"et shelves, it is easy to consume significantly greater Guantities than you would ever encounter in nature. The sugar industry has done its $est to attac" H3(. as a sweetener in the last few decades. H3(. has halved the value of the /. sugar industry since ,?@!, so they have good reason to $e concerned. Whispered campaigns a$out the evils of manufactured H3(. have raised some pu$lic dou$ts, $ut the H3(. ma"ers have cleverly hit $ac" with research that shows H3(. is no worse for you than sugar. In my hum$le opinion that&s rather li"e saying that running someone over with a red truc" is no worse than running them over with a $lue truc". However, from a chemical perspective, the H3(. producers are a$solutely correct. H3(. is a mix of fructose and glucose (usually << per cent fructose). We "now that sucrose (ta$le sugar) is a molecular $onding of fructose and glucose (<! per cent of each). +s far as our $ody is concerned, whether they are $onded at the molecular level ma"es no differenceL it splits them up anyway. H3(. is slightly worse for us gram for gram $ecause it contains slightly more fructose than sugar, $ut manufacturers use less of it anyway, so that a product containing H3(. is no sweeter than the eGuivalent sugar-

flavoured product. H3(. is $arely used in +ustralia. We have way too much sugar availa$le here to $e $othered muc"ing a$out chemically altering corn syrup. There is one su$stitute for sugar that no manufacturer is promoting. It isn&t a manufactured industrial chemical. It tastes as sweet as sor$itol. It contains no fructose and is not converted to fructose $y your liver. -our $ody is perfectly adapted to consume this su$stance without destroying your appetite system. It won&t ma"e you gain weight or give you a (4*, dia$etes, cancer, tooth decay or any of the other nasty side effects of fructose (or sweetener) consumption. This miraculous sweetener is glucose. That&s right, glucose, the other half of sugar. .ugar with the fructose removed. +ll of the studies on sugar have consistently proved that when rats were fed Fust glucose, none of the ill-effects created $y sugar were o$served. +nd this is certainly logical. -our $ody converts all car$ohydrates (except fructose) and most protein to glucose anyway. -our appetite-control system is perfectly adapted to dealing with glucose. In fact, it has evolved on the assumption that what you eat will either $e glucose or $e converted to it. When this dawned on me, I hotfooted it to the supermar"et to $uy a pac"et of pure glucose. It wasn&t the easiest thing in the world to find. It wasn&t in the sugar section or with the other $a"ing items li"e flour and salt. Instead, I located it in the home$rew section. It&s called dextrose, is sold in ,"g $ags (for a$out Q;) and apparently plays some sort of role in the construction of homemade $eer. *extrose is a little more than half as sweet as sugar and loo"s a little li"e caster sugar. I proudly returned home with my find and as"ed 5i99ie to ma"e a cupca"e recipe su$stituting dextrose for sugar. The resultant cupca"e is pleasant enough to eat and certainly tastes very sweet to me after a year or two without fructose, although

people who are still immersed in fructose tell me it tastes $land and a little floury. 1y investment in constructing a fructose-free glucose recipe has to this point $een limited to the cupca"es, $ut having $een fructose free for so long, I have limited motivation to ma"e sweet foods at all. I thin" that with $arely any real investment, the food industry (should it $e so inclined) could easily recreate most fructose-flavoured foods using recipes that include glucose instead. If this "ind of food were easily availa$le, it would ma"e the tas" of going fructose free much easier.

1(= IT9S ALL A.O)T 4ONE;

+s" anyone in the to$acco $usiness. +n industry that exploits hardwired evolution for profit is a licence to print money. .ugar is much $etter than to$acco though. )very$ody consumes your product every day (not Fust the ones with an addiction) and you don&t need to $other with all that complicated licensing and annoying pro$lems a$out how and where you advertise and sell your products. +nd while your sugary products are costing the health systems of most nations $illions of dollars, no-one is $laming (or suing) you. In fact, if the finger of $lame is pointed at anyone, it is pointed at your customers for not having the willpower to resist your products. +ustralia, the /nited 2ingdom and the /nited .tates all spend more than C! per cent of their respective health-care $udgets on the treatment and %prevention& of symptoms and diseases that the evidence shows are caused $y fructose. +nd the demand is accelerating. The largest direct $eneficiaries of this spending are the drug companies. 3orty cents in every dollar spent on pharmaceuticals are for drugs used in the management of meta$olic syndrome ((4*s and type II dia$etes), chiefly $lood pressure and cholesterol-lowering drugs, and insulin and drugs to enhance the effect of insulin. 1uch of the remainder relates to drugs used in the treatment of various cancers. The drug companies donate money to the various national heart and dia$etes foundations, so they can collectively continue their mission of educating the pu$lic as to the dangers of meta$olic syndrome and associated symptoms and, in +ustralia, lo$$y the government for more drugs to $e included in the pharmaceutical $enefits scheme. We need loo" no further than the +ustralian Heart 3oundation for an example of this. Its primary corporate sponsors are the maFor international

pharmaceutical companies. #esides pic"ing up the ta$ for the health effects of sugar, the taxpayer also su$sidises the production of sugar. #ecause it is a product that is su$Fect to unrelenting demand regardless of the economic cycle, sugar has always $een the target of government fundraising efforts. When the product is as popular as sugar, no$ody "nows or cares if the government ta"es its toll on the way through. +s a result, sugar production has $een su$Fect to significant taxation and government-driven price manipulation for most of its commercial life. 3or centuries, sugar has $een one of the world&s most controlled foods. It is rationed during wars and used as a commodity to swap for foreign currency. It&s also a weapon of international diplomacy and economic policyma"ing. #ecause of the politics influencing sugar, there is virtually no free trade or true mar"et competition in the world sugar $usiness. The maFority of nations, $oth importers and exporters, regulate either sugar production or consumption and price. 1ost sugar exporters, +ustralia $eing one of the largest, su$sidise their sugar farmers and then sell sugar in the world mar"et for less than its production cost during periods of world surpluses. The largest producer, #ra9il, has very intelligently designed its economy to accommodate diversion of sugar to ethanol production (all #ra9il&s cars can run on ethanol or petrol) during times of depressed prices for sugar consumption and $ac" again when prices improve. The /nited .tates& sugar policy has $een affected $y statute since ,>@?, when the 3irst (ongress of the /nited .tates imposed a tariff upon foreign sugar. The purpose of this and later tariffs was to provide revenue for the government. #eginning in the ,?>!s, the energy crisis, inflation and glo$al commodity shortages struc" at the $asic foundation of the /. federal sugar program. The result was a dramatic increase in

sugar prices and a significant decrease in the amount of sugar in the +merican diet. 3or seven years the price of sugar in the /nited .tates varied with world prices, causing chaos for /. sugar planters. 3urious lo$$ying $y the sugar industry resulted in sugar $eing included for the first time in the /. 3arm +ct in ,?@,. .u$sidies were no longer paid, $ut price supports were reintroduced and Guotas on foreign sugar were used to control supplies and support the price of sugar to producers. The com$ination of price supports and su$sidies costs the +merican consumer and taxpayer roughly Q= $illion every year. The /. sugar program provides a price floor, $ut no price ceiling, meaning the /. *epartment of +griculture prevents prices from falling $ut does not prevent prices from rising. The sugar Guotas "eep the price of sugar in the /nited .tates at a$out twice the world level. With the sugar price artificially inflated, there has $een a ready mar"et for H3(. in the /nited .tates since the reintroduction of sugar Guotas in ,?@,. The resultant damage to sugar consumption caused $y the loss of the food manufacturers, and particularly the $everage companies, has meant that sugar refining as an industry in the /nited .tates has $een in unprofita$le decline for the last two decades. H3(. is manufactured $y chemically converting corn syrup (almost ,!! per cent glucose) into a mix of fructose and glucose. It tastes almost identical to sugar. The artificial price maintenance of sugar gave the corn producers an opportunity that they gra$$ed with $oth hands in the late &>!s. Today almost half of all the corn produced in the /nited .tates ends up $eing turned into H3(.. +ll that corn largely ends up in soft drin"s. H3(. is only marginally cheaper than sugar, $ut in an industry where $illions of grams are $eing purchased every year, fractions of a cent per gram ma"e $ig differences. The taxpayer still foots the $ill.

(orn is even more heavily su$sidised than sugar. The /. government su$sidised the corn industry to the tune of Q ; $illion over the five years from ,??< to ;!!!. +lmost all /. sugar refiners have now sold up, and what remains of the industry is run largely $y grower cooperatives. #ig $usiness has Guit the sugar industry in the /nited .tates and is in the process of moving towards the future of /. sweeteners, H3(. and low-Foule sweeteners. The /. .ugar +ssociation (a lo$$y group formed in ,? = to push the interests of /. sugar growers and producers) is fighting hard against H3(., sucralose and the other sweeteners, $ut it is a $attle that it is losing on multiple fronts. #esides sugar refiners, other casualties of the /. sugar and corn programs are the people of eGuatorial third-world nations dependent on sugar exports to prop up their economies. #ecause /. sugar imports have $een cut $y @! per cent since ,?>< as a result of su$sidised sugar and corn, the economies of (entral +merica and the 6hilippines have $een pulverised. The /. .tate *epartment estimates that reducing /. sugar imports costs friendly third-world governments almost a $illion dollars a year, forcing many former sugar farmers to ta"e up more profita$le export crops such as mariFuana and heroin. In +ustralia, we are less generous with our sugar producers and we don&t have a corn industry worth propping up, $ut su$sidies are still present. +ustralia&s sugar industry consists of C<!! farms spread across too many electorates for the average politician to ignore. It competes in a world where Fust a$out every$ody is not playing $y the rules. The )uropean /nion and the /nited .tates massively underwrite their industries and this results in a mar"et that can $e dangerous territory for producers without su$sidies. In ;!!=, the +ustralian government decided to give small sugar producers incentives to leave the industry so that it could $e %rationalised for long-term economic

sustaina$ility&. +lmost half a $illion dollars was committed to the program. It&s $arely a drop in the ocean compared with the $illions pouring into the sugar industry in the /nited .tates and )urope, $ut it shows that even in +ustralia we are not immune from having to pay for sugar twice. 3irst to prop up the industry that ma"es it, and second to fix the damage it causes. The real winners from inflated /. sugar prices are, however, the three companies that $etween them control ?, per cent of the mar"et for H3(., and their three $iggest customers. The producers are +rcher *aniels 1idland (+*1), which controls =C per cent of the /. H3(. mar"etL (argill, which controls =< per centL and the world&s largest sugar refiner, Tate and 5yle, which $rings up the rear with ;! per cent through its /. su$sidiary, .taley. The customers are (oca-(ola, 6epsi(o and (ad$ury .chweppes. Tate and 5yle operates over C< sugar production facilities in ;? countries, predominantly in )urope, the +mericas and .outh)ast +sia. Tate and 5yle was founded in the /nited 2ingdom in ,?;, $y the amalgamation of the separate refining $usinesses of Henry Tate and +$ram 5yle. In the mid-,?=!s Tate and 5yle $egan to purchase land and set up production facilities in :amaica, Trinidad, #eli9e and 1auritius. In ,?C<, Tate and 5yle diversified into agri$usiness and chemical research, leaving fewer resources to improve sugar technology or yields. In the mid-,?>!s Tate and 5yle sold its plantations and $egan to concentrate on importing and refining in the /nited 2ingdom. This left countries that produce and sell raw sugar with the most ris"y part of the $usiness. In ,?@<, Tate and 5yle too" a significant sta"e in the /. sugar$eet-refining mar"et, $uying eight refineries operating under the name Western .ugar. + year later Tate and 5yle tried to $uy into the /2 $eet-processing mar"et. The #ritish 1onopolies and 1ergers (ommission vetoed this acGuisition $ecause it

would have given Tate and 5yle control over ? per cent of the #ritish sugar mar"et. In ,?@@ Tate and 5yle made an ill-fated move to consolidate the fragmented /. sugar-refining mar"et, purchasing +mstar (a cane refiner using the $rand name *omino .ugar) and .taley (ontinental (a producer of H3(.). In the late ,??!s, Tate and 5yle, in response to the volatile sugar mar"et in the /nited .tates, $egan see"ing a $uyer for its sugar holdings. In ;!!,, Tate and 5yle sold the *omino .ugar $rand to the .ugar (ane 'rowers (ooperative of 3lorida and the 3lorida (rystals (orp. + year later, over ,!!! sugar $eet growers in (olorado, 7e$ras"a, Wyoming and 1ontana united to form the Western .ugar (ooperative and purchase Tate and 5yle&s remaining /. sugar-refining interests. 6rior to the sale, Tate and 5yle accounted for more than ;! per cent of the /. sugar mar"et. Tate and 5yle is still the "ing of the world sugar industry, $ut much li"e an oil company investing in solar energy, it is ma"ing sure it has its fingers in the alternative pies as well. Tate and 5yle is the owner of the sucralose patent (developed all those years ago with the help of the Nueens (ollege team investigating the evils of sugar). .ucralose is the runaway train of the alternative sweetener mar"et and I wouldn&t mind $etting that Tate and 5yle are ensuring they are well positioned if the world suddenly decides sugar is too dangerous. +*1 and (argill are as /. home-grown as they get. #oth can trace their roots to the linseed-crushing industries that flourished in the /. 1idwest from the ,@>!s to the ,?;!s. 5inseed was crushed to produce linseed oil, a polyunsaturated oil suita$le for use in oil paint, a slow-drying, hard-wearing external paint that was perfect for the rapidly expanding settlements of the /nited .tates. #ut $y the ,? !s oil of a different "ind was ma"ing the linseed oil $usiness loo" decidedly ordinary.

#lac" gold, Texas tea, was cheaper and easier to use than linseed oil. The lac" of interest in linseed oil (it was to $e several decades $efore *r 2eys got everyone all hot and $othered a$out eating polyunsaturated oils rather than mixing them with paint) forced +*1 and (argill to diversify into corn and soy. +s it turns out, corn and soy were exactly the right things to $e growing when )urope ran out of food at the end of World War II. +*1 and (argill made a "illing exporting heavily su$sidised /. grains as part of the effort to re$uild )urope. #oth companies ended up in the H3(. $usiness as a direct extension of their grain $usinesses. Today they are heavily diversified commodity houses, $ut each controls onethird of the /. H3(. $usiness, which is worth a$out a Guarter of a $illion dollars in profit to each of them every year, most of it as a direct result of government su$sidisation. .ixty per cent of the output from all those sugar growers, corn growers, multinational sugar corporations and grain $uyers ends up in the car$onated soft drin"s made $y Fust three companies, (oca-(ola and 6epsi(o in the /nited .tates and (ad$ury .chweppes in the /nited 2ingdom. #ut these three don&t Fust sell car$onated soft drin"s. +ll have diversified into %sports& drin"s and Fuices as well. They are not the only suppliers of fructose in the world, $ut together they account for a significant and growing slice of the mar"et. In ;!!C, 6epsi(o made a profit of almost Q;.< $illion, and (ad$ury .chweppes, Q= $illion. #oth were a mere shadow of (oca-(ola&s almost Q,, $illion. Together, these three chal"ed up Q,C.< $illion in profit A a$out the same as the $ig two of the to$acco industry, +ltria (6hillip 1orris) and #ritish +merican To$acco A on sales of over Q,!! $illion, and it was Fust an average year in the softdrin" game. There&s nothing wrong with $eing in the $usiness of selling products that every human on the planet is hardwired to consume. The difference $etween sugar and to$acco is that the sugar industry has us all convinced it is our fault we&re fat,

not theirs.

+nother sector that $enefits from the mass self-delusion that we are to $lame for $eing fat is the dieting industry. 'oing to the gym is a popular %cure&. 6eople in the /nited .tates spent Q;, $illion doing that in ;!!C. They also spent Q;! $illion on diet soft drin"s, Q $illion on meal replacements, Q= $illion on low-Foule meals, Q= $illion on pharmacy diet programs, Q;.< $illion on artificial sweeteners, Q; $illion on diet $oo"s, Q; $illion on weight-loss centres and a mere Q, $illion on anti-o$esity drugs. The total /. weight-loss industry is worth over Q<@ $illion a year and is growing at a$out the same rate as our waistlines (C per cent per annum).

(haos theory is infamously misGuoted as saying that a hurricane in the /nited .tates can $e caused $y the flap of a $utterfly&s wings in To"yo. 3ructose is the mother of all $utterfly-wing flaps. + small meta$olic difference in the way our $odies process fructose versus glucose has resulted in a large percentage of the human race developing varying stages of meta$olic syndrome. (onsumers spend $illions $uying the stuff, governments spend $illions ensuring that consumers can continue to $uy it and then hundreds of $illions %treating& the health pro$lems created $y it. +nd all the while, we all "eep getting fatter and sic"er, apparently $ecause we lac" the willpower of our grandparents. If a nanoportion of the money spent on any one of the conseGuences of fructose were instead directed towards removing fructose from our diet, the world would $e a significantly healthier place A and we&d stop having to listen to those endless government commercials $eseeching us to show restraint and go to the gym for 'od&s sa"e. .ure, some very $ig companies would have to find something else to do with their time, $ut they are full of smart peopleL I&m sure they can figure

out something to do. 3at in our arteries "ills us. We are designed not to eat too much fat. We are also designed to see" out sweet food $ecause it shouldn&t "ill us. 3ructose, the su$stance that ma"es food sweet, does not occur in significant Guantities in nature. #ut we were smart enough to figure that out and extract the fructose. When we concentrate fructose so we can ma"e everything sweet, we open up a loophole in our $ody&s evolved assumptions a$out what we will $e eating. 3ructose is converted to fat, $ut there is no control in place to stop us eating too much of it. 7ow the fat that we would normally eat fills our arteries, plus the fat converted from fructose. Worse than that, the fructose ruins our a$ility to tell when we are full. 1y generation (I was $orn in ,?CC) is the first to receive an infusion of fructose every day of their lives. The results are in. If you feed humans fructose for the first ! years of their lives you get an o$esity epidemic, and massive health system costs associated with treating cardiovascular disease, type II dia$etes, oral health, cancer and miscellaneous other pro$lems. It&s time to stop. -ou can stop eating fructose $y using the fructose detector in your mouth. +n even $etter solution would $e for those who produce food to use glucose instead. .elling fructose ma"es you rich, so there are many very wellheeled groups and corporations who will not li"e the message in this $oo", and I expect the attac"s will come from all Guarters. #ut we now "now enough a$out the chemistry of the human $ody to $e a$solutely certain that fructose is a "iller of epidemic proportions, and any amount of muddying of the waters $y the vested interests should $e treated in very much the same way as those in the to$acco industry were. 5et the food fight $eginO

NOTES 1= Startin out

The Sa''harine Disease $y T. 5. (leave (:ohn Wright V .ons, #ristol, ,?> ) is usually availa$le secondhand from +ma9on.com for under Q<!. + few of the sites I found particularly useful when searching for trusted articles on medical mum$o Fum$o wereD www.med$io.info, a site that I was too ignorant to understand when I started out, $ut later discovered to $e a goldmine of relevant information. 8ver and over again I found the summaries and references on this site to $e invalua$le "ic"ing-off points for further research. The site is authored (without any real fanfare) $y 6rofessor )meritus 0o$ert Horn from the Institute of 1edical #iochemistry, /niversity of 8slo, 7orway. www.pu$medcentral.nih.gov, a massive online li$rary of articles covering the life sciences and $iochemistry. 61( is managed $y the /. 7ational Institute of Health&s 7ational (enter for #iotechnology Information (7(#I) in the 7ational 5i$rary of 1edicine. It is as comprehensive as it is authoritative and, $est of all, it is free. There are a lot of online li$raries that will let you access Fournal articles for a fee, $ut few can match the coverage of 61(. httpDPPFn.nutrition.org, an extensive online li$rary of articles which appear in the +ournal of -utrition, pu$lished $y the +merican .ociety of 7utrition (www.nutrition.org). 7ot all the articles are free $ut significant num$ers are, and it is a very decent resource in the area of nutrition research.

 www.wi"ipedia.org, an invalua$le resource. *on&t worry, I didn&t ta"e it as gospel on medical research, although I discovered it was right more often than not (the tric" is pic"ing when it&s wrong). Where it came in terri$ly handy was in providing me with a layperson&s definitions of words that medical researchers threw a$out with no explanation whatsoever. Throughout the $oo" I have used <g as an approximation for the amount of ta$le sugar in a teaspoon. 6urists will "now that it&s actually .;g, $ut using that figure Fust ma"es the calculations messier without adding a greater degree of clarity to the story. The figures on lactose intolerance rates come from an article on e1edicine.com (www.emedicine.comPmedPtopic= ;?.htm), with some cross-referencing for +ustralia to an article $y *avidson, '.6. ,?@ , %5actase deficiency diagnosis and management&, Medi'al +ournal of Australia, .ept ;?, pp. ;A . In +ustralia, the figure of >! per cent is more than reversed, with only ,! per cent of the adult population experiencing lactose intolerance. This will change into the future as more

and more of our immigrant population comes from a non)uropean $ac"ground.

$= Theories of fatness
-ou can read the %official& version of the life and times of *r +t"ins at his company we$site www.at"ins.com. William #anting&s $oo", A /etter on Cor&ulen'e (Harrison, ,@C=), is availa$le in full online at www.lowcar$.caPcorpulenceP, $ut $e warnedD it isn&t exactly easy reading. This from the introductionD
%8f all the parasites that affect humanity I do not "now of, nor can I imagine, any more distressing than that of

8$esity, and, having emerged from a very long pro$ation in this affliction, I am desirous of circulating my hum$le "nowledge and experience for the $enefit of other sufferers, with an earnest hope that it may lead to the same comfort and happiness I now feel under the extraordinary change,Wwhich might almost $e termed miraculous had it not $een accomplished $y the most simple commonsense means.&

*r .tillman&s first $oo", The Do'tors 1ui'k Weight /oss Diet, first pu$lished in ,?C> $y 6rentice Hall, has $een repu$lished as recently as ,?@> ($y *ell). -ou&ll struggle to find it new anywhere, $ut there are usually secondhand copies availa$le on +ma9on. He followed this $oo" up with The Do'tors 1ui'k "n'hes %ff Diet (6rentice Hall) in ,?C?, The Do'tors 1ui'k Teen2Age Diet in ,?>, and his 34 Day Sha&e 5& Program (*elacorte 6ress) in ,?> . Dr Atkins Diet ,e!olution (#antam) was first pu$lished in ,?>;. It was repu$lished $y +von in ,??; as Dr Atkins -ew Diet ,e!olution and is still in print today. -ou should $e a$le to o$tain a copy of it from your local $oo"store. The most recent and outrageously popular +ustralian version of the low-car$ diet is The CS",% Total Well eing Diet, pu$lished in ;!!< $y the good fol"s who $rought you this $oo" and availa$le at all good $oo"shops (hopefully my cheGue is in the mail).

%= &o' 'e turn food into ener y

If you want to read a$out *r 3rederic" #anting (no relation to our fat friend, $ut an extraordinary coincidence) and 6rofessor :ohn 1ac5eod and the story of how insulin was discovered as a treatment for dia$etes, go to the 7o$el 6ri9e we$site at httpDPPno$elpri9e.orgPno$elXpri9esPmedicinePlaureatesP,?;=P. -ou can read their acceptance speeches, see photos of them and

drill into the detail of why the pri9e was awarded to them. This site is a great resource for information on each of the numerous 7o$el 6ri9e winners that I discuss from this point on. The graph comparing high-'I and low-'I foods has $een reproduced from the Wi"ipedia commons. It was prepared $y .tudio= in +ugust ;!!C. *r :ennie #rand-1iller&s )" .a'tor6 The )lu'ose ,e!olution (Hodder Headline, ;!!;) was the first in a series of $oo"s she pu$lished a$out 'I, including recipe $oo"s, "ids& $oo"s, reference $oo"s and more $oo"s on how 'I is used. 1ost of these $oo"s are still availa$le today from your local $oo"shop.

(= )sin stored ener y

If you really li"e reading a$out the detail of some of the early discoveries in endocrinology such as #anting (from the last chapter) and 1urlin, then it might $e worth pic"ing up a copy of 4ictor (ornelius 1edvei&s The History of Clini'al 7ndo'rinology6 A Com&rehensi!e A''ount of 7ndo'rinology from 7arliest Times to the Present Day, (6antheon, ,??=). It&s unfortunately not easy to come $y and a li$rary might $e your $est $et. It&s not as dry as it sounds, really. 2oFima and 2angawa&s paper on the discovery of ghrelin is availa$le in full online at httpDPPphysrev.physiology.orgPcgiPcontentPfullP@<P;P ?<, $ut I don&t recommend reading it unless you are well on your way to completing your $iochemistry studies. They say they named ghrelin %after a word root (YghreZ) in 6roto-Indo-)uropean languages meaning YgrowZ&. I still rec"on they named it the way I suggest in the text and sought out an academic explanation for it, $ut you $e the Fudge.

*= +at !a"es you fat , or does it#

3or those who don&t indulge in %reality& television, The Biggest /oser is a long-running show that sGuee9es hundreds of hours of entertainment out of torturing a $rigade of heavily o$ese individuals with extreme exercise routines (and some mind games for fun). The graph showing fat consumed was prepared $y me using data from the /. *epartment of +griculture (/.*+). The /.*+&s )conomic 0esearch .ervice maintains an extraordinarily detailed open-access dataset on consumption of most foods and food groups in the /nited .tates (many, such as fats, going $ac" to ,?!?). This excellent resource is located at www.ers.usda.govPdataP3ood(onsumptionP. +n excellent summary of the .even (ountries .tudy is availa$le on the /niversity of 1innesota We$site at www.epi.umn.eduPresearchP>countriesPoverview.shtm. +ncel 2eys and his wife 1argaret first pu$lished their 1editerranean *iet in ,?<?. The $oo" was called 7at Well and Stay Well and was pu$lished $y *ou$leday. It&s out of print now $ut you can usually get a second-hand copy on +ma9on. If your su$scription to the Ameri'an +ournal of 7&idemiology is up to date, you will find a copy of *r 1ann&s 1aasai study in 4olume ?< on page ;C. 3or the rest of us, a free a$stract is availa$le at httpDPPaFe.oxfordFournals.orgPcgiPcontentPa$stractP?<P,P;C. *r -ud"in&s first $oo", Sweet and Dangerous6 The -ew .a'ts A out the Sugar 0ou 7at as a Cause of Heart Disease# Dia etes# and %ther (illers, *avid 1c2ay (o, ,?>;, is an excellent read, if for no other reason than to get detailed insight into the earliest experiments on intentionally feeding animals sugar and measuring the results. 5i"e Fust a$out everything else

I recommend you read, it is out of print, $ut can still $e o$tained easily on +ma9on. The +merican *ia$etic +ssociation&s ;!!; directive to avoid fructose is contained in the report entitled %)vidence-$ased nutrition principles and recommendations for the treatment and prevention of dia$etes and related complications&, which can $e found online at httpDPPcare.dia$etesFournals.orgPcgiPcontentPfullP;CPsupplX,Ps<,. .trangely, the ,?@ recommendation that people should eat fructose is not online anywhere.

-= .ioche!istry 1/1
+lmost no$ody $others to explain any of the $asic terminology or concepts when they write $iochemistry papers for pu$lication. .omething that helped me enormously in coming to grips with this stuff was a $oo" my father-in-law *r Tony 1orton (see ac"nowledgements) gave me. I heartily recommend you o$tain a copy of Har&ers "llustrated Bio'hemistry (1c'raw Hill) if you want to drill any further into the complex world of the $iochemist. I use the ;!!C edition, $ut I&m sure you&ll $e a$le to pic" up a later edition at your local university li$rary. The ;!!C edition doesn&t have much coverage of fructose, $ut it does provide a foundation to the concepts discussed in this chapter. 2eep it $y your side when reading $iochemistry papers you discover on the internet. -ou&ll need it, or something li"e it.

0= &oney 'ithout 1ees

The sweetness receptor gene in humans was first identified in research pu$lished $y the Howard Hughes 1edical Institute in ;!!, (7elson, ', Hoon, 1, (handrashe"ar, :, Bhang, -, 0y$a, 7 V Bu"er, (, %1ammalian .weet Taste 0eceptors&, Cell, vol.

,!C, Issue =, pp. =@,A?!, online at www.cell.comPcontentParticlePa$stractM uid[6II.!!?;@C> !,!! <,;). 3ollow-up research in ;!!< suggests that domestic cats ($eing carnivores) have not evolved the gene and therefore are not attracted to sweet food. -ou can read the pu$lished cat research at www.plosgenetics.orgParticlePinfoD doiP,!.,=>,PFournal.pgen.!!,!!!=. The /.*+&s +gricultural 0esearch .ervice (yep, the people who run #eltsville) maintains a fa$ulous online data$ase of the nutrient contents of over ><!! foods. -ou can access it at www.ars.usda.govPmainPsiteXmain.htmMmodecode[,;=< <!!. We don&t have anything eGuivalent to the pu$lic version of the /.*+ data$ases in +ustralia, $ut if you want to do a $it of analysis you can pull together data on what +ustralians eat from the 7ational 7utrition .urvey (77.) and the 7ational Health .urvey (7H.). The 77. was a one-off, $ut the 7H. is conducted every three years $y the +ustralian #ureau of .tatistics. #oth are availa$le from www.a$s.gov.auP. The price of sugar through the centuries is extracted from 7oel *eer&s ,? ? two-volume epic, The History of Sugar ((hapman V Hall). His prices have $een fed through an inflation calculator and currency converter to present them in ;!!> +ustralian dollars. 8$viously they are, at $est, guesses, $ut they give a relative feel for the cost of white gold through the ages. 7oel points out that sugar in , !!s )ngland was almost seven times as expensive as honey (which wasn&t all that cheap to $egin with). I created the graph of fructose consumption $efore I wrote even a word of this $oo". It was extraordinarily difficult to gather together all the information reGuired. It existed, $ut not in any one place. The data from ,?!? onwards was pulled from the /.*+ data$ases, one foodstuff at a time, $y $rea"ing out the

percentage of the food (e.g. sugar, <! per cent) that was fructose for each year and then totalling it. The figures prior to ,?!? came from the 5nion Army Data Set. This incredi$le resource crossmatches the medical records of more than =< !!! men mustered into the /nion +rmy with the /. census results from ,@<! to ,?,!. It provides Guite an accurate representation of sugar consumption in the /nited .tates at that time, as well as lots of other interesting stuff a$out soldiers& socioeconomic circumstances and health. It&s freely availa$le at the /niversity of (hicago&s (enter for 6opulation )conomics we$siteD www.cpe.uchicago.eduPunionarmyPunionarmy.html.

2= Porrid e in the arteries

The #1I calculator has $een reproduced from the Wi"ipedia commons. It was prepared $y InvictaH8' in .eptem$er ;!!C and is $ased on World Health 8rgani9ation data, which can $e viewed at www.who.intP$miPindex.FspMintro6age[introX=.html. That WH8 site is a fascinating resource. It allows you to do graphical and map-$ased comparisons of #1I data $etween countries and over time for most of the world. Ta"e a loo", it&s worth it. The /. overweight and o$esity graph was created $y me $ased on data from the /. (enters for *isease (ontrol&s 7ational (enter for Health .tatistics ((*(-7(H.). If you want to drill down further on /. health statistics, ta"e a loo" at their site at www.cdc.govPnchsP. There is an eGuivalent site maintained $y the +ustralian government. The +ustralian Institute of Health and Welfare&s site is located at www.aihw.gov.auP. 1ost of the statistics on disease prevalence and incidence in this and the following chapters come from one or other of these two sites.

3= 4ore "i55ers
The World Health 8rgani9ation maintains Guite thorough worldwide data on the prevalence of dia$etes. -ou can chec" out their latest data and, more importantly, their predications at www.who.intPdia$etesPfactsPworldXfiguresPenP. The lung cancer versus smo"ing graph was created using lung cancer death rates from the (*(-7(H. and the /. 1ortality 4olumesL you can access this at www.cdc.govPnchsPdatawhPstata$Punpu$dPmorta$sPhistta$s.htm. That data was com$ined with /.*+ cigaretteconsumption data to produce the graph. The graph comparing fructose consumption and prostate cancer death is not prepared using sophisticated medical statistic models. When I loo"ed at the fructose consumption statistics, I Fust noticed that the curve loo"ed similar to that of the prostate cancer data (from the mortality data referred to earlier), and fashioned a prediction $y simply copying the rest of the fructose curve and attaching it to the end of the prostate cancer curve. The maths might not $e there, $ut it loo"s pretty convincing to my untrained eye. The 7urses& Health .tudy has $een used to study Fust a$out every disease affecting women in the /nited .tates since ,?>C. -ou can read more a$out it at www.channing.harvard.eduPnhsP.

1/= What a1out e6ercise#

3ood energy is measured in Foules or calories. 3our "iloFoule is the amount of energy reGuired to increase the temperature of ,g of water $y one degree centigrade. To heat enough water for a cup of coffee from room temperature to $oiling point would ta"e a$out @! !!! "iloFoules of energy. + Foule is a very small unit of measurement, so dieticians always use "iloFoules or

often a$$reviate "ilocalories (thousands of calories) to %(alories& (capital %(&) as a sort of shorthand. Heating the cup of coffee would actually ta"e Fust ;! (alories in the sense most people understand, as used in food la$elling. +s discussed previously the metric eGuivalent of the calorie is the Foule, and is calculated using )instein&s famous eGuation )[mc;, where 7 is energy in Foules, m is mass in "ilograms and ' is the speed of light in metres per second. 8ne calorie (small %c&) is eGuivalent to .,@< Foules and one (alorie (capital %(&) is the same as .,@< "iloFoules ("F). Where I&ve used (alorie throughout the $oo" its always $een in lower case, where one calorie eGuals .,@< "iloFoules. :ean 1ayer was responsi$le for much more than convincing us all that exercise caused weight loss. 3or a full run-down on his achievements, ta"e a loo" at his o$ituary in the -ew 0ork Times, which you can loo" up in their archive at www.nytimes.com. The 1ayo (linic&s summary of the seven $enefits of exercise can $e found at www.mayoclinic.comPhealthPexercisePHN!,C>C. /nli"e many in the fast-food industry, 1c*onald&s pu$lishes comprehensive nutrition data on every type of food they sell. -ou can download the complete dataset from the 1c*onald&s +ustralia we$site at www.mcdonalds.com.auPHT15PnutritionP. The graph comparing "iloFoule inta"e and soft-drin" consumption was created using data from the /.*+&s )conomic 0esearch .ervice online data$ase mentioned previously.

11= A reci7e for co5d tur"ey

What is supposed to $e on a food la$el in +ustralia is determined $y 3ood .tandards +ustralia and 7ew Bealand. Their we$site at www. foodstandards.gov.auP contains a mine of information.

The $rea"fast cereal graph was created $y wandering the aisles of the local supermar"et and Fotting down the sugar and fat content of every cereal I could find. -es, I did loo" seriously weird doing that, $ut it is the only way to find this stuff out in any sort of methodical fashion. Whenever you see me give a num$er for the percentage of fructose in a vegeta$le or fruit, it is an average. The actual amount will depend on the variety, where it was grown, how ripe it is and, of course, the si9e. I&ve tried to $e very fair and choose middling num$ers for dry uncoo"ed fruit and vegeta$les in all instances.

1$= So is this a diet#

3or a comprehensive summary of current information on trans fats, you could do worse than the +merican Heart +ssociation we$site. I don&t agree with much that the +H+ says a$out fat, $ut this is worth a loo"D www.americanheart.orgPpresenter.FhtmlMidentifier[=! <>?;.

1%= A5ternati8es to fructose

The graph on artificial sweetener consumption is created from data pu$lished $y the /.*+ )conomic 0esearch .ervice.

1(= It9s a55 a1out !oney

*ata on the +ustralian sugar industry comes from www.canegrowers.com.au, a lo$$y group for +ustralian sugarcane growers. *on&t worry, I crosschec"ed with data from the +ustralian #ureau of .tatistics where it was availa$le. Information a$out each of the companies discussed in this chapter was gathered from their respective corporate we$sites and annual reports.

AC<NOWLEDGE4ENTS
1any people helped me to write this $oo". .ome of them intended to, $ut for Guite a few it was the last thing on their mind. .ome mem$ers of the medical fraternity (who pro$a$ly last loo"ed at a $iochemistry text$oo" sometime $efore 6rincess *i&s wedding) found the fructose theory Guite amusing. Their dou$t forced me to ma"e sure I understood the current research at the deepest possi$le level. 5i99ie tired very Guic"ly of my regaling everyone I met with the latest article on the chemical interactions of the '5/T transports, and politely suggested that perhaps I could write a $oo" a$out it. :udith (a pu$lished author) had the misfortune to sit next to me at a $usiness $rea"fast. The horrors of fructose ruined her meal, $ut her encouragement put me on the path to writing this $oo". 5i99ie supported me without Guestion (and with considera$le patience) through all my strange experiments with food and convoluted explanations. .he denies har$ouring a hope that if I wrote it down I would shut up a$out it. #ut if that was her plan, it $ac"fired $adly when 3ran" (my good friend and %agent&) convinced :ulie and Ingrid from 6enguin that my thoughts were worth inflicting on more than those within hearing distance. The only person who has read every draft of this $oo" since it was ,! pages long, and fastidiously corrected (almost) all the split infinitives along the way, is my father-in-law, *r Tony 1orton 03*, 1##., 1., 1*, 1.c+ppl, 3+7B(+ (retired). He hates any $ig show $eing made of his Gualifications, $ut it gave me enormous comfort to "now that someone with as impressive a list as that was loo"ing over my shoulder. Tony

wrote a $oo" on medical statistics in his retirement (Fust for fun), so he was a good person to ma"e sure I didn&t get too cra9y with the conclusions I was drawing or the sources I was using. .haron and 'ordon (also a doctor) have shown a level of interest and support normally reserved for fanatical adherents of cult religions. That, com$ined with their lifelong a$ility to $e Fust ahead of the trend curve in everything from cars to music, gives me hope that this $oo" will start the revolution we need to have in understanding o$esity. I&m still not sure if the only doctor I "now who is actually an endocrinologist entirely $elieves everything I say a$out fructose. #ut at least +dam is no longer pointing and laughing. His early warning that I should stic" to well-regarded Fournals stood me in very good stead. #roo"e had the unenvia$le Fo$ of "noc"ing all the rough edges off my manuscript (and ma"ing me thin" I wrote it that way in the first place). +nd Fust when I thought it was loo"ing pretty good, along came :ane and triple-chec"ed everything again. I tend not to $e detail oriented when it comes to finishing things I start, so having #roo"e and :ane drag me that last mile was invalua$le indeed. +ny mista"e that escaped the 6enguin editorial process well and truly deserves its freedom.