face

11 Sports science professor Tim Noakes goes full

low-carb, part 1.
By Alan Aragon

14 Why is nutrient timing still such a controversial

topic?
By Alan Aragon

Copyright © September 1st, 2012 by Alan Aragon

Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 Aspartame linked to cancer & leukemia, planet

panics.
By Alan Aragon

5 Improvement in coronary heart disease risk

factors during an intermittent fasting/calorie
restriction regimen: Relationship to adipokine
modulations.
Kroeger CM, et al. Nutr Metab (Lond). 2012 Oct
31;9(1):98. [Epub ahead of print] [Pubmed]
6 Alternate day fasting (ADF) with a high-fat diet
produces similar weight loss and cardio-protection
as ADF with a low-fat diet.
Klempel MC, et al. Metabolism. 2012 Aug 10. [Epub ahead
of print] [Pubmed]

7 Protein supplementation augments the adaptive

response of skeletal muscle to resistance-type
exercise training: a meta-analysis.
Cermak NM, et al. Am J Clin Nutr. 2012 Nov 7. [Epub
ahead of print] [Pubmed]
8 Do the non-caffeine ingredients of energy drinks
affect metabolic responses to heavy exercise?
Pettitt RW, et al. J Strength Cond Res. 2012 Oct 3. [Epub
ahead of print] [Pubmed]

9 Changes in atherogenic dyslipidemia induced by

carbohydrate restriction in men are dependent on
dietary protein source.
Mangravite LM, et al. J Nutr. 2011 Dec;141(12):2180-5.
Epub 2011 Oct 26. [Pubmed]
Alan Aragon’s Research Review – September 2012 [Back to Contents] Page 1
 Study strengths
First off, this study has plenty of real-world relevance. As
Aspartame linked to cancer & leukemia, planet panics.
mentioned in the manuscript, aspartame is used in more than
By Alan Aragon 6000 commercially distributed foods & beverages worldwide,
and annual aspartame use in the US is estimated at 5000-5500
Intro & background tons. Unlike previous human data that examined aspartame
Aspartame is a non-nutritive sweetener produced by joining intake at only one point in time, this study used data spanning
phenylalanine and aspartic acid. It was first synthesized in 1965 multiple time points within two large cohorts – the Nurses’
and was approved by the FDA for use in beverages and beverage Health Study (NHS) and Health Professionals’ Follow-Up Study
syrup bases in 1983.1 Its approval for general use in foods did (HPFS), totaling 47,810 men and 77,218 women. As such, this is
not happen until 1996. Aspartame’s history is littered with the most comprehensive long-term human study to-date
scientific, political, and legal warfare. It’s making headlines investigating the potential link between aspartame intake and
again, and this time sending everyone into perhaps the largest cancer risk. The prospective nature of the study (information
panic ever garnered by an artificial sweetener. The storm was was collected before the onset of disease) reduces the
unleashed as soon as a study by Schernhammer et al made its confounding effects of recall bias.
way toward publication in the American Journal of Clinical
Nutrition,2 and rapidly into headlines across the cyberscape. Study limitations
There’s plenty of scare-mongering as well as dismissal of this The main limitation of this study is shared by all
study, so let’s calm down a bit and pick it apart for strengths and epidemiological research – it’s observational, not controlled. The
limitations. From there, we can speculate over implications and possibility of multiple rogue variables is inevitable.
potential applications. Here’s the abstract: Observational/correlational research cannot demonstrate cause-
and-effect; only randomized controlled trials (RCTs) can.
Consumption  of  artificial  sweetener‐ and  sugar‐containing  soda 
and risk of lymphoma and leukemia in men and women.  
Another limitation common to epidemiological studies is the use
  of a food frequency questionnaire (FFQ), which was developed
Schernhammer ES, et al. Am J Clin Nutr. 2012 Dec;96(6):1419‐28.  out of the need for a simple, inexpensive means to collect survey
doi: 10.3945/ajcn.111.030833. Epub 2012 Oct 24. [Pubmed]  data from large populations. Self-reported data from FFQs
 
BACKGROUND:  Despite  safety  reports  of  the  artificial  sweetener  should be viewed with caution. For example, in the Nurses'
aspartame,  health‐related  concerns  remain.  OBJECTIVE:    We  Health Study, FFQ data was mailed out & collected in annual
prospectively  evaluated  whether  the  consumption  of  aspartame‐  intervals. Imagine attempting to recall the details of your
and sugar‐containing soda is associated with risk of hematopoetic  average dietary intake over a one-year period, particularly if
cancers.  DESIGN:  We  repeatedly  assessed  diet  in  the  Nurses' 
your intake is haphazard or not highly consistent – which is a
Health  Study  (NHS)  and  Health  Professionals  Follow‐Up  Study 
(HPFS).  Over  22  y,  we  identified  1324  non‐Hodgkin  lymphomas  distinct possibility for many. From my field observations, the
(NHLs), 285 multiple myelomas, and 339 leukemias. We calculated  diets of nurses are anything but consistent; they largely resemble
incidence  RRs  and  95%  CIs  by  using  Cox  proportional  hazards  a whirlwind of chaos. The following quote from Kristal et al
models. RESULTS: When the 2 cohorts were combined, there was  puts the relevance & validity of FFQs into perspective:3
no  significant  association  between  soda  intake  and  risks  of  NHL 
and multiple myeloma. However, in men, ≥1 daily serving of diet  “Three relatively recent developments have focused bright
soda  increased  risks  of  NHL  (RR:  1.31;  95%  CI:  1.01,  1.72)  and  lights on the limitations of FFQs. The first is the growing
multiple  myeloma  (RR:  2.02;  95%  CI:  1.20,  3.40)  in  comparison  lack of consistency both within and across studies examining
with  men  who  did  not  consume  diet  soda.  We  observed  no  diet and cancer risk. [...] The evidence is mounting that much
increased risks of NHL and multiple myeloma in women. We also  of the inconsistency, and some of the null results, in studies
observed  an  unexpected  elevated  risk  of  NHL  (RR:  1.66;  95%  CI:  of diet and cancer are due to poor dietary assessment. One
1.10,  2.51)  with  a  higher  consumption  of  regular,  sugar‐ incontrovertible conclusion is that we need new strategies for
sweetened  soda  in  men  but  not  in  women.  In  contrast,  when  dietary assessment that can be practically incorporated into
sexes  were  analyzed  separately  with  limited  power,  neither  large cohort studies.”
regular  nor  diet  soda  increased  risk  of  leukemia  but  were 
associated  with  increased  leukemia  risk  when  data  for  men  and  The authors of the present study acknowledge the limitations of
women were combined (RR for consumption of ≥1 serving of diet  self-reported data. However, they also attempt to defend their
soda/d when the 2 cohorts were pooled: 1.42; 95% CI: 1.00, 2.02).  approach. They contend that collecting the cumulative average
CONCLUSION:  Although  our  findings  preserve  the  possibility  of  a  aspartame intake via repeated FFQs provided a long-term picture
detrimental  effect  of  a  constituent  of  diet  soda,  such  as  of intake that accounts for changes over time. I would argue that
aspartame,  on  select  cancers,  the  inconsistent  sex  effects  and 
repeated use of a particular method does not automatically
occurrence of an apparent cancer risk in individuals who consume 
regular  soda  do  not  permit  the  ruling  out  of  chance  as  an 
increase its reliability, especially if it’s faulty to begin with. The
explanation.  SPONSORSHIP:  NIH/National  Cancer  Institute  (grant  authors acknowledge that unmeasured confounders cannot be
CA130054,  “Aspartame  Intake  and  the  Risk  of  Cancer”;  primary  ruled out. For example, a positive correlation between non-
investigator:  ESS)  and  in  part  by  a  Nutritional  Epidemiology  of  Hodgkin lymphoma (NHL) and regular sugar-sweetened soda
Cancer Training Grant (R25 CA098566; to KB). The Nurses’ Health  was seen, and the authors concede that sugar itself was not
Study  cohort  is  funded  through  NIH  grant  CA87696,  and  the  associated with increased risk. Therefore, appearance of
Health  Professionals  Follow‐Up  Study  cohort  is  funded  through  increased NHL risk from implausible foods calls the culpability
NIH grant CA055075.  of aspartame into question.
Alan Aragon’s Research Review – September 2012 [Back to Contents] Page 2
Findings & strangeness
The main findings of this study were that men consuming one or
more daily servings of aspartame-sweetened diet soda had an
increased the risk of NHL and multiple myeloma compared to
non-consumers. These risks were not detected in women, which
is another curious result calling the validity of the outcomes into
question, unless we accept the possibility of sex-specific
difference in response to aspartame. When data from both sexes
were pooled together, the risk of leukemia increased as a result
of consuming one or more servings of diet soda per day. Due to
a lack of statistical power, this increased risk was not detectable
when the sexes were viewed separately. Regular soda increased
the risk of NHL in men but not women – another weird outcome.
Speaking of strange outcomes, epidemiological research has no
shortage of them. Exemplary in this regard is research showing
that the consumption of protein/fat-based foods such as red meat
and eggs increase diabetes risk.4,5 The idea of protein/fat-based
foods being diabetes agents is humorously implausible since
diabetes is largely an impairment of carbohydrate metabolism.
But, this is often the nature of observational research. This is
why epidemiological findings are useful for generating
hypotheses for more rigorous study under controlled conditions,
not for drawing firm conclusions.
Questions of relevance & plausibility
On the note of plausibility, aspartame’s potential to cause cancer
is not completely devoid of basis. Aspartame is broken down
into phenylalanine, aspartic acid, and methanol – all of which
enter systemic circulation. Methanol metabolizes into
formaldehyde and then to formate (also called formic acid). The
focus of this conceptual model is formaldehyde’s carcinogenic
potential. Schernhammer et al repeatedly mention that
formaldehyde is classified as a known carcinogen by the
International Agency for Cancer Research (IACR).6 However,
they neglect to mention that formaldehyde is an naturally
occurring physiological chemical within all normal living cells.7
It’s important to note that the IACR’s classification of
formaldehyde as a carcinogen was based on a completely
different context from aspartame ingestion through foods and
beverages. Excessive formaldehyde exposure occurs primarily in
industrial workers involved with the production of formaldehyde
or formaldehyde-containing products.8 Other individuals at risk
are mortuary personnel and laboratory technicians exposed to
high concentrations of formaldehyde used for the preservation of
biological specimens. Exposure happens mainly through the
inhalation of formaldehyde gas, and less commonly by
absorbing formaldehyde through the skin.
A side-note related to the methanol/formaldehyde pathway is
that men who drank less than the median intake of alcohol (6
g/day, or the equivalent of about half of one beverage serving)
had a higher risk of NHL when 2 or more daily servings of diet
soda were consumed. This was not seen in men who drank
above the median alcohol intake. A potential explanation for this
is that alcohol (ethanol) consumption increases the enzymatic
activity of alcohol dehydrogenase type I (ADH), which inhibits
the metabolism of methanol.9 Thus, the authors speculated that a
lower intake of alcohol potentially resulted in a higher
Alan Aragon’s Research Review – September 2012
conversion of methanol to formaldehyde. But as we’ll see, this
line of speculation is questionable.
Aspartame→methanol→formaldehyde→cancer→baloney?
Although the aspartame→methanol→formaldehyde conversion
pathway has been proposed as a basis for carcinogenicity, this is
not without dispute from within the scientific community. For
example, Stegink et al administered three aspartame doses
considered to be at the abuse level (100, 150, and 200 mg/kg
bodyweight).10 No significant increases in formic acid levels
were seen compared to pre-dosing conditions. The relevant
implications of this finding are illustrated in the following
excerpt by Magnuson:11
“The fact that methanol and formaldehyde are breakdown
products of aspartame sounds scary to consumers. Therefore,
it is important to know that formaldehyde is produced by our
bodies every day in amounts thousands of times greater than
you would ever get from aspartame, as it is a key metabolite
that is needed to make other essential compounds, including
DNA. Also, the known toxic effects of methanol relate not to
formaldehyde, but to the build-up of formic acid in the
blood.”
Illustrating the questionability of this proposed pathway, a
serving of tomato juice yields 4-6 times more methanol than the
equivalent amount of an aspartame-sweetened beverage.11 This
concept is echoed by Butchko et al, who contend that common
staple foods such as meat, dairy, fruits, and vegetables provide
much greater amounts of aspartic acid, phenylalanine, and
methanol than that produced by aspartame-sweetened
beverages.12 Very high doses of methanol (far higher than what’s
normally derivable from aspartame ingestion) still fail to cause
formaldehyde accumulation. Within the body, formaldehyde is
used within seconds or converted to formate, which then is either
used or excreted via conversion to water or carbon dioxide.13
This rapid degradation occurs through multiple enzyme systems,
including the formaldehyde dehydrogenase complex, which is
widely distributed throughout various bodily tissues. The
aspartame→methanol→formaldehyde→cancer hypothesis is
stiffly challenged by the fact that even in methanol-poisoned
humans, formaldehyde increases are undetectable in blood or
tissues.12 Therefore, it appears that the proposed mechanism of
aspartame’s alleged carcinogenic effect is not likely without
certain leaps of faith to bridge the gaps.
Rats to dispute the ADI
The acceptable daily intake (ADI) of aspartame set by the FDA
is 50 mg/kg of bodyweight, which for adults is the equivalent of
roughly 18-19 cans of diet soda.13 The European Food and
Safety Agency (EFSA) sets the ADI similarly, at 40 mg/kg.
These limits are based on the evidence at-large, indicating that
aspartame is not a threat to human health.12,15-17 However, the
authors of the present study contend that human toxicological
data showing the safety of aspartame is still open for debate,
especially in light of Soffritti et al’s recent “megaexperiment” in
1800 rats showing a dose-dependent increase in lymphomas,
leukemias, and transitional renal cell tumors resulting from lower
aspartame doses than what’s currently deemed safe.18 In response
to Soffritti’s research, I would counter that while humans and rats
[Back to Contents] Page 3
share some metabolic similarities, they are more different than they
are alike in their processing of nutrients and drugs. There’s some
very interesting (yet little-known & highly underappreciated)
research on the critical physiological differences between human
and rat liver cells.19,20 The relevance of this is that the liver plays a
crucial role in the metabolism of all the compounds being discussed.
Furthermore, recent research by Sweeting et al suggests that
comparing human and rodent metabolism of methanol is not valid,
since rodents and non-rodents use completely different enzyme
systems (catalase and ADH, respectively) for this task.21
Industry-sponsored vs. independent research
Unsurprisingly, there have been disparate outcomes between
industry- & non-industry-funded research. In response to an
editorial by Lean & Hankey giving aspartame glowing marks for
safety,22 Briffa pointed out the possibility of commercial bias. To
quote his critique:23
“This review is particularly worrying as it shows that,
although 100% of industry funded (either whole or in part)
studies conclude that aspartame is safe, 92% of
independently funded studies have found that aspartame has
the potential for adverse effects.”
Magnuson calls this argument misleading and false, citing large-
scale non-industry-funded research coming to the conclusion
that aspartame is not a carcinogen.24,25 Notably, most industry-
sponsored research examines aspartame ingestion in the form
of foods and beverages. In contrast, independent research tends
to exploit unrealistic situations, such as direct injection into the
blood, brain, or other organs at doses thousands of times greater
than normal human consumption levels.13
Concluding notes
Ultimately, this study adds another strand to the evidence pile,
which is subject to continued scrutiny. There’s no certainty that
aspartame is a human carcinogen, but Schernhammer et al’s
results are thought-provoking, nevertheless.2 If nothing else, the
data will force scientists to dig deeper for the truth of the matter.
Will the FDA, EFSA, and other health organizations adjust their
positions on safe intake levels of aspartame? Only time and the
march of research (and politics) can determine that. For anyone
worried enough, several major brands of diet soda are aware of
the aspartame scare, and have answered consumer concerns by
developing aspartame-free versions of their products. It’s a
simple matter of checking the ingredient label. Should regular
consumers of aspartame be worried? This is a personal judgment
call since the human evidence showing adverse potential is
scarce and largely uncontrolled. For some folks, maintaining
peace of mind might be worth forgoing the pleasure of their
favorite aspartame-sweetened diet drinks. For those unwilling to
do so, the weight of the human evidence is currently still in your
favor. In any case, caution and skepticism are advised.
References
1. Gold MD. Docket # 02P-0317 Recall Aspartame as a Neurotoxic
Drug: File #7: Aspartame History. Jan 12, 2003. [FDA]
2. Schernhammer ES, et al. Am J Clin Nutr. 2012 Dec;96(6):1419-28.
doi: 10.3945/ajcn.111.030833. Epub 2012 Oct 24. [Pubmed]
3. Kristal AR, et al. Is it time to abandon the food frequency
questionnaire? Cancer Epidemiol Biomarkers Prev. 2005
Dec;14(12):2826-8. [Pubmed]
Alan Aragon’s Research Review – September 2012
4. Pan A, et al. Red meat consumption and risk of type 2 diabetes: 3
cohorts of US adults and an updated meta-analysis. Am J Clin Nutr.
2011 Oct;94(4):1088-96. Epub 2011 Aug 10. [Pubmed]
5. Radzevičienė L, Ostrauskas R. Egg consumption and the risk of type 2
diabetes mellitus: a case-control study. Public Health Nutr. 2012
Aug;15(8):1437-41. Epub 2012 Mar 6. [Pubmed]
6. International Agency for Research on Cancer Working Group.
Formaldehyde, 2-butoxyethanol and 1-tert-butoxypropan-2-ol. In:
WHO, ed. IARC Monographs on the Evaluation of Carcinogenic Risks
to Humans. Lyon, France: IARC, WHO, 2006. [IARC Monographs]
7. Swenberg JA, et al. Formaldehyde carcinogenicity research: 30 years
and counting for mode of action, epidemiology, and cancer risk
assessment. Toxicol Pathol. 2012 Nov 16. [Epub ahead of print]
[Pubmed]
8. National Cancer Institute. Formaldehyde and Cancer Risk (NCI fact
sheet). Reviewed June 10, 2011. [NCI]
9. Lee SL, et al. Oxidation of methanol, ethylene glycol, and isopropanol
with human alcohol dehydrogenases and the inhibition by ethanol and
4-methylpyrazole. Chem Biol Interact. 2011 May 30;191(1-3):26-31.
Epub 2010 Dec 15. [Pubmed]
10. Stegink LD, et al. Blood methanol concentrations in normal adult
subjects administered abuse doses of aspartame. J Toxicol Environ
Health. 1981 Feb;7(2):281-90. [Pubmed]
11. Magnuson BA. Relationship between aspartame, methanol, and
formaldehyde explained. Aspartame Expert Work Group (2008).
Evidence Analysis Library of the Academy of Nutrition & Dietetics.
[AND]
12. Butchko HH, et al. Aspartame: review of safety. Regul Toxicol
Pharmacol. 2002 Apr;35(2 Pt 2):S1-93. [Pubmed]
13. Magnuson B. Aspartame – facts and fiction. N Z Med J. 2010 Mar
19;123(1311):53-7. [Pubmed]
14. Mattes RD, Popkin BM. Nonnutritive sweetener consumption in
humans: effects on appetite and food intake and their putative
mechanisms. Am J Clin Nutr. 2009 Jan;89(1):1-14. Epub 2008 Dec 3.
[Pubmed]
15. Magnuson BA, et al. Aspartame: a safety evaluation based on current
use levels, regulations, and toxicological and epidemiological studies.
Crit Rev Toxicol. 2007;37(8):629-727. [Pubmed]
16. Butchko HH, Stargel WW. Aspartame: scientific evaluation in the
postmarketing period. Regul Toxicol Pharmacol. 2001 Dec;34(3):221-
33. [Pubmed]
17. Spiers PA, et al. ame: neuropsychologic and neurophysiologic
evaluation of acute and chronic effects. Am J Clin Nutr. 1998
Sep;68(3):531-7. [Pubmed]
18. Soffritti M, et al. First experimental demonstration of the
multipotential carcinogenic effects of aspartame administered in the
feed to Sprague-Dawley rats. Environ Health Perspect. 2006
Mar;114(3):379-85. [Pubmed]
19. Kotokorpi P, et al. Physiological differences between human and rat
primary hepatocytes in response to liver X receptor activation by 3-[3-
[N-(2-chloro-3-trifluoromethylbenzyl)-(2,2-
diphenylethyl)amino]propyloxy]phenylacetic acid hydrochloride
(GW3965). Mol Pharmacol. 2007 Oct;72(4):947-55. Epub 2007 Jul
12. [Pubmed]
20. Aragon AA. Newsflash: rats are not humans. AARR. March, 2010.
[AARR]
21. Sweeting JN, et al. Species- and strain-dependent teratogenicity of
methanol in rabbits and mice. Reprod Toxicol. 2011 Jan;31(1):50-8.
Epub 2010 Oct 16. [Pubmed]
22. Lean ME, Hankey CR. Aspartame and its effects on health. BMJ. 2004
Oct 2;329(7469):755-6. [Pubmed]
23. Briffa J. Aspartame and its effects on health: independently funded
studies have found potential for adverse effects. BMJ. 2005 Feb
5;330(7486):309-10; author reply 310. [Pubmed]
24. National Toxicology Program.. NTP report on the toxicology studies
of aspartame (CAS No. 22839-47-0) in genetically modified (FVB
Tg.AC hemizygous) and B6.129-Cdkn2atm1Rdp (N2) deficient mice
and carcinogenicity studies of aspartame in genetically modified
[B6.129-Trp53tm1Brd (N5) haploinsufficient] mice (feed studies).
Natl Toxicol Program Genet Modif Model Rep. 2005 Oct;(1):1-222.
[Pubmed]
25. Lim U, et al. Consumption of aspartame-containing beverages and
incidence of hematopoietic and brain malignancies. Cancer Epidemiol
Biomarkers Prev. 2006 Sep;15(9):1654-9. [Pubmed]
[Back to Contents] Page 4

Improvement in coronary heart disease risk factors
during an intermittent fasting/calorie restriction
regimen: Relationship to adipokine modulations.
Kroeger CM, et al. Nutr Metab (Lond). 2012 Oct 31;9(1):98.
[Epub ahead of print] [Pubmed]
BACKGROUND: The ability of an intermittent fasting (IF)-
calorie restriction (CR) regimen (with or without liquid meals) to
modulate adipokines in a way that is protective against coronary
heart disease (CHD) has yet to be tested. OBJECTIVE:
Accordingly, we examined the effects of an IFCR diet on
adipokine profile, body composition, and markers of CHD risk
in obese women. METHODS: Subjects (n = 54) were
randomized to either the IFCR-liquid (IFCR-L) or IFCR-food
based (IFCR-F) diet for 10 weeks. RESULTS: Greater
decreases in body weight and waist circumference were noted in
the IFCR-L group (4 +/- 1 kg; 6 +/- 1 cm) versus the IFCR-F
group (3 +/- 1 kg; 4 +/- 1 cm). Similar reductions (P < 0.0001) in
fat mass were demonstrated in the IFCR-L (3 +/- 1 kg) and
IFCR-F group (2 +/- 1 kg). Reductions in total and LDL
cholesterol levels were greater (P = 0.04) in the IFCR-L (19 +/-
10%; 20 +/- 9%, respectively) versus the IFCR-F group (8 +/-
3%; 7 +/- 4%, respectively). LDL peak particle size increased (P
< 0.01) in the IFCR-L group only. The proportion of small LDL
particles decreased (P < 0.01) in both groups. Adipokines, such
as leptin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-
alpha), and insulin-like growth factor-1 (IGF-1) decreased (P <
0.05), in the IFCR-L group only. CONCLUSION: These
findings suggest that IFCR with a liquid diet favorably
modulates visceral fat and adipokines in a way that may confer
protection against CHD. SPONSORSHIP: This study was
funded by Isagenix LLC., Chandler, AZ.
Study strengths
This study helps to expand the small but very intriguing body of
intermittent fasting (IF) research. This is the first IF study to
examine the effect of a fasting day combined with calorie
restriction the rest of the week. It’s also the first to compare this
regime with versus without liquid meals. Sample size (60
subjects, 54 completed the study) was fairly large compared to
the piddly numbers commonly seen in diet trials. Body
composition was assessed via dual X-ray absorptiometry (DXA).
Dietary intake was assessed & software-analyzed by a trained
dietitian at weeks 1, 3, & 10, and physical activity was tracked
electronically with a pattern recognition monitor.
Study limitations
I would like to have seen a longer diet phase than 7 weeks. Also,
the intermittent fasting/calorie restriction with liquid meals
(IFCR-L) was more tightly controlled, since two of the 3 meals
per day were provided by the lab in the form of a pre-measured
packet of powder. In contrast, none of the 3 daily meals in the
solid food condition (IFCR-F) were lab-provided. This leaves
greater error potential due to the inherent lack of precision and
tendency to underestimate/under-report self-provided intakes in
the IFCR-F group. Furthermore, the results of this study may be
limited to the absence of a formal or intensive training program.
Alan Aragon’s Research Review – September 2012
Comment/application
Overall, while both diets reduced bodyweight and improved
markers of coronary heart disease (CHD) risk, the liquid diet
outperformed the solid diet in weight loss, waist circumference
reduction, and total & LDL cholesterol reduction. Notably, only
the liquid diet increased LDL particle size, which is considered
to be anti-atherogenic.
Before chalking these results up to the funding source (Isagenix,
seller of the meal replacement powder tested), the above chart
showing dietary variables reveals potentially confounding
differences despite the lack statistical significance. Notice first
how during the 7-week diet period, the reduction in total energy
intake in IFCR-L was 453 kcal compared to baseline (26.52%).
Total energy reduction in IFCR-F it was reduced by 250 kcal
(14.52%), which is a more subtle drop. Next, take a look at the
protein intakes. Habitual intake was slightly higher in IFCR-L,
and this increased from 75 g to 84 g/day during the diet phase. In
contrast, IFCR-F’s protein went from 67 g to 65 g/day. From a
proportional standpoint of protein intake, IFCR-F consumed
0.69 g/kg, while IFCR-L had 0.88 g/kg. Both intakes were sub-
optimal, but even more so IFCR-F. The combination of a higher
protein intake along with a lower total energy intake could at
least partially explain the more favorable bodyweight &
anthropometric changes in the liquid diet group. Interestingly, no
differences were seen in subjective ratings of appetite/hunger.
In addition to the above, IFCR-L showed reductions in pro-
inflammatory/pro-atherogenic adipokines, whereas IFCR-F
showed no significant reductions. However, it’s unknown
whether these improvements are inherent to the meal
replacement product or merely the greater reduction in body fat
(which included visceral fat reduction). The authors
acknowledge that IFCR-L’s greater improvement in lipid profile
and adipokine levels were likely due to greater reductions in
body weight & visceral fat mass. To this end, the authors
diligently acknowledge the limitation I mentioned earlier:
“This study is limited in that it did not carefully control for food
intake by providing food-based meals to the intervention groups,
i.e. dinner meal for the IFCR-L group, and 3 meals/d for the
IFCR-F group.”
The idea that the meal replacement product used (Isalean Shake
by Isagenix) had health advantages beyond better energy intake
control is far-fetched, unless plenty of faith is placed in the
‘magic’ of milk proteins and fructose, which are the product’s
primary ingredients. Here are the labels of chocolate and vanilla.
[Back to Contents] Page 5
Alternate day fasting (ADF) with a high-fat diet
produces similar weight loss and cardio-protection as
ADF with a low-fat diet.
Klempel MC, et al. Metabolism. 2012 Aug 10. [Epub ahead of
print] [Pubmed]
OBJECTIVE: The goal of this study was to determine if these
beneficial changes in body weight and coronary heart disease
(CHD) risk can be reproduced if an HF background diet is used
in place of an LF diet during ADF. METHODS: Thirty-two
obese subjects were randomized to an ADF-HF (45% fat) or
ADF-LF diet (25% fat), which consisted of two phases: 1) a 2-
week baseline weight maintenance period, and 2) an 8-week
ADF weight loss period. All food was provided during the study.
RESULTS: Body weight was reduced (P<0.0001) by ADF-HF
(4.8%±1.1%) and by ADF-LF (4.2%±0.8%). Fat mass decreased
(P<0.0001) by ADF-HF (5.4±1.5kg) and ADF-LF (4.2±0.6kg).
Fat free mass remained unchanged. Waist circumference
decreased (P<0.001) by ADF-HF (7.2±1.5cm) and ADF-LF
(7.3±0.9cm). LDL cholesterol and triacylglycerol concentrations
were reduced (P<0.001) by both interventions (ADF-HF:
18.3%±4.6%, 13.7%±4.8%; and ADF-LF: 24.8%±2.6%,
14.3%±4.4%). HDL cholesterol, blood pressure, and heart rate
remained unchanged. There were no between-group differences
for any parameter. CONCLUSION: These findings suggest that
an ADF-HF diet is equally as effective as an ADF-LF diet in
helping obese subjects lose weight and improve CHD risk
factors. SPONSORSHIP: University of Illinois at Chicago,
Department of Kinesiology and Nutrition, Departmental
funding.
Study strengths
This is innovative since it’s the first study to ever compare a
high-fat alternate-day fasting diet (ADF-HF) with a low-fat
alternate-day fasting diet (ADF-LF). And, like the previous
study I reviewed, it’s a welcome addition to the small but
intriguing body of research on intermittent fasting regimes. All
meals were provided by the lab, which is a rare level of dietary
control. All uneaten food was weighed and recorded. Meals were
provided, but not consumed at the lab, so adherence logs were
assessed weekly. Body composition was assessed via dual
energy X-ray absorptiometry (DXA).
Study limitations
This study was well designed & executed. So, to grope for
limitations, one of them is the absence of a formal exercise
program, which is a common limitation of diet research in
general. Something that I’d love to see is the effect of resistance
training on intermittent fasting regimes. Another limitation was
the absence of tracking energy expenditure or physical activity.
The authors acknowledge this, mentioning that future research in
this area should control for physical activity by using
quantitative means such as an accelerometer. A limitation
pointed out by the authors was the occurrence of weight loss in
both groups during the initial 2-week phase, which was
supposed to be a baseline maintenance period. They speculated
that the subjects could have neglected to eat all of the food
provided due to an eagerness to lose weight. They also speculate
that physical activity could have increased during this time.
Alan Aragon’s Research Review – September 2012
Comment/application
The main findings of this study were a lack of significant
between-group differences in the reduction of total weight, fat
mass, waist circumference, LDL-cholesterol (LDL-C), and
triacylglycerol (TG). In fact, no significant between-group
differences were seen in any of the measures compared. This
study exemplifies the flexibility of dietary carb/fat proportion in
achieving similar results when protein is matched. However,
there were some notable outcomes regarding body composition
and lipid profile. ADF-LF caused a nonsignificant increase in
HDL-C. This is surprising since higher-fat (especially saturated
fat) diets are better than low-fat diets at raising or preserving
HDL-C.1-3 Another odd outcome was the lack of difference in
TG reduction; lower-carb and/or higher-fat diets have a tendency
to lower TG compared to their low-fat counterparts.
As seen above, both diets were relatively low in protein (another
typical property of research diets), and both diets relatively high
in carbohydrate – particularly for weight loss diets. It would
have been interesting to see the sugar content of each diet. One
of the most intriguing outcomes was the non-significant gain in
lean mass in both groups (1.2 kg in ADF-HF, 0.5 kg in ADF-LF)
despite the loss of fat mass (5.4 kg in ADF-HF, 4.2 kg in ADF-
LF). This finding is in line with a recent review by Varady
examining 11 daily caloric restriction (DCR) studies and 7
intermittent calorie restriction (ICR) studies.4 Both diet types
have similar effects on total bodyweight reduction, but ICR has
thus far been more effective for lean mass retention.
Specifically, 3 of the ICR studies showed no significant decrease
in LBM, while all of the DCR studies showed decreased LBM.
An important note is that the majority of the ICR trials used
bioelectrical impedance analysis (BIA) to measure body
composition, while the majority of DCR studies used dual X-ray
absorptiometry (DXA) or magnetic resonance imaging (MRI). It
would be interesting to see if resistance training amplifies or
diminishes any lean mass-retaining advantage of ADF and other
intermittent fasting variants compared to linear diet models.
The present study had subjects consume 125% of their
maintenance energy needs on feeding days and 25% on fasting
days, averaging out to 75% or their maintenance needs (or a
25% deficit) overall. An interesting avenue of research would be
the comparison of various deficit/surplus permutations. For
example, would 150% of maintenance on feeding days and 0%
on fasting days have yielded the same results on health markers
and body composition as the present protocol? Another untapped
area of study is the systematic comparison of deficits varying in
severity. This line of investigation could seek out deficit
thresholds beyond which lean mass is no longer preserved.
[Back to Contents] Page 6

Protein supplementation augments the adaptive
response of skeletal muscle to resistance-type
exercise training: a meta-analysis.
Cermak NM, et al. Am J Clin Nutr. 2012 Nov 7. [Epub ahead of
print] [Pubmed]
BACKGROUND: Protein ingestion after a single bout of resistance-
type exercise stimulates net muscle protein accretion during acute
postexercise recovery. Consequently, it is generally accepted that
protein supplementation is required to maximize the adaptive response
of the skeletal muscle to prolonged resistance-type exercise training.
However, there is much discrepancy in the literature regarding the
proposed benefits of protein supplementation during prolonged
resistance-type exercise training in younger and older populations.
OBJECTIVE: The objective of the study was to define the efficacy of
protein supplementation to augment the adaptive response of the
skeletal muscle to prolonged resistance-type exercise training in
younger and older populations. DESIGN: A systematic review of
interventional evidence was performed through the use of a random-
effects meta-analysis model. Data from the outcome variables fat-free
mass (FFM), fat mass, type I and II muscle fiber cross-sectional area,
and 1 repetition maximum (1-RM) leg press strength were collected
from randomized controlled trials (RCTs) investigating the effect of
dietary protein supplementation during prolonged (>6 wk) resistance-
type exercise training. RESULTS: Data were included from 22 RCTs
that included 680 subjects. Protein supplementation showed a positive
effect for FFM (weighted mean difference: 0.69 kg; 95% CI: 0.47, 0.91
kg; P < 0.00001) and 1-RM leg press strength (weighted mean
difference: 13.5 kg; 95% CI: 6.4, 20.7 kg; P < 0.005) compared with a
placebo after prolonged resistance-type exercise training in younger and
older subjects. CONCLUSIONS: Protein supplementation increases
muscle mass and strength gains during prolonged resistance-type
exercise training in both younger and older subjects. SPONSORSHIP:
Supported by a postdoctoral research fellowship from the Canadian
Institute of Health Research.
Study strengths
This meta-analysis is the first of its kind, examining both
strength and hypertophic effects of protein supplementation
during chronic resistance training. A wide range of populations
were analyzed (healthy younger adults, trained athletes, and
older individuals. Subgroup analyses were conducted for age and
training status. Only randomized controlled trials (RCTs) lasting
a minimum of 6 weeks were included, which eliminates the
confounding variability & limited nature of acute studies.
Inclusion criteria for body composition assessment was limited
to more sophisticated methods (hydrodensitiometry, air
displacement plethysmography, and dual X-ray absorptiometry).
Sensitivity analyses were conducted to determine whether the
effects on fat-free mass (FFM) were due to 1) age range cutoffs
and 2) different sources of protein.
Study limitations
Meta-analyses fall under the umbrella of observational research;
they cannot show causation, despite the examination of
randomized controlled trials. In addition, a large amount of studies
were excluded. 139 studies met the initial criteria for consideration,
but only 22 of those studies made it into the analysis (although 2 of
the tables in the manuscript list 23 studies). 5 studies that met the
inclusion criteria were excluded because the corresponding authors
Alan Aragon’s Research Review – September 2012
could not be reached. The authors of the present study also point out
that the potential for publication bias among the chosen studies
cannot be ignored. An additional limitation was the heterogeneity of
the placebo treatments across studies: 16 studies used carbohydrate,
3 used water, 2 used a low-protein diet, and 2 used exercise-only.
Another limitation was the heterogeneity in protein supplementation
timing across studies. 15 of the studies supplemented protein near
and/or during the training bout, whereas 7 studies did not involve
specific timing. Supplementation dose varied widely as well,
ranging from as little as 6 g EAA to 106 g whey & casein.
Comment/application
The main finding of this study was that protein supplementation
augments gains in FFM and 1-RM leg press strength in both
younger and older subjects. However, age-related differences were
seen. Type I & II muscle fiber hypertrophy was seen in younger 49
years old or less) but not older subjects (50 years old or more) in
protein-supplemented conditions. This lack of fiber hypertrophy in
older subjects was seen despite a 33% greater increase in leg press
strength. Protein source did not have any significant influence on
the results. It’s notable that the greater FFM gain in the protein-
supplemented groups were approximately 1 kg greater than the
placebo groups after 12 weeks of resistance training, so we’re not
looking at anything spectacular. However, if this advantage can
persist over periods of years, then the small, statistically significant
difference can become concretely meaningful. An interesting
finding was that resistance-trained subjects were even more
responsive to protein supplementation than untrained subjects. This
shows how ‘newbie gains’ can mask treatment effects.
The younger subjects, both trained & untrained, were consuming
approximately 1.2 g/kg (which the authors called “more than
adequate”), and protein supplementation on average added roughly
50 g to this. Taking an 80 kg person for example, this would raise
protein intake to about 1.8 g/kg. In light of this, there are a couple of
important points to make. Firstly, 1.8 g/kg is not grossly higher than
the ranges listed in recent authoritative recommendations for
athletes. For example, the joint position stand of the American
Dietetic Association, Dietitians of Canada, and the American
College of Sports Medicine lists 1.2-1.7 g/kg as an appropriate
range.5 The International Society of Sports Nutrition position
stand lists 1.4-2.0 g/kg.6 Other recent reviews’ recommendations
range 1.2 to 2.2 g/kg.7-9 The second point is that athletes whose
main goal is muscular size and strength typically consume
protein amounts exceeding the ~1.8 g/kg in the present study.
For example, Lowery et al found that ‘protein-seeking’ strength
trainers reported (via diet journals) an intake of 2.5 g/kg.10 In
another example, Kim et al studied the dietary habits and
nutritional status of elite Korean bodybuilders, who reported an
intake of 4.3 g/kg.11 In my observations, bodybuilders and
strength athletes habitually consume ~2.2-3.3 g/kg.
Therefore, the authors’ conclusion that protein supplementation
is an effective means to augment muscular adaptations to
resistance training might only apply to individuals whose protein
intake does not exceed 1.2 g/kg (the low end of most
authoritative recommendations). The conclusion does not apply
to individuals with a pre-existent abundance of dietary protein
typical of strength-training populations who consume amounts
far above that seen in the present study. Total daily amount is
what really counts. If this daily target is achieved with both
whole foods and supplements, then great – but supplementation
should not be viewed as necessary or optimal.
[Back to Contents] Page 7
Do the non-caffeine ingredients of energy drinks affect
metabolic responses to heavy exercise?
Pettitt RW, et al. J Strength Cond Res. 2012 Oct 3. [Epub ahead
of print] [Pubmed]
BACKGROUND: Energy drinks (ED) such as Red Bull (RB)
are marketed to enhance metabolism. Secondary ingredients of
EDs (e.g., taurine) have been purported to improve time-trial
performance; however, little research exists on how such
secondary ingredients affect aerobic metabolism during heavy
exercise. OBJECTIVE: The purpose of this study was to
investigate the effect of the secondary ingredients of RB on
aerobic metabolism during and subsequent to heavy exercise.
DESIGN: In double-blind, counterbalanced, and crossover
fashion, 8 recreationally trained individuals completed a graded
exercise test to determine the gas exchange threshold (GET).
Subjects returned on two separate occasions and ingested either
an 245 ml serving of RB or a control (CTRL) drink with the
equivalent caffeine prior to engaging in two, 10-min constant-
load cycling bouts, at an intensity equivalent to GET, with 3 min
of rest between bouts. RESULTS: Accumulated liters of O2 (10
min) was higher for the first (17.1 ± 3.5 L) versus the second
(16.7 ± 3.5 L) bout but did not differ between drinks. Similarly,
excess post-exercise oxygen consumption was higher following
the initial (RB: 2.6 ± 0.85 L; CTRL mean: 2.9 ± 0.90 L) versus
second bout (RB mean: 1.5 ± 0.85 L; CTRL: 1.9 ± 0.87 L) but
did not differ between drinks. No differences occurred between
drinks for measures of heart rate or rating of perceived exertion.
CONCLUSIONS: These results indicate that the secondary
ingredients contained in a single serving of RB do not augment
aerobic metabolism during or subsequent to heavy exercise.
SPONSORSHIP: College of Graduate Studies and Research at
Minnesota State University, Mankato.
Study strengths
This study is conceptually strong since the commercial success
of Red Bull energy drink is rather staggering and currently on
the rise. To quote the company’s figures reported on their
website:12 “A total of 4.631 billion cans of Red Bull were sold
worldwide in 2011, representing an increase of 11.4% against
2010. Company turnover increased by 12.4% from EUR 3.785
billion to EUR 4.253 billion. [...] As of the end of 2011, Red Bull
employed 8,294 people in 164 countries (end 2010: 7,758 in 161
countries).” Suggesting a high prevalence of use for the goal of
sports performance, Froiland et al surveyed 203 varsity athletes
at a Division I university, and found that 72.9% of them used
energy drinks such as Gatorade, Powerade, All Sport, and Red
Bull.13 Indeed, Red Bull sponsors several high-profile
professional sports teams and athletes (as seen on their site). The
small sample size of the present study (8 subjects) was alleviated
by the within-subject crossover design. Subjects logged their
habitual food intake 24 hours prior to each trial, and duplicated
this intake on the subsequent trial. Dietary duplication was
confirmed by software analysis.
Study limitations
As mentioned, the sample size was small (8 subjects). This can
be viewed as a statistical compromise, but again, the subjects
served as their own controls, so inter-subject response variability
was minimized. The results of this study might be limited to the
testing protocol, which examined aerobic metabolism, rather
Alan Aragon’s Research Review – September 2012
than exercise performance per se. This would best be assessed
via time trial of a fixed distance to complete in the shortest time
possible, or a fixed time during which the most work would be
attempted. The outcomes might also be limited to the type of
training used in testing (aerobic training rather than strength or
resistance training). The authors pointed out that future
investigations should control for differences in beverage
carbonation, which can potentially affect expired VCO2 (volume
of carbon dioxide) values, which can introduce error in oxygen
uptake and respiratory exchange ratio (RER).
Comment/application
The main findings were a lack of significant difference in the
effect on aerobic metabolism between Red Bull and the caffeine-
matched control condition. Specifically, the key non-caffeine
ingredients in Red Bull (taurine, glucoronolactone, B vitamins)
did not increase oxygen uptake and excess postexercise oxygen
consumption (EPOC), nor did it reduce RER, rate of perceived
exertion (RPE), or heart rate compared to the control treatment.
In summary, no greater enhancement in aerobic metabolism
during or after training was seen as a result of Red Bull
compared to caffeinated ginger ale.
The performance-enhancing potential of Red Bull energy drink
has been examined in previous studies.14-16 Unsurprisingly, it
outperformed low- & non-caloric controls that did not contain
caffeine. However, The more interesting question is whether or
not the taurine content of Red Bull (1000 mg) contributes an
ergogenic effect in conjunction with the other ingredients.
Nearly two decades ago, Geib et al16 compared the following
versions of Red Bull: 1) without taurine & glucoronolactone; 2)
without taurine, glucoronolactone, & caffeine; 3) the original
formula of Red Bull, which contained all of the previous
compounds. In endurance-trained athletes, the original formula
caused greater endurance capacity, and more favorable hormonal
responses than the other treatments. The authors attributed these
effects specifically to the taurine content of the beverage.
Recent research on the independent effects of taurine on exercise
performance have been mixed and generally unimpressive.
Balshaw et al found that in trained middle distance runners, 1g
taurine improved the performance of a simulated 3-km time trial
compared to placebo (magnitude-based inferences showed the
likeliness of taurine’s benefit to be 99%).17 In contrast,
Rutherford et al found that in well-trained cyclists, 1.66 g taurine
failed to increase endurance performance (steady-state follwed
by time trial) compared to a non-caloric taurine-free control, and
a placebo beverage which subjects were told contained taurine.18
Interestingly, however, the taurine condition showed a 16%
greater fat oxidation compared to the control & placebo
conditions. Galloway et al found that 7 days of 1.66 g taurine
supplementation failed to increase muscle taurine content or
affect substrate metabolism during 2 hours of cycling at 60%
VO2max.19 Armentano et al saw no significant improvements in
push-up performance after 7 days of taurine (or creatine)
supplementation.20 Glucuronolactone is commonly used in
energy drinks for purposes that are unclear. Red Bull does not
make any specific claim behind its use of glucuronolactone.
Thus far, there is no human research showing its isolated
benefits on exercise performance. The same can be said for B
vitamin supplementation outside of correcting deficiency.21-23
[Back to Contents] Page 8

Changes in atherogenic dyslipidemia induced by
carbohydrate restriction in men are dependent on
dietary protein source.
Mangravite LM, et al. J Nutr. 2011 Dec;141(12):2180-5. Epub
2011 Oct 26. [Pubmed]
BACKGROUND: Previous studies have shown that multiple
features of atherogenic dyslipidemia are improved by replacement
of dietary carbohydrate with mixed sources of protein and that these
lipid and lipoprotein changes are independent of dietary saturated
fat content. OBJECTIVE: Because epidemiological evidence
suggests that red meat intake may adversely affect cardiovascular
disease risk, we tested the effects of replacing dietary carbohydrate
with beef protein in the context of high- vs. low-saturated fat intake
in 40 healthy men. METHODS: After a 3-wk baseline diet [50%
daily energy (E) as carbohydrate, 13% E as protein, 15% E as
saturated fat], participants consumed for 3 wk each in a randomized
crossover design two high-beef diets in which protein replaced
carbohydrate (31% E as carbohydrate, 31% E as protein, with 10%
E as beef protein). The high-beef diets differed in saturated fat
content (8% E vs. 15% E with exchange of saturated for
monounsaturated fat). Two-week washout periods were included
following the baseline diet period and between the randomized diets
periods. RESULTS: Plasma TG concentrations were reduced after
the 2 lower carbohydrate dietary periods relative to after the
baseline diet period and these reductions were independent of
saturated fat intake. Plasma total, LDL, and non-HDL cholesterol as
well as apoB concentrations were lower after the low-carbohydrate,
low-saturated fat diet period than after the low-carbohydrate, high-
saturated fat diet period. CONCLUSION: Given our previous
observations with mixed protein diets, the present findings raise the
possibility that dietary protein source may modify the effects of
saturated fat on atherogenic lipoproteins. SPONSORSHIP:
Supported by the Beef Checkoff through the National Cattlemen’s
BeefAssociation and by NIH National Center for Resarch
Resources, University of California, San Francisco Clinical and
Translational Science Institute grant no.UL1 RR024131.
Study strengths
This study is innovative since it’s the first to examine the effect
of varying saturated fat content on atherogenic dyslipidemia
within the context of a low-carbohydrate diet. Lunch and dinner
were prepared/provided for the subjects by the lab. All of the
beef protein was provided within these entrees. A crossover
design was implemented, giving all subjects a chance to undergo
both diets, minimizing confounding differences in inter-subject
variability.
Study limitations
The trial period (3 weeks per dietary condition) was short.
Questions remain about how the dietary effects may have
progressed or diminished over a longer period. The 2-week
wash-out period between trials was short as well, potentially
leaving insufficient time for all parameters to completely return
to pre-trial levels. Crossover designs are subject to ‘order
effects’ where the relative positioning of each treatment (i.e., the
high- before the low- SFA diet & vice-versa) could have
influenced the outcomes. However, the authors counter that,
“...there was no evidence for an association of diet order with
any of the reported measurements.” A final limitation was the
Alan Aragon’s Research Review – September 2012
absence of a formal training protocol. In fact, no tracking or
accounting of physical activity was reported. This opens up the
possibility for confounding differences between subjects. I’d
also add that a structured training program stands the chance of
narrowing the diet-mediated differences seen in lipid profiles. It
might also be important to note that maintenance, rather than
hypocaloric conditions were imposed. This might limit the
relevance of these outcomes to non-dieters.
Comment/application
The main findings of this study were as follows: The low-
carb/low-saturated fat diet (LCLSF) significantly lowered total
cholesterol, LDL, and non-HDL cholesterol as well as apoB
concentrations. The low-carb, high-saturated fat diet (LCHSF)
did not significantly lower any of the aforementioned
parameters. In fact, LCHSF actually raised small LDL while
LCLSF lowered it. Both diets lowered TG similarly, with the
LCLSF having a nonsignificant edge in this regard. This
collectively shows that the diet with less saturated fat (8% vs
15% of total kcal) outperformed its counterpart for improving
markers of atherogenic dyslipidemia, with the exception of a
lack of significant difference in the lowering of TG.
There are a few interesting aspects of this study which you can’t
glean from the abstract. One of them is that total dietary
cholesterol was very similar between LCLSF and LCHSF (463
& 467 mg/day, respectively). Another detail missing from the
abstract is that SFA from beef was only a minor component of
both diets. The abstract might have the tendency to mislead
people into thinking it was lower-fat beef that outperformed
higher-fat beef, when that was not the case. The higher SFA
content in LCHSF was achieved via fortifying the diet with full-
fat dairy products. However, what the full text still doesn’t tell
us is exactly what food sources comprised the diets. Menu
information would be useful in attempting to speculate over the
outcomes and draw potential recommendations. LCLSF was
higher in mono-unsaturated fatty acids (MUFA), and this might
have contributed to the favorable outcomes.24 Both diets’
carbohydrate content was 31% of total energy, and the text
indicates that the sugar:starch ratio in both diets was an even 1:1,
which is not ideal. In a typical maintenance diet of 2200 kcal,
this would amount to roughly 85g starch and 85 g sugar.
Previous research by the authors of the present study found that
an increased intake of saturated fat within the context of a
reduced-carbohydrate diet does not adversely affect measures of
atherogenic dyslipidemia.25 However, the latter study’s diet had
a mix of protein sources, as opposed to the present study’s
singular reliance on beef. To quote the authors, “Hence, the
present findings suggest an interaction between saturated fat
and one or more nonfat components of beef on lipoprotein
metabolism.” Notably, there was no specification of the diet’s
proportion of processed red meat, which has been more strongly
implicated in the increase of various chronic diseases than
unprocessed red meat. Keeping in mind the study’s limitations,
potential practical applications would be to a) vary your protein
sources instead of just getting it from beef, b) reduce your high-
fat dairy intake if you refuse to eat any other protein source but
beef, or c) either of the previous, while predominating your
carbohydrate intake with whole foods and maintaining a sensible
training program and favorable body composition.
[Back to Contents] Page 9
 19. Galloway SD, et al. Seven days of oral taurine
supplementation does not increase muscle taurine content or
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May;6(3):216-34. Epub 2012 Apr 13. [Pubmed] 2008 Jun 26. [Pubmed]
2. Nordmann AJ, et al. Effects of low-carbohydrate vs low-fat 20. Armentano MJ, et al. The effect and safety of short-term
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analysis of randomized controlled trials. Arch Intern Med. Med. 2007 Mar;172(3):312-7. [Pubmed]
2006 Feb 13;166(3):285-93. [Pubmed] 21. van der Beek EJ, et al. Thiamin, riboflavin and vitamin B6:
3. Samaha FF. Effect of very high-fat diets on body weight, impact of restricted intake on physical performance in man.
lipoproteins, and glycemic status in the obese. Curr J Am Coll Nutr. 1994 Dec;13(6):629-40. [Pubmed]
Atheroscler Rep. 2005 Nov;7(6):412-20. [Pubmed] 22. van der Beek EJ, et al. Thiamin, riboflavin, and vitamins B-
4. Varady KA. Intermittent versus daily calorie restriction: 6 and C: impact of combined restricted intake on functional
which diet regimen is more effective for weight loss? Obes performance in man. Am J Clin Nutr. 1988 Dec;48(6):1451-
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9. [Pubmed]

Alan Aragon’s Research Review – September 2012 [Back to Contents] Page 10

 Well, that’s something you don’t see every day – a low-carb fan
discrediting Atkins and praising Gary Taubes in the same
Sports science professor Tim Noakes goes full low- thought. What’s even more unusual is that Noakes is, or at least
carb, part 1. was, a man of science. I read a lot of stuff, and I have not come
By Alan Aragon across a single scientifically valid point Gary Taubes has made
about nutrition or exercise – at least not from his interviews and
articles since the release of his first diet book. All that I’ve
gathered is that he has an excellent sense of sensationalism and
entertainment. Gary Taubes’ material has made two appearances
in AARR (May 2009, May 2012) mainly because his
pseudoscientific claims are so outrageous that they demand
some commentary from the side of science & reason.

Second  the  reason  why  this  eating  plan  has  been  so 
extraordinarily  effective  in  my  case  is  because  it  matches 
precisely  my  particular  biological  needs,  perhaps  because  like 
Mr Banting, my lineage is from England. In brief I inherited from 
my  father  and  his  lineage,  a  predisposition  to  develop  adult‐
onset  diabetes  because  I  am  what  is  known  as  “carbohydrate 
resistant” (CR) and hence “pre‐diabetic”. My biology is such that 
I  am  unable  effectively  to  clear  from  my  bloodstream,  the 
Tim who? breakdown  product  of  ingested  carbohydrate,  glucose.  As  a 
Tim Noakes is best known in academic circles as the scientist result my pancreas must over‐secrete the hormone, insulin, one 
who illuminated the concept of a “central governor” as it applies of  whose  normal  functions  is  to  direct  the  glucose  from  the 
to exercise. The general idea is that the central nervous system bloodstream into the liver and muscles.   
 
protects homeostasis by regulating the amount of work done But instead, in my case, under the action of insulin most of the 
before the perception of fatigue sets in, preventing further carbohydrate that I ingest is directed into my fat cells where it 
performance capacity, thus insuring survival. He also discovered contributes  to  progressive  weight  gain,  continual  hunger, 
exercise-associated hyponatremia (critically low blood sodium lethargy  and,  in  time,  pancreatic  failure  and  the  onset  of  the 
levels from the overconsumption of plain water during training). irreversible and universally fatal condition, adult‐onset diabetes. 
It’s not an overstatement to say he’s a legend in the field. Lay I  am  as  certain  as  I  can  be  that  this  eating  plan  is  the  only 
folks familiar with Tim Noakes have likely heard of his book effective  long‐term  health  solution  for  anyone  who  shares  this 
The Lore of Running. Within the latter, Noakes vigorously Banting/Noakes biology. 
championed a high intake of carbohydrate for the purpose of
maximizing performance. Alright, a couple of things here... First of all, it’s mildly
However, with the recent launch of his new book Challenging astounding how Noakes appears to be making assumptions about
Beliefs: Memoirs of a Career, he’s made numerous media his current physiological status based on wild guesses about
appearances renouncing his former high-carb stance and genetic predispositions. The idea that English lineage is a risk
preaching the low-carb gospel. I don’t have his book, so I don’t factor for diabetes is not only amusing, but it’s unfounded. A
know how much of it is dedicated to low-carb raving, but I’ve recent review by Elbein discussing the genetics of type 2
stumbled upon enough recent Noakes interview material to be diabetes mellitus (T2DM) reported the following:
surprised if he doesn’t give low-carbing at least a generous plug “Several lines of evidence suggest that genetic susceptibility
or two. In the following discussion, I will interject my plays a major role in the pathogenesis of T2DM. First, risk
thoughts with quotes of his from a recent (and rather shocking) varies widely across populations, from 5% or less in white
article that’s been making waves in science-oriented fitness and Asian populations to 50% or more among Pima Indians
circles.1 In the spirit of his passion for endurance, Noakes’ and South Sea Island populations.”
article runs on endlessly, so I’ll cover this in two parts to
preserve the attention and sanity of the readers. So, it looks like Tim is in the genetically gifted club, along with
myself (granted that I have traces of Asian and not Martian).
...the  eating  plan  I  follow  was  first  prescribed  in  1861  by  a  Secondly, it’s senseless to merely assume you’re glucose-
Harley Street surgeon Mr William Harvey with great success to a  intolerant, carbohydrate-resistant, insulin-resistant, or however
corpulent  London  undertaker,  Mr  William  Banting.  Thus  it  is  you choose to describe it. I’m hoping that Noakes, with all of his
more  appropriately  named  the  Harvey/Banting  diet.  [...]  Dr  influence and resources, was able to get evaluated for insulin
Robert  Atkins  re‐discovered  “banting”  in  1974  and  his  name  is  sensitivity via hyperinsulinemic-euglycemic clamp, instead of
now incorrectly used as if he was the first to describe this eating  merely guessing that this is what Fate has decided for him. His
plan.  The  history  of  Harvey  and  Banting’s  original  contribution  mentioning of being “pre-diabetic” makes it plausible that his
was  re‐discovered  by  Gary  Taubes  and  is  described  in  Taubes’  blood test results, while overweight (he claims to have lost a
momentous books Good Calories, Bad Calories and Why we get  significant amount of weight while low-carb dieting for roughly
fat and what to do about it.  the past year), showed objective signs of glucose intolerance.
Alan Aragon’s Research Review – September 2012 [Back to Contents] Page 11
Still, projecting some personal low-carb epiphany upon the
public is just cheesy (no pun intended). He chose to indulge in
excess for an extended period, so now he must undo the damage
– just like anyone else who has screwed up some aspect of their
lives and now has to pick up the pieces. It happens to the best of
us. However, my issue is with the claim that an extreme stance
against carbohydrate is optimal universally (though he briefly
disclaims this), particularly for those whose primary objective is
weight loss.
The third point is that this is not a diet, it is an eating plan for life 
– it is a life style, it is a new eating behaviour. This is not the way 
to  go  for  anyone  who  wishes  a  quick  fix  to  lose  weight  and  to 
improve  their  health  by  changing  their  eating  patterns  for  as 
short a time as possible. Once you “bant”, you have to stick with 
it  for  life.  Because  those  who  successfully  lose  weight  on  this 
eating  pattern  will  regain  that  weight  and  more  within  a  short  It’s often overlooked that resistance training is the trump card
time of going back to eating the way they did before – that is,  for improving insulin/glucose metabolism (and other measures).
returning to eat the foods that precipitated the problem in the  Aerobic training covers only part of what’s optimal. For
first place.  example, Bweir et al found that resistance training improved
 
The  point  is  that  the  metabolic  abnormality  (CR)  driving  the 
problem is not ever going to normalise regardless of how much 
weight  is  lost  or  even  how  much  exercise  is  performed.  For 
those  of  us  with  CR,  our  metabolism  is  the  problem  and  if  we 
want  to  do  the  best  for  our  bodies,  then  we  have  to  change 
forever the nature of the foods that we eat. But I argue that this 
change  is  much  easier  than  most  would  ever  believe. 
Unfortunately it is also the advice that many dieticians may be 
scared  to  prescribe  for  the  reason  that  they  have  been  taught 
that  high  fat,  low  carbohydrate  Banting  diets  full  of  “artery‐
clogging”  saturated  fats  are  dangerous.  But  this  is  an 
unsubstantiated dogma that does not stand up to an intelligent 
and  independent  interpretation  of  the  complete  scientific 
literature. 
The excerpt above sounds like the process of making a decision
to join the convent or priesthood. Once you’re in, you’ve made a
commitment toward self-denial of the pleasures of this planet –
and you better stick to it OR ELSE. So, there it is again, that
lovely extremist bent. Inflexible approaches to dieting have been
associated with a double-whammy of adverse outcomes. Smith
et al found a positive correlation between flexible dieting and
lower bodyweight, as well as the absence anxiety and
depression.3 Additionally, rigid dieting was found to be
associated with overeating and increased bodyweight. Along
these lines, Stewart et al found that rigid dieting was associated
with symptoms of an eating disorder, mood disturbances, and
anxiety.4 This was not the case with flexible dieting that did not
involve an all-or-nothing approach.
Noakes’ next point that carbohydrate resistance (CR) is “not
ever going to normalise regardless of how much weight is lost or
even how much exercise is performed” is a steamy load of bunk
as well. Weight loss is an independent factor in the improvement
of glucose control. This has been demonstrated repeatedly in the
literature, even in inherently treatment-resistant populations. For
example, Jazet et al found that in a loss of 50% of excess weight
(20.3 kg or 44.7 lbs) normalized basal endogenous glucose
production and improved insulin sensitivity.5 Notably, these
Alan Aragon’s Research Review – September 2012
changes occurred in type 2 diabetics, and no formal exercise
program was imposed. A recent study by Snel et al involving
large-scale weight loss and an exercise program (cycle
ergometer training), the loss of 23.7 kg (52.1 lb) resulted in
improved insulin-stimulated glucose disposal, as well as insulin
signaling at the molecular level.6 Once again, this occurred in
type 2 diabetics, so the improvements occurring in this
population are much harder-won than improvements in pre-
diabetics and people with normal glucose tolerance. To quote a
review by Østergård et al:7
“Several large-scale studies have documented the fact that
increased physical activity can reduce or at least postpone
the development of type 2 diabetes, and low physical fitness
is a clear independent risk factor for the development of type
2 diabetes.”
pre- and post-exercise HbA1c readings to a greater degree than
aerobic training in type 2 diabetics.8 Similarly, Arora et al found
that progressive resistance training improved blood lipids and
measures of glucose control and general well being to a greater
extent than aerobic training in type 2 diabetics.9 Of course, it
never hurts to do both types of exercise. To illustrate this, Sigal
et al reported that both resistance and aerobic training are
effective at improving glycemic control in type 2 diabetics, but
combining the two types of training was more effective than
either type on its own (note that this could have been due to a
greater training volume overall).10
For  to  change  one  has  to  rid  oneself  of  an  addiction  for  easily 
assimilated  carbohydrates  –  an  addiction  that  is  at  least  as 
powerful  as  those  associated  with  cigarette  consumption  and 
some  recreational  drugs  like  heroin.  It  is  not  easy  to  give  up 
addictions.  And  like  all  addictions,  addicts  have  to  take  each 
moment of their recovery one day at a time. In a sense those of 
us  who  are  unable  to  metabolise  carbohydrates,  are  never 
cured of that addiction. We are always in recovery. We have to 
take each new day of our cure, one day at a time. 
 
But for those who like me are convinced that they have a really 
good  reason  to  change  (in  my  case  to  avoid  dying  from  adult‐
onset diabetes – the fate that struck my father and his brother) 
and  are  prepared  to  change  what  we  eat  for  the  rest  of  our 
lives, then we may be up for the challenge. 
 
The fourth point is that this is not a “fad” diet ‐ the reason why 
it works so well is because there are solid biological reasons why 
it  must  produce  a  successful  outcome  if  followed  faithfully  by 
those with CR. 
First of all, Noakes is drawing the false implication that being
carbohydrate-intolerant and carbohydrate-addicted are inevitably
conjoined. This appears to be another personal projection he’s
taking liberty to make. However, the idea of carbohydrate
(especially refined types) being addicting is intriguing, and has
indeed gotten some exposure in the recent scientific literature.
Those more accepting of the idea that food can be addictive
[Back to Contents] Page 12
point to similar neural and behavioral effects of foods and
addictive drugs.11-13 However, even the most open-minded
authors (including Robert Lustig) must concede the following
anti-climactic fact:12 “Sugar addiction, including tolerance and
withdrawal, has been demonstrated in rodents but not humans.”
Proponents of the validity of carbohydrate addiction have a large
burden of proof to bear, particularly when referring to
population-wide effects as opposed to individual cases. There
are several challenges to the sugar addiction→obesity epidemic
model, including the following:
ƒ A key characteristic of addiction is loss of control. A very
small energy surplus accumulating over a sustained period
of time can account for the increases in body mass index
(BMI) distributions of populations. This suggests that any
measurable loss of control of eating (an essential criteria of
addiction) is miniscule in most of the obese population.14
ƒ The latest report from the ERS/USDA shows an increase of
445 kcal compared to 40 years ago (2169 kcal/day in 1970
vs 2614 kcal in 2010).15 Of this increase, caloric sweeteners
contributed only 42 kcal (less than 10% of the total
increase). The majority of the increase came from equal
contributions from grains (mainly refined grains) and added
fats, with minor contributions to the total from dairy fats,
fruits & vegetables, and meats. Therefore, putting the blame
on sugar ignores where the bulk of the contributions are
coming from.
ƒ An estimated 142 kcal decrease in occupation-related daily
energy expenditure occurred from the early 1960’s to the
early 2000’s.16 Combined with the USDA/ERS data, this
puts the energy surplus at 587 kcal greater than it was in the
1960’s -1970’s. Bear in mind that this is not including
decreases in recreational energy expenditure, which are
difficult to measure, but are likely inevitable due to physical
play replaced by digital play. A conservative estimate of
100 kcal would bring the surplus total to 687 kcal. Thus,
allegedly uncontrolled increases in carbohydrate (refined or
other) cannot be singled out as the all-encompassing obesity
culprit.
ƒ Sugar addiction is often claimed to share parallels with drug
addiction. In addition to a loss of control, key characteristics
of the classic addiction model are craving, tolerance, and
withdrawal. The proposed food addiction equivalent to
tolerance is increasing amounts of food required to reach
satiety. However, this is not a convincing equivalent to drug
addiction because it assumes a direct relationship between
satiety and intoxication.14 Even in the case of binge eating,
it occurs in the absence of hunger, and eating is done to the
point of physical discomfort.
ƒ Withdrawal symptoms upon drug cessation include
dysphoria and autonomic symptoms such as sweating and
tremors. Distress during the cessation of sugar (or other
carbohydrate) can be merely a survival signal of an energy
crisis within the body rather than a signal to get intoxicated.
There is simply no objective evidence for human
withdrawal syndromes upon cessation of any food – sugar
included.14
ƒ Aside from the obvious fact that humans are not rats, the
demonstration of sugar ‘addiction’ in the rodent model was
done under “a highly prescribed and atypical feeding
procedure.”17 The outcomes furthermore demonstrated a
Alan Aragon’s Research Review – September 2012
food preference for palatability, rather than sugar per se.
This does not mean that palatable foods are physically
addictive, but rather that the particular lab protocol (which
included deprivation) can artificially produce a reaction to
food that’s similar to the response to addictive drugs.
ƒ The drug addiction model predicts progressively increased
cravings alongside the duration of drug cessation. However,
in the case of food, fasting in humans has been observed to
result in decreased food cravings.17 Furthermore, unlike the
drug tolerance model would predict, children like intensely
sweet tastes, but this preference declines through
adolescence.
References
1. Noakes T. Tim Noakes on Carbohydrates. June 18, 2012. [Health
24]
2. Elbein SC. Perspective: the search for genes for type 2 diabetes in
the post-genome era. Endocrinology. 2002 Jun;143(6):2012-8.
[Pubmed]
3. Smith CF, et al. Flexible vs. Rigid dieting strategies: relationship
with adverse behavioral outcomes. Appetite. 1999 Jun;32(3):295-
305. [Pubmed]
4. Stewart TM, et al. Rigid vs. flexible dieting: association with
eating disorder symptoms in nonobese women. Appetite. 2002
Feb;38(1):39-44. [Pubmed]
5. Jazet IM, et al. Loss of 50% of excess weight using a very low
energy diet improves insulin-stimulated glucose disposal and
skeletal muscle insulin signalling in obese insulin-treated type 2
diabetic patients. Diabetologia. 2008 Feb;51(2):309-19. Epub 2007
Dec 14. [Pubmed]
6. Snel M, et al. Effects of adding exercise to a 16-week very low-
calorie diet in obese, insulin-dependent type 2 diabetes mellitus
patients. J Clin Endocrinol Metab. 2012 Jul;97(7):2512-20. Epub
2012 May 8. [Pubmed]
7. Østergård T, et al. The effect of exercise, training, and inactivity
on insulin sensitivity in diabetics and their relatives: what is new?
Appl Physiol Nutr Metab. 2007 Jun;32(3):541-8. [Pubmed]
8. Bweir S, et al. Resistance exercise training lowers HbA1c more
than aerobic training in adults with type 2 diabetes. Diabetol Metab
Syndr. 2009 Dec 10;1:27. [Pubmed]
9. Arora E, et al. Effects of resistance training on metabolic profile of
adults with type 2 diabetes. Indian J Med Res. 2009
May;129(5):515-9. [Pubmed]
10. Sigal RJ, et al. Effects of aerobic training, resistance training, or
both on glycemic control in type 2 diabetes: a randomized trial.
Ann Intern Med. 2007 Sep 18;147(6):357-69. [Pubmed]
11. Fortuna JL. The obesity epidemic and food addiction: clinical
similarities to drug dependence. J Psychoactive Drugs. 2012 Jan-
Mar;44(1):56-63. [Pubmed]
12. Garber AK, Lustig RH. Is fast food addictive? Curr Drug Abuse
Rev. 2011 Sep;4(3):146-62. [Pubmed]
13. Gearhardt AN, et al. Can food be addictive? Public health and
policy implications. Addiction. 2011 Jul;106(7):1208-12.
[Pubmed]
14. Ziauddeen H, et al. Obesity and the brain: how convincing is the
addiction model? Nat Rev Neurosci. 2012 Mar 14;13(4):279-86.
[Pubmed]
15. United States Department of Agriculture – Economic Research
Service. Food Availability (Per Capita) Data System: Summary
Findings: Food patter equivalents and dietary trends. Updated Aug
20, 2012. [USDA/ERS]
16. Church TS, et al. Trends over 5 decades in U.S. occupation-
related physical activity and their associations with obesity. PLoS
One. 2011;6(5):e19657. Epub 2011 May 25
17. Benton D. The plausibility of sugar addiction and its role in obesity
and eating disorders. Clin Nutr. 2010 Jun;29(3):288-303. Epub
2009 Dec 28. [Pubmed]
[Back to Contents] Page 13

Why is nutrient timing still such a controversial topic?
By Alan Aragon
____________________________________________________
In the Q/A section of the December 2011 issue of AARR, I
addressed the “lingering controversy & confusion” surrounding
nutrient timing. The question was asked by Eric Helms before he
exploded into superstardom (by bro standards, anyway - haha).
Essentially, he asked what’s the deal with my apparent
downplaying of the importance of timing nutrients (protein in
particular) in close proximity to the training bout despite
recommendations to the contrary from the ivory tower. My
answer, in short, was that the body of research evidence as a
whole is painfully equivocal. Acute studies show a remarkable
consistency of positive benefit in timing nutrients near training,
while chronic studies have been hit-and-miss. The mixed results
Alan Aragon’s Research Review – September 2012
in chronic studies are primarily due to differences in study
design. This includes differences in subject profile, nutrient
doses, training protocols, measurement instruments, and funding
sources (yup, I had to go there). The chart below is an expanded,
more inclusive version of a chart in a collaborative review paper
I wrote with the great Brad Schoenfeld that’s making its way
through peer review. The chart in the yet-to-be published paper
focuses on hypertrophy as a result of immediate post-exercise
nutrient ingestion. However, the chart below includes notes on
total protein before and during supplementation, as well as
strength results. It also includes two studies that were left out of
our paper since they weren’t dealing specifically with the
immediate post-exercise “anabolic window.” The goal of the
chart below is to provide an aerial view, and a better grasp of the
current state of affairs in chronic nutrient timing research in the
context of resistance training. Color coding notes are at the
bottom of the chart, references are on the following page. I
realize how small the text is, so prepare to hit the zoom control.
[Back to Contents] Page 14
References in the order they appear on the chart:
1. Esmarck B, et al. Timing of postexercise protein intake is
important for muscle hypertrophy with resistance training in
elderly humans. J Physiol. 2001 Aug 15;535(Pt 1):301-11.
[Pubmed]
2. Cribb PJ, Hayes A. Effects of supplement timing and
resistance exercise on skeletal muscle hypertrophy. Med Sci
Sports Exerc. 2006 Nov;38(11):1918-25. resistance exercise
does not enhance postexercise muscle protein synthesis. J
Appl Physiol. 2009 May;106(5):1730-9. [Pubmed]
3. Willoughby DS, et al. Effects of resistance training and
protein plus amino acid supplementation on muscle
anabolism, mass, and strength. Amino Acids.
2007;32(4):467-77. [Pubmed]
4. Verdijk LB, et al. Protein supplementation before and after
exercise does not further augment skeletal muscle
hypertrophy after resistance training in elderly men. Am J
Clin Nutr. 2009 Feb;89(2):608-16. [Pubmed]
5. Hoffman JR, et al. Effect of protein supplement timing on
strength, power and body compositional changes in
experienced resistance trained men. Int J Sport Nutr Exerc
Metab. 2009 Apr;19(2):172-85. [Pubmed]
6. Burk A, et al. Time-divided ingestion pattern of casein-
based protein supplement stimulates an increase in fat-free
body mass during resistance training in young untrained
men. Nutr Res. 2009 Jun;29(6):405-13. [Pubmed]
7. Hulmi JJ, et al. Acute and long-term effects of resistance
exercise with or without protein ingestion on muscle
hypertrophy and gene expression. Amino Acids. 2009
Jul;37(2):297-308. [Pubmed]
8. Wycherley TP, et al. Timing of protein ingestion relative to
resistance exercise training does not influence body
composition, energy expenditure, glycaemic control or
cardiometabolic risk factors in a hypocaloric, high protein
diet in patients with type 2 diabetes. Diabetes Obes Metab.
2010 Dec;12(12):1097-105. [Pubmed]
9. Erksine RM, et al. Whey protein does not enhance the
adaptations to elbow flexor resistance training. Med Sci
Sports Exerc. 2012 Sep;44(9):1791-800. [Pubmed]

Here is a link to the Powerpoint presentations (in PDF) of each

speaker in the 2012 Sports Performance Research Institute, New
Zealand (SPRINZ) Strength & Conditioning Conference,
featuring a smashing presentation by my friend & colleague Eric
Helms.

If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles you’d like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.

Alan Aragon’s Research Review – September 2012 [Back to Contents] Page 15