What is Life?

On the origin and mechanism

of living systems.

Christopher Busby


 

 Maxwell’s Demon

Lots of questions arise. And I have no intention of

answering them. What I want to do is to provide
material for thought and confusion.

Paul Feyerabend
The Tyranny of Science
Polity Press 2011



What is Life? On the origin and mechanism of living
systems
Christopher Busby

Published December 2015

QTP Publications
Address: 10 Bratwell Road, Coleraine, BT51 4LB, UK

Typeset in Times New Roman 11.

Cataloguing information: Busby Christopher—What is
Life? On the origin and mechanisms of living systems.
A catalogue for this book is available from the British
Library
ISBN: 978-0-9565132-1-2

All rights reserved, including the rights of reproduction

in whole or in part in any form whatsoever. The book is
sold subject to the condition that it shall not, by way of
trade or otherwise, be lent, resold, hired out or otherwise
re-circulated without the publisher’s prior consent, in any
form or binding or cover other than that in which it is
published and without a similar condition being imposed
upon the subsequent publisher.

The drawings or Maxwell’s Demon were scribbled by

Saoirse Morgan on a A4 pad at the time I was describing
all this to her in 2006; They can be all be found in my
poetry book Our Mother who art in Everything Sosiumi
Press 2009 but I have slotted them in here also to lighten
up the mood.



 Contents

page

Foreword 1

Moscow conference abstract 2

Chapter 1. The drug receptor concept 9

Chapter 2 What kT did 21

Chapter 3 Maxwell’s Demon 33

Chapter 4 Molecular Communication 41

Chapter 5 Proteins 53

Chapter 6 Mechanism 65

Chapter 7 The origin of life 79

Chapter 8 Proposed experiments 99

Chapter 9 Molecular Communication & Cancer 107

Chapter 10 Endnote and Warning 123

Select Bibliography 126



 

 Foreword

I won’t apologize for stealing Schrödinger’s 1943 title: I

couldn’t really see another one as pithy and appropriate
for what I have to say. Nor will I apologize for the size
of the book, which will not be great.

It is customary for scientists to write their works with

citations for everything they put down (although
Schrödinger did not). Thus, like spiders, they spin an
extension to the existing complex web linking all the
evidence and observations together with filaments made
of their own interpretations and experimental additions;
this has become the way it is done. But what if all your
ideas are connected together in an entirely separate way?
It is impossible to go back and undo the web if the error
is at the beginning. I have had a lot of trouble with this in
publishing papers on radiation and health where the
spider-web is based on the idea of dose, which came in
right at the beginning, at the centre of the system of
thinking. In the end you have to bypass the historical
structure with its conclusions and present a different and
entirely separate one. But in this book, for reasons which
I will outline below, I don’t intend even to do that. The
time I have is too short and I am getting old. Old people
are allowed some leeway, and I will take all I can. I will
spin a new web out of different ideas altogether.

I have always been interested in the big questions, and

began this investigation into the molecular mechanism of
life in about 1971 when I was working at the Wellcome
Research Laboratories in Beckenham. I left Wellcome at

1

the age of 29 to follow a life where I combined a sort of
primitive natural philosophy of thought with living
outside the system as much as possible, especially
without working for anyone. I am proud that after
Wellcome I have never had a job, apart from one year as
a Postdoctoral fellow at the University of Kent (I fled
before the contract ended). So I could devote a lot of
time to thinking “outside the box” as they say. This
makes me quite rare. Most scientists work for a
company, a university, an institute or the military. They
have to do what they are told. I have never done what I
was told. I have always done as I pleased. My mother
used to say to the aunties: Christopher does as he pleases.
Correct.

So between 1970 say and this year, 2015, that is 45 years

of independent thinking, I have mulled over the scientific
paradoxes of living systems to try and figure out what is
going on. Why is a dead duckling dead and a living one
living, both apparently with an identical molecular
structure. And what about our little friend the amoeba.
One cell. Watch her through the microscope tootle about.
What’s going on there? I fell in love with Ms amoeba.

I have (with hardly any money--you don’t get much if

you don’t work) built electronic machines to investigate
my ideas, buying components from the amateur
electronics suppliers and whole lumps of equipment from
ebay in the USA (where they chuck out the most
sophisticated and complex equipment and you can buy it
for a song). By 1990 I believe I had the answer. I had

2

built the equipment and shown that the idea was sound.
But then a number of blocks were there to stop me going
public. First, like Darwin, I was afraid it was nonsense
and didn’t want to be laughed at (it may still be
nonsense, but it is entertaining, so bear with me). I put it
in a drawer to think about it some more. A second thing
was that I started my research on radiation and health.
This is what I am most known for and it has taken up 25
years of my life, fighting to get what is so clearly
obvious accepted. A third thing was that if I am correct it
is not a small idea: it has both positive (cancer cure) but
also a negative (military) potential. Do I want to go down
in history (asks one of my women) as the inventor of the
death ray. Etc. I had some final experiments to make, and
by 2005 I had read about Luca Turin’s ideas and
experiments with deuterated perfumes. I had used some
of the money I made in radiation court cases to stock a
laboratory to create machines that employed the
principles, but never seemed to get the time to do the
work. Everything conspired against it. In 2008 I was
invited to Moscow by Elena Burlakova to give a paper
on my ideas, but for various odd reasons was unable to
get a visa in time. I present the outline of what I sent her
after this foreword. Then I ran out of money and had to
sell my house and move to Riga: the contents of the lab
were put in storage.

So I will just sit down on my boat Marius, and write it all

out chapter by chapter. I will refer to some people and
ideas but will generally not bother. This approach is so
delightful that I am really looking forward to the freedom

3

to just throw it at you, like a bucket of thoughts and
results. I intend to write this in 10 days, as this is all I
have spare at the moment. But if I don’t do it now, it will
drag on, and I will lose track of it, or get too old to think
straight or perhaps even just fall down dead. After all,
Handel wrote Messiah in three weeks, so I am sure that I
can put together the essentials.

Fasten your seat belts.

Christopher Busby
MV Marius, Somewhere in France
And (another 3 days at) 1117 Latvian Academy of
Sciences, Riga, Latvia
September/ October 2015.

4

 4th International Conference
Mechanisms of Super Low Dose Action
Moscow, Russia, 28th to 29th October 2008

MAXWELLS DEMON, MOLECULAR

COMMUNICATION AND LIVING SYSTEMS:
OUTLINE OF AN EXPLANATION OF THE
ORIGIN AND DYNAMICS OF LIFE

C.C.Busby, Green Audit/ Department of Molecular

Biosciences, University of Ulster

Castle Cottage, Sea View Place, Aberystwyth

SY231DZ UK

Abstract
Consideration of the bankruptcy of current chemical
models of the living cell leads to an alternative proposal
for the nature of living systems and their origin.
I begin with pharmacology. The conventional
explanation of pharmacological activity at the living cell
involves chemical information exchange through
hormone-receptor or drug-receptor interactions. This is
presented in the historical and current model as a
sequence of specific targeted chemisorption by a small
molecule at some preferred electronically conjugate
surface followed by some unelaborated further sequence
of steps, implicitly assumed to be chemical in nature. Yet
despite a number of clear and massive problems with
such a model no alternative has been suggested.
Problems include: (1) The enormous difference in

5

chemical shape and chemical nature of substances which
are shown by reciprocal plots to activate the same
receptor. (2) The fact that proteins can act at the same
receptor as small pharmacologically active molecules
even though they are orders of magnitude larger. (3) The
difficulty in creating a model in which an adsorbate at
the surface of the cell can cause changes inside the cell
over the large molecular distances involved: the second
messenger problem.
(4) Cells respond to pharmacological agents at
concentrations where the agent is stochastically absent.
There are other problems with living systems and
their origins. First, living systems contravene the 2nd law
of Thermodynamics. They do not operate thermo-
dynamically as spontaneous processes and do not
increase their system entropy. Instead they are able to
take energy from their surroundings (metabolism) and
utilize this energy to increase their organization. Since
the unit of life is the single cell, this behaviour must be
explainable within the single cell and its workings. It
must also have been present in some form at the
beginning when inanimate molecules became in some
sense alive. A strictly chemical reaction, however
complex, will not do this, and could not have begun
spontaneously to do this when life began.
Second, the chemical model for cell activity is
usually described in terms of diffusion controlled
processes in dilute solution. Yet the most obvious aspect
of the living cell is clutter and impediments to diffusion:
the curtains of lipoproteins which divide the cell up into
many layers and labyrinths seem to be designed to reduce
molecular diffusion not assist it. Why are they there?
Third, the machinery of the cell clearly relies
mainly upon proteins, yet chemically proteins are
enormous, slow moving in terms of diffusion and

6

chemically rather similar though physically very
different. What is their role? How do they contribute to
the cell operation?
I propose a new model in which the cell is seen
as an electromagnetically switched system operated
through molecular energy exchanges at vibrational
frequencies. The essence of all living systems is that they
are hot: life developed on a hot planet. It is an interesting
fact that kT for the narrow range of vibrational energy
exchanges of all molecules (3300-200cm-1) spans the
range of commonly occurring living environments. Cell
dimensions define cavity array oscillators for water
absorption. It is also the case that traditional
thermodynamics has been overtaken by quantum
specificity. Second Law considerations of molecular
energy exchange described by the Maxwell’s Demon
thought experiment are broken by quantum energy
exchanges at vibrational frequencies. Thus molecular
communication of energy can occur exclusively between
hot molecules that share vibrational modes whilst other
molecules in the same cell will be transparent to such
exchanges. Experiments I carried out in the 1980s with a
modified Callendar Differential Thermal Balance
confirm this. In the model, the components of the cell are
now seen primarily as units for electromagnetic energy
exchanges rather than for diffusion-controlled chemical
reactions. Proteins act as resonators through specific
selection of surface infrared absorbers through
evolutionary selection of tertiary folding, the folding
being determined by the amino acid sequences. In the
cell, switching occurs by blanketing the surface with
specific vibrational absorbers, the pharmacologically
active agents, and local reaction rates increase due to
local pockets of energy (heat). It is the vibrational
absorption and emission spectrum of the drug or

7

hormone that is the relevant quality and not the shape. In
support of this idea I describe the experiments of Luca
Turin on acetophenone and d-6acetophenone and I draw
attention also to pheromone observations in insects. The
idea can answer the questions I began with and also can
account for the spontaneous origin of life on earth.

8

 Chapter 1

The drug receptor concept

1.1 Drug receptor interactions

My early research at Wellcome was on the physical

chemistry of pharmacologically active compounds at the
molecular and cell level. What drug companies like
Welcome want to do is find compounds which have quite
selective effects on human physiology or on the
molecular reactions which control the development or
function of bacteria, viruses, parasites, and the many
hostile entities that cause disease. Research has
discovered many small chemical compounds (molecular
weight up to about 500) which control the behaviour of
physiological systems, compounds which exert positive
or negative influences on heart action, stomach acid, the
nervous system, the chemical neuro-transmitters and so
forth. When I was there in the 70s, one of the things we
were interested in was the histamine response which
controlled stomach acid secretion. Two guys from Smith
Kline & French (I think French has gone and they were
taken over) Black and Ganellin, had postulated the
existence of a second “receptor” for the substance
histamine which until then most drug people had
associated with the allergic reaction, and where
Wellcome had a pretty good drug that blocked its allergic
effects, triprolidine. So, if you like, it was our territory.
The Black Ganellin drug that stopped the stomach acid
secretion was called Burimimide, and looked a bit like
histamine. Triprolidine looks nothing like histamine, nor

9

do the other H1 blocking agents. They named the
receptor “H2” to distinguish it from the H1 allergy
receptor. It was a very important drug, and more recent
versions of it can be bought over the counter for
indigestion. Ulcers are a thing of the past because of this:
when I was young, people regularly died from stomach
ulcers.

Up to the time I began at Wellcome, the way that drugs

were found had been to have a Chemical Research
Laboratory in which a team of organic chemists
synthesized what they thought might be biologically
active compounds. These were clever fellows; sort of
gentlemen scientists who followed hunches and created
compounds that were similar to ones that either were
known to do something or else were natural compounds
which already existed in the body but to which they
made a slight chemical addition or subtraction. A
Chlorine atom here, a Sulphur substitution there. That
kind of thing. It was the inspired lottery school of drug
design. When the molecule was made and we checked
spectroscopically that it was what they thought it was, it
went to the pharmacologists to do their frightful
experiments on the rats, guinea pigs, dogs (in the case of
the stomach acid) and cats. But about the time I was
there, the clever chemists were getting on in age, and
there had been a lot of developments in technology
which enabled us to begin to look more closely at the
interactions at the molecular level between
pharmacologically active compounds (like histamine)
and the cells that they switched on (or off). We were to

10

supplant the chemists with “rational drug design”. The
idea then was, and still is, that there was a structure on
the outside of the cell, which was like a keyhole switch;
it was called the “receptor”.

The idea of the drug receptor developed through most of

the last century and is superficially an attractive one. It
has been called “pharmacology’s big idea” and it is. The
surface of the cell, which faces outwards to the big world
of the extracellular environment, the blood etc. is
believed to have a finite number of active sites which
have a surface shape and electronic charge conformation
which is complementary to the shape and charge
conformation of the substance (called by the
pharmacologists a “ligand”) which somehow locates
itself up against the receptor and causes some change
there which then communicates with the inside of the cell
somehow and throws the master switch. The
mathematical treatments which go with this are similar to
those which describe surface (Langmuir) adsorption, and
many measurements of drug concentration versus
activity have been made. These data generally suggest
that receptors are finite in number and that above a
certain concentration of drug (ligand) there is no further
effect; the system has been saturated. The idea of course
requires that the receptor has a high and specific affinity
for the drug under normal physiological concentrations.
It also allows for both agonists and antagonists: thus
there are substances which have a high affinity but don’t
throw the switch, and these then block access of the real
substances which also have affinity but do switch on the

11

effect. The receptor occupancy model predicts a
logarithmic relation between concentration and effect; a
reciprocal plot of the logarithm of the concentration
versus the effect is a straight line. The effect of a
competitive antagonist at a receptor is predicted to shift
the line parallel to the original and this is found to be so.

So it does seem as if there are active sites on the surface

of the cell, and that both agonists and antagonists stick
there through chemical affinity and this causes the
switching on of the cell. So far so good. But what if the
observations can be interpreted differently?

1.2 Interpretation and science

Science builds itself, always built itself, on

interpretations of a selection of observations. Built into
any interpretation is a set of “givens”. Facts which are
assumed based on a different set of interpretations of a
different set of facts. For example, the drug-receptor
theory assumes that we are dealing here with chemistry,
and that the chemical interaction at the receptor site is a
real phenomenon. I mean, it may be a real phenomenon--
we know that there is such a thing as adsorption on
surfaces, but questions remain about how the switch is
thrown and effects begin to occur inside the cell and also
about the chemical / morphological nature of the
receptor.

My friend Dr David Davis, the medical anthropologist,

whom I visited in Alderney to measure radiation from La
Hague, believed that all we had to do, to get the truth in

12

any area, was to stick up on a large board all that was
really known about the issue in question and look at it
all. The interpretation would, he maintained, be clear.
But I thought: what if there are several interpretations?
The several interpretation school died long ago, toward
the beginning of the last century. The reason was the
removal of Science from amateurs and the absorption of
Science into Universities. The crystallization of belief
into textbooks which copied themselves into the present.
The Black Boxes of Bruno Latour (look him up). Paul
Feyerabend. I don’t know about you but I find it easy to
believe what I read in a textbook, unless I am very
careful. It all flows off the page into my head and my
mind says: Yes, that seems very plausible. And of course
it is. But that doesn’t make it right. My dealings with the
radiation risk community and their scientists have made
it clear to me that Science is actually very like religion,
nowadays anyway. It is all about belief. Mary Midgely
was on to that.

The drug receptor idea has come forward in the

textbooks together with the accretion by Science of big
fat textbooks on cell biology, biochemistry and
biophysics. In these books you will see the most
beautiful representations of cells created by artists using
perspective and several colours and shadings. Why aren’t
they in the Louvre? These pictures have become, for the
students who are asked about them in the examinations,
the reality of the living cell. But the pictures are derived
from electron microscope photographs which are of cells
which have been killed and frozen and stained with high

13

atomic number elements (Osmium, Uranium, Gold).
They are not pictures of the living cell: the closest we can
get to that with the light microscope shows something
that is blurry and shivers as if it is cold. What’s going on
there? And second, how do we know that the
arrangements of the various bits and pieces in the cell are
the same when it is alive as when it is frozen and
stained? Same with the drugs and receptors. No one has
seen a drug receptor. I recall when at Wellcome Peter
Goodford, Head of Biophysics, which had the committee
on drug design where I was the physical chemist
member, actually paid some monstrous amount of
Wellcome’s money to have the haemoglobin molecule
built as a model. He wanted to “see” the receptor for
diphospho-glyceric acid, a substance which modulates
the haemoglobin oxygen dissociation equilibrium, so we
could suggest a synthetic analogue that might help those
with cardiac insufficiency. It was a magnificent creation:
you twirled a knob and the conformation changed. Or
you could carry out quantum mechanical molecular
orbital calculations on various molecules to work out
preferred conformations (though not with haemoglobin
as there were too many atoms). There was a guy from
Texas who did this for Histamine. But he was calculating
preferred conformations (shapes) for the substance in a
vacuum; nothing else there. This was such a waste of
effort.

There are two big problems with the drug receptor lock
and key idea. The first is: how does the binding of the
agonist at the receptor site cause the cell to switch on.

14

There has to be some telephone connection as it were
between the surface of the cell where the receptor is and
the goings-on inside. Various solutions have been
proposed for this one but they are all alike in their
implausibility. Second, how is it that the actual shapes
and the electronic shapes and indeed the chemical
reactivities of the compounds which all switch on the
same receptor are so different, in some cases enormously
different. Let’s have a look at some examples. In Fig 1.1
I show the chemical structures of Histamine and
Burimimide, which was the first of the H2 receptor
antagonists discovered by the Black/ Ganellin team. This
was praised as an example of the rational drug design
approach, for which they got the Nobel prize. It was the
rational drug design approach that I was involved in with
Peter Goodfords crew at Wellcome. Whenever someone
says “rational” I get out the garlic.

In Fig 1.2 I show the main marketed H2 receptor drugs

that followed from Burimimide. At the top is
Cimetidine, the first successful compound which was
marketed in 1976 as Tagamet. Then below that there are
Ranitidine, Famotidine, Nizatidine and Roxatidine
Acetate.

Now I can tell you, I played around with models of some

of these at the time. And since then with most of these. I
also was interested in the likely position of the NH2 on
the histamine side chain. What a laugh. This was the
subject of a complicated molecular orbital calculation by
the guy in Texas. I looked at the conformation under

15

various pH situations. How could Burimimide
electronically pretend to be Histamine so that it bound at
the same receptor? Or even physically? Those who are
chemists will immediately see that the antagonists shown
in Fig 1.2, the ones that work, are chemically very
different although if you stretch the imagination there
may be some common features. All they have in
common is the washing powder band-waggoning tag
“atidine” or “itidine”. We have four different
heterocyclic rings separated by a 4-chain containing
sulphur from some totally different terminal groups, two
of which contain a nitro group, one a cyano and one a
sulphanilamide. How can all these have any kind of
common chemical or electronic affinity for the same
receptor? And when we get to the last one, Roxatidine
acetate, there is absolutely no chance that this “atidine”
represents any kind of chemical similarity to the others or
to Histamine. No sulphur in the middle, a benzene ring.
How can any chemist (or indeed any child at school or
artist) believe that all these are complementary toward
the same receptor? The molecular weights range from
111 for Histamine through 212 Burimimide then 314
Ranitidine and 348 Roxatidine. Yet they all no-doubt
conform to the requirement of the mathematical theory,
the Schild reciprocal plot. They switch the thing on; or
rather they block histamine from switching it on.

Something wrong here. Need to think again.

16

 Fig 1.1 Histamine and Burimimide

Burimimide

Histamine

17

 Fig 1.2 The main Histamine H2 antagonists

Cimetidine (SKF, Black, Ganellin, 200mg)

Ranitidine (Glaxo; 3 times more potent than cimetidine

150mg)

Famotidine (Merck. 9 times more potent than ranitidine

40mg)

18

 Nizatidine (Lilly. Same potency as Ranitidine 150mg)

Roxatidine acetate (same potency as Ranitidine 150mg).

19

 20

 2.

What kT did.

2.1 The inside of the cell

Imagine looking at the inside of a transistor radio set on

the basis that you knew nothing at all except that it
created music when you pressed a switch. You cut it
open and look inside. You take sections. This is a lot
easier than a cell, because the thing is much larger and
you can see everything. What you see (unlike a
processed cell) is what is there when it is working
playing Radio 4. So you name all the coloured
components. You employ graphic artists to draw
illustrations. You put these into textbooks and marvel at
the wonder of it all. Others write more textbooks. But
you know nothing about the electromagnetic waves that
the system receives and amplifies. What I decided in
1974 was that we are not dealing with chemistry at all.
Except that chemistry provides the components. In fact
we cannot be dealing with chemistry except in the
construction and maintenance of the hardware and power
supply. The transistors, resistors, capacitors and battery.
My area at Wellcome was dilute solution equilibria and
thermodymamics. Awful stuff. Willard Gibbs & Co. But
it does give you a feel for what dilute solution
interactions look like. The key is the solvent, water, and
its interactions with the main foci of all the molecules of
life, the amino acids, peptides and proteins, the

21

nucleosides and the sugars: hydrogen bonding and
solvation. There are various quite serious problems with
the description of the cell we seem to have now. One is
that diffusion controlled processes are slow especially in
the larger cells. I have read that the reason most cells
have the dimensions they have, about 10 microns
diameter, is that this is a limit for diffusion efficiency.
This may be a component, but the range of cell diameters
is not large and there may also be another reason which I
will discuss below. And the more complex eukaryotic
cells are so cluttered. The big proteins will be impeded in
any transfer by their hydrogen bonding “stickiness” to
say nothing of the curtains of lipid which hang about
everywhere. What are they for? Why are they there?
And what is it that transfers the receptor signal from the
surface of the cell membrane to the inside of the cell to
switch on the energy? The Second Messenger. Right. A
Biblical concept straight out of the book of Revelations.

There is another problem for me: proteins and

particularly the “active sites” that are where the enzymes
change the substrate into the product. As with the cell
structure, the graphic design people have been enlisted
here also. The books (and scientific papers) are full of the
strange coloured pasta shapes which are supposed to
show the active sites. These are reconstructions of X-ray
crystallographic and other results, but what do these
things really look like in an aqueous solution in a living
system? How do they work?

22

2.2 The receptor

Let’s go back to the histamine H2 drugs. It is clear that

they have nothing much in common as chemicals or
electronic conjugate surfaces, or even shapes. You can
look at other drug receptors and find much the same
thing. But they all conform to the key mathematical
requirements that define a single receptor. Interestingly
also they all seem to have roughly the same activity, that
is the range of activity is quite small. This may be a
valuable pointer to what is happening.

If the drugs all appear to switch on a single unique

receptor (and they do), but the receptor cannot be defined
chemically or physically (which it can’t), what are we
left with? Clearly the receptor is not a physical position
on the surface of the cell, or at least it is not one that has
any keyhole-like Yale lock specificity. The only answer
is that either it has no specificity and the specificity lies
elsewhere and/or that it doesn’t exist at all and the action
of the drug occurs through some other process than
chemical contact. Then the reciprocal plots that define
the active sites are just Langmuir adsorption plots, which
is what everyone said they looked like.

If the quantity of each of the H2 drugs needed to cause

the pharmacological effect is roughly the same, then that
suggests that the number of individual molecules
adsorbed on the surface of the cell is roughly the same,
whatever the drug. If we take 150mg as a reasonable
dose and the molecular weight as 250 then that is 3.6 x
1020 molecules. In a human aqueous body of 50kg that is

23

about 8 x 10-6 Molar and if we say there are about 1012
cells available for adsorption that is about 4 x 108
molecules per cell. Which is not many, given the size of
the molecule and the surface area of the cell membrane.
If it were the earth, that would be a signal from every
point about 1km apart. You need mobile phone masts for
that one.

It also suggests that there is no specific receptor on the

cell surface. There is only adsorption. That is clear from
the mathematical relationship between dose and effect.
But we are still dealing with a specific signal. What kind
of signal? As soon as you ask this question, the answer
jumps up in your face and shouts at you. It must involve
an electromagnetic signal. This would satisfy all the
above. It would also answer the question of how the
signal becomes sufficiently amplified to throw all the
levers inside the cell. You don’t need a second
messenger. The ligand, the drug molecule has to
somehow reach mechanically through the cell membrane
and shake hands with something on the inside. OK, there
are proteins that span this distance. But to me it seems a
strained possibility. But electromagnetic signals are not
spatially constrained. Like radio waves they can be
detected by anything that is tuned to detect them; their
range extends and amplifies the effect of the point source
to enormous distances, which are only limited by
damping and loss of energy. And what frequency of
electromagnetic signal? Well this is easily answered, and
the answer leads us into a completely new set of

24

questions. Questions (and interesting answers) about the
universe and the origin of life itself.

2.3 The temperature range of living systems

If we leave out the mad stuff, the inhabitants of volcanic

vents and icy wastes we can conclude that the range of
temperatures that life likes to exist in is between about 10
degrees and say 60 degrees Celsius. In the Universe, this
is quite a narrow range of temperatures. Of course, it is
also inside the range of liquid water, and that has to be
part of the explanation. But apart from the water angle,
where would such a range of temperature lie in terms of
molecular energy? The mean statistical energy of any
system at absolute (Kelvin) temperature T is given by
kBT, where kB is Boltzmann’s constant. I am going to run
the show in wavenumbers, cm-1, because that is what is
easiest to do for describing the infrared region of the
electromagnetic spectrum, but you can get the
wavelength by taking the reciprocal. Wavenumber Q is
1/wavelength O lambda).Thus the frequency of infrared
absorption of liquid water at 3450cm-1 is at wavelength
2.89Pm. I am using Q nu) for wavenumber; I should
really put a little bar over it but I don’t know how to. I
will use f for frequency.

Now we have to introduce a little quantum theory (real

quantum theory, no dead cats and all that crazy stuff).
The Planck quantum equation is E = hf hc/O where h is
Planck’s constant and fis frequency (Hz), c the speed of
light. For energy, I will use electron volts eV but also

25

you can see that wavenumber Q 1/O is an energy unit
also. 1 cm-1 is equal to 1.24 x 10-4 eV so there are
8065cm-1 to one electron volt. Now we can look at the
energies in the living universe.

Table 2.1 gives the value of kT (I am leaving out the

subscript B as it is too tedious to type) in eV and
wavenumbers for the Earth temperatures of 5, 20, 40 and
60 degrees Celsius.

Table 2.1 Mean statistical energy over the region of

temperature of living systems

Temperature Temperature kT kT cm-1

(degrees C) Absolute K electron (8065
volts cms-
(8.6 x 10-5 1
/eV)
eV/K)
5 278 0.00239 192
20 293 0.00252 203
40 313 0.00269 217
60 333 0.00286 231

So the baseline energy of all living systems, the sink

energy, is in the far infrared. That means that if I were
God, I would seriously consider a design that employed
electromagnetic signals which could be sourced by
excited state molecular vibrations and sunk in a (slightly)
lower energy background.

26

2.4 Ducklings

When I asked the question in Russia, what distinguishes

the live duckling from the apparently molecularly
equivalent and identical dead duckling, the answer is that
one is hot and the other is cold. We are taught at school a
list of attributes of life, metabolism, reproduction and so
forth. No one says that living things are hot. But that is
what life is. Hotter than its surroundings. Non-living
things, pencils, spectacles, cups of coffee, crystals, all
spontaneously lose whatever temperature they began
with and end up at the temperature of the surroundings.
As does the dead duckling. But not the live duckling.
The live duckling quacks, squeaks, eats things, marches
about pecking corn, and is warm and stays warm. And in
the next chapter I will have to address the other aspect
that this observation raises, the famous and absolutely
key question which all theories of life’s origin have to
address. It was famously raised by Erwin Schrödinger
but (strangely, for one of the greatest quantum theory
scientists) not answered. The question of entropy. But I
will leave that for now and move on to the concept of
molecular temperature, which I believe I have invented,
but no doubt someone has been there.

No one can think in terms of electron volts as energy;

well there may be some young guy in a tweed jacket at
Cambridge who can, but they would be associating it
with some area of physics and not life. So I want to see if
we can imagine a temperature associated with a single
molecule. Why? Because it will give us some crude idea

27

of the advantage in reactivity that molecule might have
over the other molecules around it. Bear with me here; it
will become clear where I am going when I get there.
We can use the Boltzmann equation in reverse so as to
identify what the collective or average temperature
would be when associated with some vibrational
absorption bands, excited state levels of bands over the
infrared spectrum. The electromagnetic vibrational
spectrum lies between about 300 and 3600cm-1. Most of
the big absorption bands are in the middle of this region,
though the C-H and O-H stretch frequencies are between
2900 and 3600cm-1. As well as calculating the
Boltzmann temperature we can also use the Boltzmann
equation in a different form to establish the percentage of
molecular vibrational frequencies which are in the
excited state (i.e. hold spare energy) at the background
temperature.

Temperature is, as everyone knows, an average property

of a system (like radiation absorbed dose). The kinetic
theory of gases gives us the concept as a measure of the
mean energy of a Maxwell distribution of ideal gas
molecules, all whizzing about and hitting the walls of the
container, and of course, the bulb of the thermometer.
But here I want to associate it with a single molecule, as
if there were some kind of virtual thermometer tied to the
atoms that are vibrating. In Table 2.2 I give the energy in
eV, the Boltzmann temperature that this energy defines,
and the percentage of molecules in the vibrationally
excited state at room temperature (20 deg) for vibrational

28

transitions at wavenumbers of 200, 1000, 1800 and
3000cm-1.

Table 2.2 Energy and Boltzmann temperature, and

percentage occupation of excited states for infrared
transitions over the range of molecular vibrations.

Wavenumber 200 1000 1800 3000

cm-1
% occupied at 36 0.67 0.012 3 x 10-5
20qC
Molecular 287 1157 2307 4047
temperature qC
Boltzmann 2.48 x 1.24 x 2.23 x 3.72 x
Energy eV 10-2 10-1 10-1 10-1

Thus we see that the mean occupancy of these states is

very low. But by absorption of a single photon of
appropriate energy the effective molecular temperature is
very high. The molecule is more likely to react on
collision, dissociate or change. It has, on absorption of
infra-red energy acquired a new identity. It is a hot
molecule. And it can use this energy (indeed it will use
this energy) to do something that the cold molecules
which surround it are less likely to do. Have a lower
probability of doing. The distribution of molecules which
are in this excited state and thus more energetic will also
be a Maxwell-Boltzmann distribution of some kind. So
therefore on the wings of this excited state distribution
there will be a greater probability of the molecule
reacting to give the activated transition state that leads to

29

a product. This has significance for the spontaneous
development of life on earth as it answers the key
question asked by Schrödinger but not answered by him,
and generally avoided by those trying to explain life
since then.

It is well known that chemical reaction velocities

increase rapidly with temperature. At school we are told
the velocity increases by a factor of 2 for each 10qC rise
in temperature. These increased reaction velocities were
described by Arrhenius and his equation was put on a
theoretical footing by those developing the statistical
mechanical basis of the Transition State Theory,
(independently) Polanyi and Eyring. Polanyi, by the way
a hero of mine, once likened scientists to witch doctors.
He would have liked this I’m sure. Interestingly, one of
the equations developed to predict chemical reaction
velocity was that of KF Herzfeld who explicitly included
the frequency of the vibration in the relationship. So let
us now pin this idea to Dr David Davis’s blackboard.
Molecules which have absorbed a photon of
electromagnetic energy or rather have been pumped into
the excited state by resonant absorption at the appropriate
vibrational frequency are in a higher energetic state than
their surrounding molecules. This immediately
overcomes the Maxwell Demon arguments and allows us
a way into borrowing entropy from the surroundings as
part of the extra energy spilled into the sink by the more
energetic molecule. I intend to finally move toward an
argument in which such a molecule may be considered to
be alive, as compared with the “dead” colder molecules

30

around it. It eats infrared energy (at quite specific
frequencies which its neighbours cannot use) like a plant
eats sunlight, and it uses this energy to do things. These
things push it up the entropy slope: they assemble order
from chaos. This “alive” molecule can “eat” its
surroundings and grow, fall apart, combine with others
like itself, or unlike itself, prosper or fail in where it ends
up, just like in Darwin’s jungle. But it starts the process.
That’s the point. Using infrared energy at specific
frequencies. Let’s now look at Maxwell’s Demon.

31

 32

 3

Maxwell’s Demon

The Second Law

[The paradox is that] living organisms are composed of

inanimate molecules. Must we then say that “life” is the
interaction of all the inanimate components of this
whole? That nothing is alive in the cell except the whole
of it?

M Olomucki, The Chemistry of Life

3.1 Entropy
Schrödinger began his little book with the observation
that from the statistical thermodynamic point of view the
structure of the vital parts of living organisms differ
entirely from that of any piece of matter which physicists
and chemists have ever handled. He explains at some
length, and indeed it is the main thrust of the book, that
the enormous and fundamental difference between the
living and non-living, the duckling and the rock, has to
do with the tendency of all physical (non-living) objects
to increase their state of entropy. Entropy is not some
vague concept. It has units, it can be calculated
statistically for simple systems using probability theory,
and its changes can be measured accurately in a
calorimeter. I had one at Wellcome, a great big insulated
drum that was rotated to mix constituents in a partitioned
cell and measure the temperatures. We made
measurements of heat absorption or release by reactions

33

and could use the results to directly measure the Entropy
changes by mixing the reactants at different
temperatures. The Second Law of Thermodynamics is
the Entropy law. It states that in all spontaneous
processes the net Entropy increases. The sum of the
entropies of all the participating bodies is increased. The
Statistical interpretation of Entropy is order. Increasing
(positive) entropy is a measure of an increase in disorder.
This is what Eddington called “Time’s Arrow”. It is the
fate of Humpty Dumpty. It is the reason my lab or office
ends up in a disgraceful clutter. But I (life) tidy it up.
That’s the point Schrödinger was making. Without me it
would stay untidy (in truth, with me it stays untidy).

If I (or anyone) is going to explain life, and the most

difficult part of the question which is the spontaneous
generation of life from inanimate molecular material, this
is where it must start. This is where a mechanism must
be found which can reverse entropy right at the
beginning. Can create order out of chaos. Schrödinger
copped out. His conclusion was that life developed from
the “aperiodic crystal” of the chromosome (as we now
know) DNA. But where did the chromosome come
from? How did all that happen? Not by random
molecular syntheses in early earth conditions, because
that would have required a negative entropy component
which Schrödinger ascribed to the aperiodic crystal.
Circular logic. And the aperiodic crystal is not alive in
any sense: no more than a crystal does it needs an energy
source. Or else one replication and that’s it. We have to
find a mechanism that a priori pumps disorder uphill.

34

Given Schrödinger’s field of quantum mechanics, it is
odd that he didn’t figure it out.

3.2 Maxwell’s Demon

The original statement of the 2nd law was due to Clausius

and emerged from consideration of a perfect heat engine.
Clausius’s statement (1854) was: ‘in any spontaneous
system heat cannot pass from a cold body to a hotter
body without some other change occurring at the same
time’. In 1967, Maxwell developed a thought experiment
in which he postulated a molecular dimension intelligent
entity (later called a “demon” by Lord Rayleigh) which
sat at a door between two chambers containing a gas at
different temperatures. Maxwell’s Demon then estimated
the velocity of the gas molecules in the cold chamber and
when the high energy (hot) ones were about to impinge
on the door, he opened it and allowed them into the hot
chamber (Fig 3.1). This of course heated up the hot
chamber at the expense of the cold and decreased entropy
of the system, violating the Second Law. These laws
were developed long before quantum theory or the
discoveries of the quantization of energy states in
molecules. The energies involved in the Maxwell Demon
experiment are kinetic energies of what were modeled as
tiny hard spheres. Maxwell’s point was of course that no
such entity exists (though there have been some
entertaining attempts by the nanoparticle merchants to
build something similar).

35

Fig 3.1 Maxwell’s Demon operates the shutter and lets
the fast molecules through (Saoirse Morgan)

But what if we dispense with the boxes and rather we

create hypothetical boxes in a new thought experiment?
Rather than two boxes we now postulate one box, but
we also further postulate two different atoms, or rather
molecules. The Demon has the ability to calculate the
mean energy of the two types of molecules. Actually, so
do we. We can dispense with the Demon. And we are
now going to do something else. We are going to take the
molecules, let’s call these A and B. At equilibrium and
room or background temperature A and B will have the
same energy distribution as a result of collision
exchange. Or rather they will have a particular initial
energy of the system which is only a function of their
internal energy and the macroscopic statistical energy of
the box we have put them in.

36

Now comes the interesting part. We then expose the box
to infra-red radiation at a frequency which only
corresponds to an absorption band (a vibrational
transition) in molecule A. There is no such absorption
band in molecule B (as we have defined the experiment).
Then molecules A increase their energy but molecules B
do not. There are two hypothetical boxes now, those
surrounding all the A molecules and those surrounding
all the B molecules.
Molecule A now has a competitive advantage over
molecule B. Given suitable reactivities or potential
reactivities, molecule A can employ its extra energy to
react with molecule B (and in real systems C, D E F etc)
and pump the system of A and its reaction products back
up the entropy gradient. The existence of quantum
selection rules for vibrational transitions means that
molecules can communicate electromagnetic energy
specifically only to other molecules which share the
same absorption bands. It means that in a cell a system of
energy exchange can move electromagnetic energy at
infra-red frequencies in a way that defines an alphabet or
code based on specific vibrational quanta that are quite
invisible to some molecules in the cell but energise
others. This is a mechanism which does not really violate
the 2nd law since it utilizes electromagnetic energy to
move the system uphill against the entropy gradient.
However, it is a starting point for a number of interesting
possibilities and of course the discovery of quantum
theory came long after Maxwell and Lord Rayleigh and
Kelvin and all those superhero amateurs of long ago. The
excited state molecule A is, in Schrödinger’s terms;

37

“extracting order from the environment”. It is alive. It
does things.

First, as I will speculate later, this idea can define the

earliest living system which then can develop along the
lines of natural selection. Second, and I will now move
on to that, it is able to begin to explain the operation of
life at the cell level. This is where it gets interesting. I
have no way of telling if any of this is true. But it
entertained me. And certainly the current explanations
are highly implausible. Furthermore it lends itself to
experiments (some of which I have already done).

In reality how can this happen? I will discuss the

development of life from non-life in a different chapter
but at this stage all that we need to imagine is some
method for creating specific infrared radiation at specific
frequencies in order to separate the system of A and B
molecules which have the same temperature and energy
from each other so that the molecule A can be pumped
up into a more energetic state than B. If these two
substances were in a rock pool, the sun’s rays would heat
the water up and the molecules of A and B would share
the background temperature. The sun’s rays are not
frequency selective they are continuous in energy across
the spectrum. There will, of course be water band
resonance but we are not interested in that at the moment,
it just heats up the water. But the sun’s rays would also
heat up the rock or zeolite or whatever inorganic matrix
was the base of the pool. This would then emit quite
specific frequencies which I am permitted to identify

38

with molecule A absorptions. Thus molecule A would
get hot but not molecule B. The same thing can happen
in the cell. The cell is hotter than its surroundings; energy
flow from metabolism travels from the cell out into the
interstitial tissue. For unicellular creatures it travels into
the external environment. To do so it has to traverse the
cell surface, onto which we can stick molecules like A
and B or anything we like. If radiation with bands
corresponding to A absorptions traverse the cell surface
they will be selectively absorbed by any A molecules, or
even molecules which share the A frequencies more or
less. These will then be “active” as they will create a
resonant interchange with the internal sources of A
radiation and heat those up (or increase their energy).
This increase in energy of the internal sources of A
spectrum radiation can affect protein conformation
though interfering with the hydrogen bonding that
stabilizes the tertiary structure. It may do anything it
likes. Perhaps it interacts with the DNA? The RNA? This
raises the question of the activity of proteins and how
they work, which is something I will return to.

So at this stage, I just want to put down this marker.

Quantum specificity of vibrational transitions in the
infra-red enables a distinction in energy to exist whereby
in what seems to be a thermodynamic equilibrium system
is in fact not one and contains quite separate virtual
compartments of high energy molecules and background
energy molecules. Such a system can be seen as a
mixture of “living” and “dead” entities in that the living
items express their life in the form of their ability to

39

borrow negative entropy (in the Schrödinger sense) by
carrying out reactions with the “dead” surroundings and
thus acting to assemble order from chaos. In addition,
and the main point of the idea, it makes possible in
principle a mechanism or mechanisms whereby the cell
functions partly through exchange of electromagnetic
energy between molecular species which employ
different frequencies for information exchange and
which are tuned to those frequencies and cannot receive
information from other frequencies. It is the
electromagnetic energy which, in such a model, is the
prime and rapid mover for the slower synthetic
chemistry.
But is such selectivity real? Can we measure it? It seems
we can.

40

 4

Molecular Communication

4.1 Distinguishing molecules by absorption bands

The question which I asked in 1974 was this: can

molecules talk to one another “by radio” at specific
frequencies? Like I can in the VHF on my boat, with
different channels for different addresses. That is: if we
have molecule A and molecule B , and we direct infra-
red radiation from another molecule A which is slightly
hotter, do we selectively heat up molecule A while
molecule B shows little or no increase in temperature.
After all, it is one thing to predict this, but maybe it is
wrong. Maybe the effect is too small. In the last chapter
I wrote about molecule A and molecule B as if they had
each one single vibrational transition, which was
different in each case. Of course, complex molecules like
the H2 drugs or Histamine have quite a few absorption
bands. I show the solid spectrum of Histamine
dihydrochloride in Fig 4.1 below.

41

Fig 4. 1. Infrared absorption spectrum of histamine
dihydrochloride; Potassium Bromide disc.

For those who can’t understand the spectrum, here is

what it means. Infrared radiation from a hot piece of
ceramic which contains (like the sun) all the different
wavenumbers (wavelengths) is passed through the
sample, which in this case is mixed with a material like
rocksalt (which is transparent and a window for infrared)
and compressed into a disc about 3mm thick. The broad
band infrared containing all the wavenumbers is directed
through this disc to a device called a grating
monochromator which can separate out individual
wavenumbers according to the angle of incidence of the
beam of the radiation on the device. A motor moves the
monochromator angle and the energy of the infrared at
the different wavenumbers is detected on a special heat
detector. The output from this detector gives the
percentage transmission through the material, in this case
histamine. So you see that for this sample, at about 3000
wavenumbers the % transmission is about 5%. This

42

means that at that wavenumber (wavelength) the
histamine almost completely absorbs the radiation. But at
the wavenumber of 1900cm-1 the histamine lets all the
radiation through: it is transparent, like glass is to light.
By the way, glass blocks infrared, so we have to use
windows of rocksalt, fluorspar, potassium bromide and
similar inorganic materials with vibrations which are in
the far infrared. There is another way of doing this that
dispenses with the monochromator and uses a different
device employing an interferometer rather than a
monochromator. It is called the Fourier transform or (FT)
method but it gives the same spectrum.

What if all these bands were energised? Note that Fig 4.1
shows the absorption bands of the protonated (acid) form
of the base where both the basic hetero nitrogen and the
terminal chain amine nitrogen have been protonated and
are charged (don’t worry if this is Greek to you). In
neutral physiological solution maybe only one is charged
depending on the environment of the molecule;
furthermore there will be solvation effects. But this
shows that there are quite a few modes where energy can
in principle be transferred from and to. What is needed
here is some way of looking at the aqueous solution:
which in 2003 I eventually obtained, an attenuated total
reflectance cell.

In 1982 I ended up in Wales with my wife and three

girls, a dog and little money. We lived up a mountain in
two caravans by a river with a ruined house. I decided to
rebuild the house and also address the issue of molecule

43

A and molecule B. When I was at Wellcome, if I wanted
anything, they bought it. I could sign for capital items up
to £20,000. If I wanted some electronic machine made, I
had only to ask the technician Alan Strutt (descendant of
the famous physicist Lord Rayleigh who named
Maxwells Demon). Strutt, who I saw as an electronics
genius, would knock it up with a breadboard and
transistors and operational amplifiers etc. In Ivy Cottage
in Wales there was no money and no Alan Strutt. So I
decided to teach myself electronics: and I did. Those of
you who want to do experiments in physics should know
that it is unbelievably cheap to put together the most
sophisticated electronic devices. You can buy
extraordinarily powerful operational amplifiers in a chip
for less than a pound sterling. You can put these together
with a few pence worth of components, transistors,
resistors and whatnot and make your machine for less
than £20. So put away your iPhones and do something
interesting and useful.

I built a version of Callendar’s differential heat balance,

what he called a “pyranometer” using modern electronic
components. Callendar invented the device to measure
the energy coming out of the sun. It employed two pairs
of grids which were in the form of a chequerboard with
opposing plates of black enamelled or shiny platinum
bolometers (resistance grids). The black (absorbing)
resistances were compared with the shiny (reflecting)
ones in a Wheatstone bridge circuit. My version of this is
shown as a diagram in Fig 4.2. A photograph of the
apparatus (which is in storage) is shown in Fig 4.3.

44

Two hemispherical silver cups A and B of 4mm diameter
are glued with silver thermal transfer compound each to
an identical commercial micro Peltier heat pump e and f
which are in turn glued with silver compound to the face
of a solid brass cylinder G of 4cm diameter and 4cm
length which represents a heatsink. The silver detector
cups have micro low thermal-inertia thermistors glued to
the backs at the point where the Peltier cold junctions are
also attached. Each Peltier device is wired into a current
generator operational amplifier and output transistor
which is controlled by a calibrated ten turn
potentiometer. The difference in temperature between the
two silver cups A and B is measured and amplified by an
operational amplifier connected across the arms of a
Wheatstone bridge containing the sample c and reference
d thermistors. Any change in the temperature of the
sample versus the reference cup as shown by the
imbalance of the Wheatstone Bridge can be reversed by
pumping heat out of the cup into the brass heatsink by
passing current through the Peltier chips. The value of
the ten turn 100 units per turn current generating
potentiometer give the rate of heat absorption difference
between the sample and reference cup. The detector
system was embedded in potting compound.

Sample (molecule A) and reference (molecule B) were

placed in the silver cups and the apparatus placed in a
standard polystyrene coolbox with a lid.

A separate device represents the source. This consisted of

a shallow (3mm) silver dish of diameter 4cm. To the

45

back of the dish was soldered a power resistor which
could be heated to a preset temperature by driving
current with different duty cycles controlled by a
standard square wave oscillator chip (a 555) with a
variable duty cycle circuit that was informed by the
temperature of the measurement thermistor. The emitter
sample (molecule A) was coated on the surface of the
emitter to various depths usually as a solute in an
aqueous Agar gel. Other ways of linking the emitter and
detector were also employed including reflectance from a
silver mirror. I used 37qC for the emitter temperature.

There is a shutter between the source and the detector.

Fig 4.2 Molecular Communication experiment 1985

46

Fig 4.3 My Molecular Communication device for
comparing the infrared absorption of two samples. The
potentiometers on the left control current through the
Peltier chips which then pump heat from the silver cups
to the brass heatsink at the back of the detector.
Thermistors attached to the cups are part of an
operational amplifier Wheatstone Bridge with the
imbalance displayed by the meters on the right. The 10-
turn Peltier current is the value of the differential
absorption.

47

4.2 Results

The device was extraordinarily sensitive (as you might

expect with all those op-amps). I figured out it could
easily measure about 10-7 Watts. Unfortunately, having
built up the tension, I’m afraid I didn’t make as many
measurements as I wanted to. I had to build the ruined
house, we lived in 2 caravans, the big girls went off to
University, the young girl had to change schools and I
had to help teach her, my wife got sick and later my son
Joe was born. But I did enough experiments to discover
that the transfer of energy between the same molecule
compared with a different one was very real, significant
and massive. I employed various amino acids, glycine,
lysine and phenylalanine, and I generally used an oil in
the reference cup but sometimes compared the amino
acids. The signals from the amino acid versus the oil
were enormous and rapid. If you put glycine in the
emitter at 37qC and the background temperature was
22qC as soon as the shutter was pulled away the
galvanometer almost bent the pin and you had to pump
current through the sample Peltier.

In one experiment I had the glycine in the sample cup

and oil in the reference and I approached the detector
with a penny which I had heated in a Bunsen burner
flame so it was several hundred degrees. The
galvanometer barely moved. I placed my hand over the
detector at about 50 cm. The response was immediate:
the meter hit the pins.

48

Once, I had the detector on the bench wired up with the
usual agar glycine/ oil setup. I noticed that the signal
(which I outputted to a recorder) was wandering about. It
turned out to be clouds passing overhead and the
radiation from these was attenuated by the pvc roof
sheeting in the garage where I did the experiments. This
was the O-H absorption in the water in the agar of
course. Without a weighing balance I could not properly
compare the amino acids.

My results from all these experiments are in a lab

notebook which I have mislaid in the many moves I have
made since then. It is definitely somewhere. So what I
am writing here is from memory. And I never really
quantified the effect. It needed some way of carefully
weighing and dispensing the detector material. I could
not afford a balance then or micropipettes. But it was
spectacular. I intend to go back to do all this again, but
that will depend on where I end up in the next few
months and whether I have any space or money. I show
the infrared spectrum of glycine and of cooking oil in
Figs 4.4 and 4.5. You will see they share a lot of
frequencies, but remember that we do not know the
bandwidth of the effect. The width of the absorption
bands in the pictures is an artefact of the measuring
system.

The conclusion is this: the molecular communication

effect is capable of transferring heat energy between the
same molecules through space and this heat energy is not
transferred to molecules which do not share the infrared

49

emission/ absorption of the emitter. If this had been a
primitive pool on the early earth, the separation of energy
(and let’s be clear here, I am doing calorimetry,
measuring heat) between the absorber and the non-
absorber is profound.

The baseline here is that the sunlight, the temperature of

the emitter, as shown by the hot penny, is not relevant, it
heats both the molecules equivalently (so long as they
have different absorbance and specific heat capacity,
shiny vs. black etc.). It is the infrared absorption
difference which is the key to this. And, I believe, to life.
And note that the surface of the cell, the window, the cell
membrane, is made of oil.

Fig 4.4 Infrared spectrum of the amino acid glycine

50

Fig 4.5 Infrared spectrum of cooking (soybean) oil

51

 52

 5

Proteins

5.1 What are the detectors?

I believe I have established that there is molecular

communication in the infrared. We could also describe it
as resonance. If the communication between the surface
of the cell and the inside operates by this electromagnetic
mechanism, the next question is, what are the detectors?
How do they then use the signal to do things inside the
cell? How do the communication systems in the cell
work? How do enzymes work? Ribosomes? All the other
stuff. Well I don’t know, is the answer. But as I see it,
there is no good explanation from the chemistry
department either. So I will suggest an explanation. It
addresses another great mystery for me. What are
proteins for? Why does nature make such enormous
molecules which all seem much the same in their endless
and boring sequences of amino acids. How do they get
around? How can they possibly see to all the goings-on
in the cell. The proteins are not alive. But they constitute
most of what is alive, and so something is happening
here that needs to be thought about.

There are some things we know about proteins that we

can stick up on the blackboard.
x They are very big
x They are made up of 23 different amino acids
connected by amide links

53

 x The distribution of the amino acids causes the
protein to fold into various tertiary structures, or
shapes.
x This is controlled by the juxtapositioning in three
dimensions of particular amino acids which
hydrogen-bond between conjugate atoms on
different amino acids somewhere in the protein
chain.
x The tertiary structures or shapes have some
catalytic activity in certain pockets or locations
where reactions involving smaller molecules are
facilitated. No one knows how they are
facilitated as far as I can tell, though there are
various theories.
x The tertiary structures can be altered by certain
molecules so that very large changes in the shape
of the protein can be effected following some
interaction that involves very low energy. One
example from our haemoglobin work is the
binding of diphosphoglyceric acid 2,4-DPG to
the haemoglobin protein which distorts the
tertiary structure so that it can bind more oxygen
and thus shift the oxygen dissociation curve at
high altitude.

Let me start with the amino acids. If we wanted to

communicate information in the infrared we would need
a transmitter and a receiver but also an alphabet. We
would need to be able to energise specific frequencies so
that the specific detectors of those frequencies would

54

react and do something. Each of the 23 amino acids has a
different infrared spectrum.

Fig 5.1 Infrared regions of amide absorptions in a protein

(these are plotted as absorbance and so are upside down
and back to front relative to the earlier examples. (A= 1-
logT where T is transmittance)

The shapes of the absorption bands in proteins in water

are complex because many individual vibrational modes
(wavenumbers) overlap. Changes in the tertiary structure
of the proteins alter the position and intensity of the
bands. These can be measured by infrared spectroscopy,
but this is not easy to do for technical reasons. Windows
have to be insoluble in water, path lengths have to be
very short because of high absorption in aqueous
solutions.

55

The glue that holds proteins in their shapes is the
hydrogen bond. The strength of the hydrogen bond is
affected by the electron density in the bond which is
between the atom that binds the hydrogen and the next
atom to that. It also depends on the electron density of
the atom that the hydrogen bond is made with. The
hydrogen bond will be weakened or strengthened
depending on the excitation of the vibrational energy of
these bonds next to it.

There is also direction and proximity. If we take a

particular bond vibration, say an amide I. This is the
most intense absorption band in proteins. It is a
consequence of the stretching vibrations of the C=O (70-
85%) and C-N groups (10-20%). Its frequency is found
in the range between 1600 and 1700 cm-1. The exact
band position is determined by the backbone
conformation and the hydrogen bonding pattern. Within
the protein tertiary structure and close (in molecular
terms) to a -C=O group, which is energised by resonance
with a molecule on the surface of the cell, there will be a
high electromagnetic field at the frequency of the
vibration. This must affect and hydrogen bond which is
made with the group, for example

-C=O---H-NH-

Adding all these resonances together we have, in

principle, a method for altering both the conformation of
the protein and also the electromagnetic energy in any
small molecule which is close to the site where the
energised bond is located. Since the wavelengths of these

56

electromagnetic fields are comparable to or slightly
larger than the cell dimensions (between 10 and 16P it is
clear that such a communication would extend to more
than one cell. Nevertheless, the intensity of the signal
will be highest close to the emitter, the vibrating bond.

This also answers the question of the mode of action of

enzymes: the active site is one where the preferential
binding orientation of the substrate is such that the
energy from the local vibrations is focussed on the bond
in the substrate which it is proposed to break.

In passing, this is another clue to the dimensions of cells.

Most eukaryotic cells have a diameter of about 10P such
that the mean intercellular distance is one wavelength,
thus making a community of cells which form an
electromagnetic array with co-operative resonance.

So it is the tertiary structures of the proteins that

represent the main machinery in the cell, in living
systems. It is these enormous molecules which process
the smaller molecules, synthesize the requisite
compounds from the building blocks and regulate their
concentration. I am arguing that the control of all of these
processes is through electromagnetic energy in the infra-
red. The intensity of each frequency and the spectrum of
frequencies energise locations in the macromolecules
that switch their activity on and off. The focusing of the
electromagnetic energy at positions in the protein
structures enables these structures to carry out the

57

chemical changes in substrates to synthesize the
molecules necessary for the functioning of the cell.

I know. It all seems rather too much, doesn’t it. But then
the whole of life at the complex level of the cell is
equally difficult to explain. Compared with an
explanation involving chemical diffusion and molecular
collisions this explanation seems fairly straightforward.
And we do have some clues that this, or something like
this, is correct. And also it is an explanation that is
relatively easy to investigate, as I will enlarge upon in
another chapter.

It is fairly easily testable. And indeed, the infrared

communication aspect of the receptor has been tested.

At this point, so as to confound those biologists,

pharmacologists and life-origin-explainers who have
arrived at this point and are laughing their socks off, I
want to look at some evidence that supports this
approach.

5.2 Luca Turin

I came across the work of Luca Turin in the late 1990s. I

was presenting these ideas of mine to a guy from
Unilever whom I have been put in touch with by my
friend Vyvyan Howard. I was hoping for some money
and a lab to follow all this up. No luck. The Unilever guy
was not impressed. Since then I have followed with
interest the discoveries and career of Luca Turin. He was
a perfume expert. He asked the same question about the

58

perfume receptors in the nose that I asked in the 1970s
about the drug receptors in the body. He also noticed that
the shape of the molecules did not predict the way they
smell, and so the then (and still) receptor theory must be
wrong and that there must be something else happening.
Like me he figured out that it must be the vibrational
energy spectrum of the molecule that defines its odour.
He gives some examples. First, take the standard
perfume that is employed in creating the smell of
sandalwood. This is cis-3-hexeneol. You can create the
same “shape” with cis-3-hexenethiol where the terminal
alcohol –OH is substituted by a thiol –SH. This molecule
smells of rotten eggs. The OH stretch frequency of the
hexenol is at 3643cm-1 but the SH stretch is at 2650cm-1.
He points out that this region, the region of the SH
stretch is one where there are almost no other vibrational
signals from molecules. It is a frequency region which is
almost uniquely inhabited by the sulphur hydrogen
stretch. But at the same time, as a perfume expert, he
knew that the smell of rotten eggs was almost unique to
sulphur compounds which contained the SH group. His
prediction then is that a vibration at this frequency will
be associated with the smell of rotten eggs. He searched
the literature and found that boranes also shared this
frequency. The seminal authority on borane synthesis
had reported that they smelled of rotten eggs.

There is more. Turin decided to see what the effects of

deuterium substitution would have on the perfume of
various molecules with strong and identifiable smells. He
has carried out many such studies. The first one was the

59

try and recreate the almond smell of cyanide. The CN
stretch is around 2200cm-1. He took acetophenone which
smells of flowers and deuterated the hydrogens. As
Deuterium (an isotope of hydrogen) is heavier, this
pulled the CH stretch frequencies down to 2200cm-1. The
deutero-acetophenone apparently smelled of almonds and
not of flowers. This is such a clever experiment.

More recently he has applied this approach to the rational

design of perfumes. He was asked to create the smell of
coumarin which he describes as sweet herbaceous-warm,
hay like, tobacco but using a different compound.
Coumarin is a two ring heterocyclic compound with a
quite specific and complex infrared spectrum. Turin
worked with chemists to find a 3-ring sulphur
heterocyclic compound which is structurally nothing at
all like Coumarin but which shares all the same infra-red
bands. He named it Tonkene. It smells like Coumarin.
The molecular structures of the two compounds are
shown in Fig 5.1. Once again, as with the Histamine
compounds, the two chemical structures, electron
densities and shapes have little in common. A conjugate
electron density surface which was designed to fit both is
impossible to imagine.

Turin has carried out studies with fruit flies and shown
that they are able to distinguish isotopically substituted
perfumes. He has also been the object of a lot of attacks,
scorn and levity, but seems to be a tough guy. And of
course, if his theory is valuable in creating money for the
perfumiers, just like Pasteur with the fermentation

60

industry, he has some strong support. This was the
anthropologist Bruno Latour’s mechanism for getting
famous with scientific theories. Like Professor
Challenger in Conan Doyle’s “Lost World” Turin has
taken the pterodactyl out of the packing case on stage
and despite the jeers of the audience, the pterodactyl is
flying about the auditorium.

Fig 5.1 Coumarin (above) and Luca Turin’s vibrational

spectrum analogue Tonkene (below)

Turin was not the first to suggest the vibrational origin of

detection in the area of scent; it was suggested by M
Dyson 1938 and then by RH Wright in 1961 in
connection with insect pheromones. But we can say that
Turin has more or less proved it.

61

So let us consider where this gets us. First, it shows that
there is real evidence from experiments that, for olfactory
receptors at least, the mechanism is associated with
vibrational energy and not with shape. The interesting
thing about Turin is that he didn’t take the next step,
which was to extend this idea to all receptors. For if the
system can operate in the nose, why would Nature stop
there? Is it not much more likely that this is the universal
system but that he has stumbled on it because perfume
and smell are areas of investigation where we have direct
access to the receptor and can play games with it because
we can smell it working as it were. And we can imagine
that smell, or its precursor ability to detect food, must
have been one of the first senses to appear on the stage of
evolutionary development. That’s how our little friend
the amoeba figures out where to move to. It is how the
insects figure out where their mates are despite the fact
that the number of pheromone molecules available is less
that would stochastically exist in the detecting insect.

There is one more problem for Turin (and me) to solve.

That is, what is the nature of the detector? In Turin’s case
he places the receptor on the outside of the cell
membrane, or at least that’s what I think he assumes.
Then the detector has to discriminate infrared vibrations.
It has, he says, to be a spectrometer. He locates such a
“spectrometer” within a rather arcane physics based
process termed inelastic electron tunnelling, and with the
kind of arm waving that I also go in for in this book. He
says that this mechanism allows for a method whereby
molecules involved in electron transport (and thus cell

62

energisation) can be set up to be selective for frequency
and can somehow translate vibrations into nerve
impulses.

I guess we would have to then propose the existence of a

fair number of different metal ion electron transfer
proteins which would represent the various types of
smell by extending across the vibrational spectrum in the
same way as the pigmented retinal nervous system
creates the concept of colour from three electronic (rather
than vibrational) quantum energy specific detectors.
Such a system would represent a kind of nasal retina
analogue: it would have no more to say about the general
problem of drug and hormone receptor interactions in
other cells.

But there is another way this might work, one which also
would admit of a description of the vibration driven
olfactory switches discussed by Turin. I consider this in
the next chapter.

But before we leave the proteins we must ask another

question. It is not only small molecules which switch
cells on and off. It is also circulating proteins like insulin
and thyroxine. These are enormous compared with the
small compounds which the pharmacologists play with
and imagine are binding at the “receptors”. How is it that
these huge molecules, like Battlestar Galactica compared
with Luke Skywalkers X-fighter can effect changes in
the cells. Do they have to burrow their way in like some
gigantic worm. And then what?

63

What I think happens is that the tertiary structure of the
proteins is set up, or rather has evolved, to produce
selective infrared emitters. It is the spectrum of amino
acids which are on the outside of the protein molecule
which define the molecular communication signal. This
signal is just like the small molecule signal: a series of
wavenumber emissions/ absorptions. The amino acids
responsible are those which have not had their vibrations
damped out by internal intramolecular closure. They
have either been hidden in the centre of the protein, or
the vibrations have been damped by H-bonding inside
the vast protein molecule. So each protein hormone is
defined in its message by selection of information in the
infrared. These can, like the small molecules also, be
thought of as musical chords. The resonance can be seen
with musical chords. Just hold down all the keys on your
piano by weighting them with books. Then play a chord
on your guitar. The piano will answer you with the same
chord.

This would be predicted by the theory of how life began,

which is later.

64

 6

Mechanism

6.1 Molecular temperature

If we go back to the beginning, what we know is that the

cell is hotter than its surroundings. The animal is hotter
than its environment and this is because the cell is
burning material or drinking energy from its environment
and making itself hot. That is the necessary-for-life
entropy argument where we came in. We also know that
generally if a molecular system of machinery is hot, the
reactions in the machine go faster: they are energised
because the Boltzmann energy is greater. It is easier for
the reactants to achieve the intermediate activation state
necessary for the reaction to proceed to completion. So
in principle we could agree that everything that happened
in a cell at temperature T would happen faster at
temperature T + 10. Or T plus anything. Just think about
how you feel if your temperature increases by a mere
3qC.

The temperature of the cell is an average quantity. What

we are more interested in, as far as reactions are
concerned, is the energy of the molecular bonds which
are reacting to produce the activated transition state
intermediates. In the earlier chapter I suggested we could
see these as having a virtual temperature given by the
Boltzmann temperature for that energy.

65

If we think of the machinery of the cell for now just as
the proteins, and consider only one of these structures of
protein molecules, then whatever these are doing, their
identity in terms of function, will involve three things.
First the tertiary structure, the shape. Second (in my
proposal) the specific hydrogen bonds which hold then
into that shape. Third the energy density at the active site
positions where they assist the chemical reactions which
are their purpose.

All of these are affected by the vibrational energy of the

various bonds which affect electron density and alter
hydrogen bond strengths. We know that living creatures
are mostly very sensitive to temperature. That is the
average temperature. What about the molecular
temperature that I defined earlier? The energy in the
specific bonds?

The direction of flow of energy is from the inside of the

cell outwards into the environment. The cell is the
source. The environment is the sink. Turin’s model
suffers from the problem that there is no good
explanation of how such a system would set itself up in
the first place. But we can deal with that quite simply in
what I am suggesting. Much of the loss of energy from
the cell is through infra-red emission. Indeed much of the
loss of energy from the body is also from infrared
emission. But you can block this emission by
surrounding the body with something which reflects the
energy back, like one of those silver survival blankets.
And it is the same with the cell. Let’s say there is a

66

protein detector which has a specific set of frequencies
like the 5 frequencies that Turin decided were key to the
smell of coumarin and which he created in Tonkene.
What this protein does, in our thought experiment, is that
it has a conformation, a tertiary structure which is highly
dependent on the existence of hydrogen bonds which are
associated with atoms whose fundamental infra-red
vibrations are at A, B, C and Dcm-1. These are, at the
temperature of the cell (which is greater than the external
temperature of the environment) quietly radiating away
electromagnetic energy to the outside. If the cell died,
this process would continue till there was no temperature
difference with the outside and the cell would then be the
same as a rock in the garden.

Now we bring along a molecule which has A,B,C and

Dcm-1 vibrations and stick a lot of them on the surface of
the cell. Immediately they absorb the vibrations, just like
in my molecular communication machine, and they get
hot. They resonate and beam back the same ABCD
spectrum into the cell. This immediately heats up the
ABCD bonds in the protein (increases their vibrational
energy, or rather the occupation fraction of those energy
levels) and flips the protein into a new conformation, or
whatever we decide.

So the mechanism I propose is a reflection one, a reverse

of the idea that the drug communicates something to the
inside of the cell: here the cell communicates something
to the drug molecule which then reflects the energy back
and through this resonant process increases the energy of

67

the emitting system until it does something. The cell has
been wrapped in a wavenumber spectrum specific silver
blanket and it heats parts of the cell up so that they do
something. The question is: which way is the signal
going? In the traditional drug receptor theory it goes
from the outside into the cell: the same, I guess, with
Turin’s electron tunnelling. Here I am suggesting that the
cell detects the drug as a resonant mirror.

That fits well with the how did life begin argument and
all that entropy stuff but it leaves me with the problem of
the antagonists. I guess Turin has the same problem
except its hard (though not impossible) to know how you
would detect an anti-smell. You would provide a
substance which had a set of frequencies EFGH say
which prevented the protein from altering its shape or
doing whatever it was by energising different hydrogen
bonds. After all, the conformation of the protein is
dependent on a balance of sticky forces, some which pull
this way, some which pull that way. It is not difficult to
think of a set of vibrational frequencies which would
drive the reaction in the opposite direction to the one
produced by the agonist. Turin doesn’t have this problem
because like the eye and colour detection he only has to
propose an agonist effect.

I try to show this reverse process in Fig 6.1. Here we

have two possible conformations A and B of part of an
idealised protein obtained by rotating the structure about
a hypothetical axis perpendicular to the plane of the
paper. The locations where the tertiary structure is

68

stabilised by hydrogen bonding with another part of the
protein which folds back on itself for this to occur are the
ends of a chain of amide links which normally are in
position A but upon energisation by the appropriate
frequency (wavenumber) move to position B as a result
of the weakening of the OH---N – bond shown and the
stabilisation of position B by the –NH---O=C- bond. The
antagonist, in this idea, merely has to provide B
wavenumber spectrum energy to weaken the B position
of the conformation.

69

Fig 6.1 Conformation (shape) of a section of protein
rotates about an axis to be stabilised by a hydrogen bond,
as in position A, where an OH---N- bond can be
perturbed by frequencies A to weaken and move the axis
of backbone to position B which is stabilised by a NH---
O=C- hydrogen bond which is identified with infrared
energies B.

70

6.2 The far infrared

In the discussion so far I have jumped straight into the

infrared modes which affect the hydrogen bonding
properties of the molecules which have to communicate
with each other. The problem here is that this region has
many overlapping bands and there is likely to be a lot of
background noise from which the signals have to be
extracted. The region below 1000 cm-1 is the far infrared,
and below 600cm-1 it has been technically difficult to
access by the conventional dispersive spectrometers
since the devices they use to split up the frequencies,
grating monochromators, have to be constructed to give
their peak effect (to be blazed) in one region. Modern
infrared spectrometers use a different system. They
dispense with the grating and employ an interferometer.
They then change the dimensions of the interferometer
and analyse the intensity of the beam using a
mathematical process called Fourier Transform. They
can more easily deal with the far end of the IR spectrum,
but they are expensive and I can’t afford one. My
spectrometer stops at 600cm-1.

The region from 300cm-1 to 1000cm-1 has low frequency

vibrations from certain heavy atoms, but since biological
molecules consist of the light elements, for molecules
constructed from these it is combination molecular
modes which absorb in this region. These are vibrations
where the whole molecule twists and twitches and flails
about in various ways depending on how it is
constructed. Like hitting a gong, perhaps.

71

These vibrations are much more molecule specific, and if
we are looking for a set of fingerprints, retinal scans or
communication frequency sets which are unique, then
this would be where they would be. Also, this is where
the DNA nucleotides differ in their infra-red absorbance.
I haven’t so far included any mention of the DNA and
RNA. If my description of the cell and an infrared
switching machine has any basis, then we have to bring
in the DNA and RNA, since the sequences are there to
code the proteins, and presumably these sequences are
registered at the protein manufacturing machinery as an
infrared signal. I show the IR spectrum of Adenine in
Fig 6.2 and Guanine in Fig 6.3. These are the pure
substances, out of a bottle, and the spectra of these in the
cell bound up in DNA and RNA will be different. But it
is clear from the two spectra in Fig 6.1 that there are
significant differences in absorption to distinguish the
two bases. In the amide region they also differ
significantly since Guanine has the ring C=O stretch
which has a very strong absorption band at around
1700cm-1, missing in Adenine. There is no advantage in
pursuing these comparisons here as we just do not know
what the emission and absorption is in the cell at the
positions in the cell necessary to do the switching. We
can probably find out though, and I return to the
experiments in a later chapter.

72

Fig 6.2 Infrared spectrum of the main DNA base
Adenine.

Fig 6.3 Infrared spectrum of the other base, Guanine.

73

6.3 Water

The cell is largely made of water. The infra-red

properties of water are clearly of major importance to
any discussion of molecular mechanisms and life. The
infra-red spectrum of water is shown in Fig 6.2

Comparing this with the spectra of proteins and amino

acids makes it clear that water absorption is in largely the
same region as the biological molecules. The first
consequence of this is that the communication signals
being proposed may be absorbed by water molecules
interposed between the emitters and the receiver. But we
must be careful. The hydrogen bonds in water have a
very wide range of energies, as shown by the extremely
broad infra-red water bands. What this broadness shows
is the superposition of water O-H stretch and H-O-H
bending modes from molecules which enjoy a very wide
range of orientations. And this is just for bulk water. For
water in the cell, containing a wide range of hydrogen
bonded molecules and solvated to a wide range of
molecules, the water structure is less random.

74

Fig 6.2. Infra-red spectrum of water

There have been significant developments in the

understanding of the structure of water; much of the
work associated with Pollard in Washington USA. Water
shows properties which are highly dependent upon
incident infra-red background radiation, properties which
involve domains of charge separation with wide ranges
of proton concentration. Some evidence had been
brought forward by Beneviste and more recently by
Nobel prizewinner Jaques Montagnier that impacts on
the idea that water has some way of memorising the
structure (or some related identity property) of
substances which were dissolved before they were
removed by successive dilution.

75

First we must deal with the absorption issue. The
absorbance of water in the infra-red is given in Table 6.1.
It turns out that the extinction coefficient, that is the rate
at which water cuts down the incident intensity at the
main absorption bands, is only apparently large because
bulk water has a very high molarity, that is to say, its
molecular weight is low. Thus pure water has 55.5 moles
per litre concentration. Its molar extinction coefficient at
the strongest absorption in the 3400 region is about 100.
That means that 50% of the incident beam will make it
through a path length of about 2P or a 1/5th of the way
though a cell for signals in the O-H stretch region. But
for the absorption of water in the more interesting protein
amide signalling 1600 region the 50% signal will reach
about 8Por most of the way though the cell. This could
be another reason why the cell has its dimensions of a
10Pradius. That is to say each cell is isolated from the
next cell in the important protein absorption region by
the water absorption and damping of the messages. The
relevant equation for absorption is:

A = H0 l c where A = log10 I/I0 l is the path length in cm

H0 is the Molar decadic extinction coefficient (see Table

6.1).

And A = 2-log10T where T is % transmission

76

Table 6.1 Infra-red absorption of water..

Type of vibration Q0 cms- H0 M- Path for

1 1
cm-1 50% loss
(Micron P)
Stretching 3404 99.9 1.8
(asymm+symm)
Bending 1643 21.8 8.6
Protein amide II 1550 6.6 27.5
position

It turns out that the extinction coefficients of the

biological molecules in the cell are several orders of
magnitude greater than water, therefore the presence of
water in the cell does not prevent the information
exchange that I am suggesting occurs.

I turn to the issue of the water structure and the

broadness of the water absorption bands. These, as I
wrote, are the consequence of the superposition of a wide
range of vibrational modes. It may reasonably be
predicted that among the various clusters of water
molecules that represent different more stable (low
energy) types of sub-structure, there are ranges which
have vibrational characteristics which are different. If a
specific narrow bandwidth infrared beam were incident
on liquid water then this energy would be absorbed only
by those clusters of water molecules whose sub-structural
arrangement defined the same vibrational energy as the
incident band. They would store this energy and resonate
with it. This mechanism would act as a kind of water

77

memory for that frequency but it would be a memory in
the same way as a magnetic tape stores a magnetic
signal, though the relaxation time we do not know. The
increased concentration of the specific cluster that
defined that frequency would reduce as a result of
thermal motion but I cannot predict the rate of that
decay: it would have to be measured. However, as long
as the incident energy was fed in, there would be a
resonance in the water structure which would amplify the
signal though the rearrangement of the different
concentrations of the water structure vibrationally
distinct sub-units. When the signal were removed, it is
not implausible to imagine that the various sub-unit
water cluster concentration spectrum would act
differently toward a second incident infrared signal
which defined a different vibrational frequency. Thus we
have two things. First, an amplifier of infra-red
frequency information. Secondly, and this depends on the
relaxation, a potential explanation for water memory.
Finally, investigation of the molar extinction coefficient
gives us further support for the idea that the dimensions
of cells are not defined by chemical diffusion limits but
rather by the absorption frequency and extinction
properties of the main cell component, water.

78

 7

The origin of life

7.1 The failure of efforts so far

I do not propose minutely reviewing the history of efforts

to explain the origin of life. First these can be largely
divided into periods before and after the experimental
demonstrations that living creatures did not
spontaneously appear from various unlikely mixtures of
inanimate matter. Eels from horse hairs on dungheaps
and so forth. One such critical experiment in the
destruction of the spontaneous generation school can
illustrate this: the experiment of Redi (1627-1697) who
showed that the generation of maggots on meat was
associated with flies. Covering the meat with cloth
prevented maggots from “spontaneously” appearing. By
the time of Pasteur (1862) and the development of
microscopes, it was clear that life, that is living cells,
could not appear spontaneously. Pasteur carried out
clever experiments which showed that bacteria are not
created by spontaneous generation. His experiment
employed glass flasks in which nutrient medium was
placed. By using a “swan neck” and cotton plugs he
showed that if the medium was sterilized by boiling, no
bacteria were to appear in the medium, and therefore all
the bacteria that were found in open air nutrient media
were derived from bacteria in the air. I will pass over
Vitalism: the idea that life is a consequence of some
supernatural force. The need for a “vital force” reflected
the lack of knowledge of chemistry of the time. The

79

concept of vital organic molecules was shown to be
wrong by the chemical synthesis of organic compounds
in the 19th Century (e.g. Wohler: acetic acid).

The post-spontaneous generation ideas about the origin

of life began, in my opinion, with Darwin and Wallace,
although the idea of natural selection may have been
around before these two individuals articulated it (I like
to think it originated with Erasmus Darwin). What I
shall call Darwin’s idea is now well known to everyone,
and in a new form has become a kind of religion whose
high priest is Dawkins. But Darwin (and Dawkins) are
referring to the evolution of living systems, not to the
initial biogenesis of life itself. Clearly if life somehow
began, and existed in many forms, survival of the most
appropriate, the most efficient, what Darwin called the
“fittest” would occupy various niches defined by
temperature, humidity, water, chemical environment and
so forth and drive out lesser creatures. But how did these
creatures begin? We are back with Schrödinger’s 1943
question. Schrödinger’s answer seems to have been that
it began with the “aperiodic crystals” of the chemicals
comprising the chromosomes. He gave these lectures in
Dublin some ten years before Watson, Crick, Franklin
and Wilkins discovered the structure of DNA and the
complementary nature of the molecule. DNA is the
“aperiodic crystal” idea of Schrödinger, since its binary
structure enables it to divide and create copies of itself
that permit the reproduction of “life” in its many forms.
But unfortunately DNA itself is too complex to have
been spontaneously created and we are back where we

80

started. And in any event, DNA is no more alive than a
brick.

Many scientists and natural philosophers were unhappy

with the description of evolution based on the Darwin
idea. Me included by the way. Waddington (I think it
was) suggested that given the time frame that we know
from fossil records, the evolution of life forms has just
not had enough time: there must be some other process at
work. Some of the followers of Lamarck argued that it
must be that Darwinian evolution is being augmented in
some way that enables the inheritance of acquired
characteristics. Darwin himself apparently believed this.
Modern evolutionary theory (Dawkins et al) provided no
possibility of such a process since the DNA genes were
assumed to be immutable (except by random mutations
induced by radiation and spontaneous chemical errors).
In this theoretical framework the genes could certainly
not be changed to accommodate an environmental stress
that required directed alteration in the offspring. The
Dawkins people twisted themselves into knots to try and
explain the development of the eye from random
mutation or “genetic drift”, a Gaussian distribution
concept that I find hard to go along with for reasons I
won’t go into here. And most spontaneous mutations or
even accelerated radiation-induced mutations result in
death of the creation or a creature which is infertile, lacks
advantage, or breeds back to the original. Billions of
generations of fruit flies have been mutated with every
kind of mutagen: no-one has created anything but a weird
fruit fly that is either sterile or breeds back. No wasps are

81

produced. If we transfer the generation length of a fruit
fly to evolutionary time spans it is immediately clear that
the neo-Darwin explanation is difficult to accommodate.
Waddington wrote that it was like randomly throwing a
million bricks into a field and expecting them to become
a palace.

But I am not here concerned with the evolution of

species. The problem is the starting point: the first
creation of a molecule which represented something like
Schrödinger’s aperiodic crystal. And it is immediately
clear that such a molecule represents the apotheosis of all
the arguments about living and non-living processes
discussed by Schrödinger. The idea of some accidental or
random creation of such a molecule at the beginning of
life as a result of chemistry in the early Earth, or even the
early universe, brings us back to all the same arguments
levelled at the spontaneous generation merchants of the
middle ages and earlier. It is the Waddington argument
transferred from Evolution of Species to Evolution of
Life, a very much harder process to describe. And the
molecule itself is not able to sustain life without a whole
raft of attendant molecules drawing energy somehow
from the surroundings and dancing attendance on the
aperiodic crystal. The essential problem is the one raised
by Schrödinger which was the problem of entropy, which
I discussed earlier. A living structure has to create order
out of chaos by intercepting a spontaneous energy flow
and adapting itself to extract sufficient energy from that
flow to push itself back up the entropy or “unlikelihood”
gradient. Since this has to start with chemical molecules,

82

we have to find a molecule or some aggregation of
molecules which will do that trick and maintain it for the
lifespan of the molecule or aggregates of molecules
which then reproduce themselves. And this is where all
the theory of life explainers have lost their way. They
can’t figure it out. But at least they have started to
assemble the components. These just need the “kiss of
life”. That is what I will try and provide.

I should just mention in passing that other origin of life

thinkers have a different explanation but they (e.g.
Arrhenius and more recently certain cosmologists) have
copped out of the essential problem by placing the origin
of life on distant planets and even galaxies. It may well
be that they are right and that this answers some of the
time problems raised above, but these “panspermia”
theories are not, of course, ultimately helpful since they
just transfer the essential problem to a different planet.

7.2 The warm little pond

Darwin was, of course, also interested in the origin of life

itself. But he was a very religious man, and had no
difficulty ascribing this mystery to God. He wrote in
1863:

It is mere rubbish, thinking at present of the origin of

life; one might as well think of the origin of matter.

Later in 1871 he had thought some more about this,

writing:

83

 If (and Oh! What a big if!) we could conceive of a warm
little pond with all sorts of ammonia and phosphorus
salts, light, heat, electricity etc. present, that a protein
compound was chemically formed ready to undergo still
more complex changes, at the present day such matter
would be instantly devoured or absorbed, which would
not have been the case before living creatures were
formed.

As I shall argue, this paragraph contains almost all we

need to explain the origin of life; it also explains why it
could not have happened like this. For instantly devoured
read entropy. There would be no process which would
allow such a Darwin protein to remain or to copy itself
and reproduce without either energy necessary to push it
up the entropy slope or an unlimited resource of
chemicals in the warm little pond. This is also true even
if (and a very big if) we had somehow spontaneously, in
the monkey typewriter sense, arrived at the famous
aperiodic crystal and its attendants. But note also the
phosphorus salts which I will return to.

7.3 The warm little laboratory

Attempts to synthesize life based on mixing chemicals

and adding electricity are not only the stuff of Hollywood
science fiction. In 1913 Loeb synthesized glycine by
carrying out silent electrical discharges in a gaseous
mixture of ammonia, water and carbon dioxide, all of
which could be assumed to be present in early
atmospheres. Loeb had thought that he might create
biological entities by making various chemical and

84

electrical manipulations in a test tube. At the same time,
Fritz Haber carried out electrical discharges in mixures
of gases and concluded that thereby it was possible to
create “any substance known to organic chemistry”.

Later in the 20th Century, first Oparin and later Haldane

discussed the way in which in the early chemical
conditions on Earth, many of the small building blocks of
life could be formed by chemical interactions, along the
lines of Darwin’s warm little pool. Haldane proposed that
the primordial sea acted as a vast laboratory in which the
power was derived from solar energy. The early
atmosphere was reducing; was oxygen free, and the
dissolved carbon dioxide, ammonia and various salts
with photochemical reactions caused by the solar
ultraviolet would have produced a host of organic
compounds. The name given by Haldane to this sea
scenario was the prebiotic soup. It was from this soup
that Schrödinger presumably believed his aperiodic
crystal was to spontaneously appear.

An important factor was then introduced to the Oparin/

Haldane version of Darwin’s pond by Bernal. Bernal was
a chemist. He argued (quite reasonably) that chemical
reactions in such a dilute ocean would be very slow or
unlikely due to the dilution: molecules would be too far
apart to react. He proposed that reactions occurred on the
surface of minerals, predominantly the clay mineral
aluminosilicates, where adsorption and catalysis would
enable such reactions to occur.

85

Prompted by all these hypotheses, after the 2nd World
War, there began the experimental investigation of the
warm pond scenario. The first experiments were by
Melvin Calvin who used an alpha particle beam to ionise
a mixture of hydrogen, carbon dioxide and water in the
presence of ferrous ions (to supply a redox component
and presumably also to measure the dose, the famous
Fricke reaction). The idea was to simulate early
radioactivity. They found that they could easily create
most of the carboxylic acids, formic, acetic, lactic,
fumaric, succinic etc. Later Urey tried to recreate a
primitive earth condition by employing mixtures of
methane, ammonia, hydrogen and water. With his
student Miller he employed high voltage discharges over
such a gaseous atmosphere with a secondary chamber
containing water to trap any products. They were able to
synthesize a mass of organic polymers. 2% of the carbon
was recovered as some 25 amino acids including glycine,
alanine and aspartic acid. There were also several fatty
acids, hydroxy acids and amides recovered from this
early ocean model. This was an important step: it showed
that the small molecular components of living system
could have, themselves, as molecules, appeared on the
stage. But it is an almost impossible step to take this
further without solving the last big problem in life, the
Schrödinger entropy question.

To take the new prebiotic soup with its interesting mix of

possible life creating chemicals forward there was an
almost impossible hurdle, one which remains today.
Even if all these building blocks could be made under

86

prebiotic conditions, these have to be condensed into
polymers which then are organised into assemblies
capable of carrying out the behaviour of living systems.
Here we still have the live and dead duckling problem.
Attempts were made to invoke natural selection. But this
is a bootstrap problem. Not only does the assembly of
these molecules, the critical assembly to form the first
“living” structure have to somehow accidentally appear
but then it has to feed on (or assimilate aspects of) its
environment in such a way that it can reproduce and
survive. As Horowitz (1945) pointed out, only those
assemblies that learned how to synthesize the complex
molecules they needed to survive and reproduce, would
survive because by existing and reproducing they would
remove the molecular building blocks they needed from
the prebiotic soup. The first living assembly would have
to feed on something.

7.4 What KT did: EMogenesis

Those who followed the arguments presented to explain

the way in which life functions at the cell level will see
where we are going. All that is needed is to identify
Bernal’s substrate. The bottom of Bernal’s warm pond or
prebiotic sea. Whereas Bernal needed his aluminosilicate
minerals to effect adsorption and catalysis, I need some
minerals for a quite different reason. They represent
Maxwell’s Demon in that they separate molecules in the
prebiotic soup according to their vibrational absorptions.

The sun shines down on a warm pool or sea. The shores

of this sea, or the bottom of the pool, is a solid mineral Q

87

with an infrared absorption band at frequency A. The
energy spectrum of the sun is continuous: there are no
preferences. So the sun heats up all the molecules in the
aqueous phase equally. The mineral also absorbs the
sun’s rays and gets hot. But it then emits electromagnetic
(EM) radiation preferentially at a vibrational frequency A
cm-1 defined by its structure. Now of all the various
molecules in solution in the water covering the mineral
have different absorption bands. One of these has a band
at A cm-1. This molecule then becomes “hotter” (in my
terms of molecular temperature) and is more reactive
than the molecules which do not have such an absorption
band. It reacts with other molecules to create a series of
different products, some of which retain the absorption
band A cm-1. Those that do are also selected for excess
energy and can react again with surrounding molecules.
This process will continue so long as the products are
selected for extra energy A. In a sense then, these
molecules are “alive”. They eat certain chemicals in their
environment. How do they reproduce? Well we can
envisage polymers of such molecules, which we select in
our thought experiment, and when these reach a certain
size, they break in half to produce two sub sections of the
polymer. Each subsection then adds more molecules
through chemical reactions until it reaches some critical
size and then it breaks, and so forth. This whole process
is under Darwinian control, of course. The energy from
the substrate mineral selects the living from the dead.

Once we have created the system and provided the

separation between the living and dead molecules, or

88

rather our Maxwell demon has, we can just let nature
take its course: in other words we have supplied the
missing energy ingredient that pumps entropy uphill, the
factor that Schrödinger identified. We can now look for
the mineral that causes this wonder.

7.5 Looking for Maxwell’s Demon

There are two approaches to an attempt to find the

minerals that might have supplied the energy necessary
to separate out the living from the dead molecules. One is
to look at what minerals there are that would probably
have been around on an early earth. The other is to look
at living creatures and see what they are made of.
Because if the EMogenesis model has any basis in
reality, we could reasonably assume that whatever it was
that supplied the magic vibrational energy band to set up
the life system is likely to be part of the life system that
exists today. So we can work back from current living
forms to the early earth and its prebiotic soups and ask
what there is in common.

Such approaches have been part of the search-for-life

enthusiasts’ armoury already. So of course there had to
be questions asked about the early possibilities of
creating the known building block chemicals. Let’s list
these:

Starting with the primary constituents we have:

Carbon, Hydrogen, Nitrogen, Oxygen, Phosphorus.

These elements are in living systems at proportions

89

greater than a few percent. Then there are secondary
constituents which are present below about 1%. These
include Sodium, Magnesium, Calcium, Sulphur, Chlorine
and Potassium. We can ignore, for the purposes of
biogenesis the trace elements. Those in search of the first
molecules always concentrate on the organic compounds.
They need to populate the warm pool with amino acids,
the purine and pyrimidine bases, constituents of DNA
and RNA, and they include these nucleotides and
nucleosides. Then we need the lipids and their
precursors, the fatty acids and alcohols, the sugars and
the energy molecules in the various energy cycles. There
are vitamins and coenzymes, proteins. And finally we
have to have water, carbon dioxide, ammonia and the
oxides and oxy-acids of phosphorus.
If we are interested in minerals in current life that might
have been the original Maxwell Demon we do not find
silicates, and we do not find sulphates. It is possible that
we find carbonates, but not as organo-carbonates as they
are too unstable. We may be interested in sulphides, but
there are not any sulphides in living systems. What there
is in living systems in very large amounts is phosphates.
Indeed the DNA “aperiodic crystal” is a polymeric
phosphate. The fundamental energy transfer molecules in
the cell are phosphates. And if we are seeking to identify
our primal mineral at the base of the soup pool it is most
likely that we have found it. As did Darwin.

90

7.6 Phosphorus

Phosphorus always occurred combined, it is a common

element on Earth, and the average percentage in the
lithosphere is 0.157 and in ordinary soil 0.1%. The
primary minerals are Apatite 3Ca3(PO4)2.CaF2 and
chlorapatite 3Ca3(PO4)2.CaCl2 which are hard and
practically insoluble even in dilute acids. From them, soft
phosphate deposits occur of Ca3(PO4)2, calcium
metaphosphate.
Phosphate compounds occur in vegetable and animal
tissues, especially in seeds in which it is concentrated in
the germ. Cereal grains contain 0.4% of P. Egg yolks,
nerves and brain and bone marrow contain the fatty
esters of phosphoric acid, lecithins or glycerophosphates.
In order to repair tissues and provide phosphate for
bones, phosphorus compounds are essential in foods.
Plants take this from the soil as calcium phosphate. Fresh
bones contain about 58% of calcium phosphate. The
natural mineral phosphates contain salts of ortho-
phosphoric acid H3PO3 . This is tribasic and forms three
series of salts, primary e.g. KH2PO4, secondary, Na2HPO4
and tertiary, e.g. Na3PO4. The alkali phosphates are
soluble; generally the alkali earth phosphates are not. The
alkali primary phosphates are weakly acid, the secondary
phosphates are practically neutral and the tertiary
phosphates are alkaline. Thus ortho-phosphoric acid is an
ideal molecule to act as an amphoteric ion capable of a
whole range of reactions in aqueous solution, and with a
very strong P=O absorption in the infrared. The ion can
combine with itself to form pyrophosphates and can

91

polymerise to form long chain polyphosphates, or chains
coupled as linked secondary esters the most famous of
which are the ribose esters RNA and DNA. It reacts with
organic compounds to form such esters and indeed
almost with any organic molecule with a functional
group to give an enormous range of organo-phosphates.
If we are looking for our most likely substrate molecule
it is a phosphate. The infra-red spectrum of apatite is
shown in Fig 7.1 and hydroxyapatite in 7.2.

Fig 7.1 IR spectrum of Apatite

92

Fig 7.2 IR spectrum of Hydroxyapatite (note different
wavenumber scale)

The spectrum is essentially that of Calcium phosphate

but the very strong absorptions and emissions of the
phosphate P=O stretch are at about 10 microns, roughly
the resonant wavelength diameter of the cell, and
possible another clue to support phosphate as the key
emitter in the Maxwell Demon scenario. Calcium
phosphate hydroxide has the same spectrum and this is
shown in Fig 7.3

93

Fig 7.3 IR spectrum of Calcium phosphate hydroxide

Note the very high absorbance of the P=O stretch, which

has a much higher extinction than the OH stretch of
water at 3500cm-1.

There are other early minerals which would have M-O

stretch frequencies that could have assembled hot
molecules in a primeval soup, the silicates for example
like zircon, and the carbonates also. Fig 7.4 is of the
Infrared spectrum of one of the earliest minerals, the
silicate Zircon. But silicates do not seem to figure in
Earth life forms though a number of science fiction
writers have envisaged silicate creatures. It is probably a
solubility issue. The Si=O stretch is not far from the
phosphate stretch which I will turn to below, but PO4

94

seems to be the moiety of choice for life, and so we can
pass over the silicates as candidates.

Fig 7.2 Infrared spectrum of Zircon

Near hydrothermal vents we have sulphides with M=S

stretch frequencies and maybe there are other early
insoluble infra-red emitters I haven’t thought about. But
my money is on phosphate. Here is why.

7.7 The phosphate polymerisation scenario

In the supernatant liquid of the little warm pool over the

apatite, there will be all the life-precursor amines,
amides, alcohols, fatty acids, and whatnot all ready to
react. We know this from the Urey experiments. There
will also be low concentrations of phosphate ion, derived
from the apatite substrate. Certainly at the surface, where
these reactions are more likely due to adsorption:
Bernal’s idea. Now these phosphate ions will be in
resonant interaction with the hot apatite substrate. They

95

will represent our hot molecule A. They can react with
other hot phosphate molecules to form, polymers. What
they also can do is react with any of the other molecule B
substances which are dissolved in the pond. They will do
both. So let us react hot molecule A phosphate with
biogenesis molecule B. I shall write hot phosphate as
PO4* and biogenesis organic compounds as B, C, D and
so forth. I will not concern myself with stoichiometry
(e.g. BPO3, BCPO2 and so forth). You can do that.

Here is what happens:

PO4* + B = B PO4*

B PO4* + PO4* = B PO4* PO4*

(Also B PO4* + C = BC PO4* and sequences following

from this e.g. PO4*BC PO4* which in principle is the
start of the ribose and RNA chain sequence)

B PO4* PO4* + C = B PO4* CPO4*

B PO4* CPO4* + PO4* = B PO4* CPO4* PO4*

B PO4* CPO4* PO4* + D = B PO4* CPO4* DPO4*

What is being built up is a long polyphosphate chain

substituted with various organic compounds and/or an
interspersed polymeric chain of organic/ phosphate/
organic/ phosphate and so forth. Of course it is possible
that B = C = D and so forth, or any combination. And if
B, C, D have hydrogen bonding affinities they can cross
link to a separate polyphosphate chain.

96

The chain polymer can, of course become terminated.
But if it continues to build up, it will at some point break
at the weakest point to create two substituted polymeric
chains, both of which will then grow until the same size
restriction will cause them also to break in two. Thus we
have a living creature, we have life. It feeds on
vibrational energy which is redirected through a kind of
global warming effect. The apatite minerals are blue or
green and highly absorbing of short wavelength energy,
sunlight in the visible and UV region. Thus they will get
hot and will re-emit the energy as long wavelength P=O
frequencies around 1000cm-1 (10P, which is the mean
cell diameter). This is my preferred Maxwell Demon
frequency.

Phosphate is absolutely ready-made for the origin of life.

It is primeval: hydroxyapatite has been found on the
moon and thus will certainly have been around at the
beginning of life. It is a tribasic acid and thus can form
all kinds of wonderful esters and carbon nitrogen
compounds.

This phosphate based creature eats infrared energy. It

grows. It reproduces. And it mutates, because it can
basically build itself up out of whatever molecules there
are in the warm little pond. Some of the versions will be
more efficient (will have more absorbance at the
phosphate frequencies) than others.

Enter Darwin and natural selection.

97

This idea supplies the missing piece in the generation of
life from non-life discussion. For it is not enough to stick
all the precursor chemicals together. Whatever they
rearrange themselves into, whatever they react to
produce, the product, however complex and weird it is,
even if somehow it was Schrödingers aperiodic crystal
DNA created by the molecular version of the monkey,
the typewriter and Hamlet, it must have energy to
function. Otherwise it is as dead as a brick, since
whatever clever thing it did, it would end up as itself plus
the clever thing, just sitting there.

But as I wrote above, the best clue to the identity of the

Demon is the astonishing range of absolutely critical
compounds of phosphates which are associated with
living systems. We begin with the DNA and RNA
system. We have the ATP/ADP oxidative
phosphorylation energy system. We have the cell
membrane itself, an extended biopolymer based on long
chain paraffin phosphate esters. We have the skeleton. I
leave you to make a table of all the absolutely critical
molecules which are essentially substituted or extended
phosphates.

So that’s my idea. It seems fairly simple to investigate

experimentally. I have a small piece of apatite in front of
me; I bought it on ebay for a few pounds and I look at it.
It is as blue as the eyes of a Latvian princess. So
beautiful and so strange. It looks back at me.
Astonishing.

98

 8

Proposed experiments

There are two areas where, if this is correct, or even

slightly correct, we can carry out experiments. There is
also an area where this idea might yield interesting
medical effects, and I will devote a chapter to treatments
for cancer. I should say at the beginning that I have
already carried out some of these experiments, but I do
not intend to provide any results in this book. I wrote the
book because I felt that if I were right then I ought to flag
up the idea and allow everyone to have a go who might
be interested. I really also don’t want some guy patenting
this so I will flag this up as prior knowledge right here.
Especially as I don’t have the resources to do some of the
experimental work I should like to, and I have, at the age
of 70, now entered a rather precarious period of my life,
which many call the Valley of the Shadow of Death. So
I wouldn’t want to suddenly be struck down without
writing this up. Recently, my friend Michael Meacher,
the Environment Minister left us i.e. died at 75. Other
friends of mine have disappeared and others are
increasingly looking dicky. To say nothing of losing
your marbles, another possible fate. Alice Stewart the
radiation epidemiologist kept her mind sharp to her death
in her 90s: fingers crossed.
And pass the  .

99

8.1 Molecular communication

I have already described a molecular communication

experimental setup. Other possibilities may be easily
devised. The rates of reaction of enzymatic processes
with and without the input of specific frequencies or sets
of frequencies would be of interest. Cross beam
experiments are also of interest. The issue is whether it
is possible to separate two or more sets of mixed
compounds or affect specific reaction velocities between
any two on the basis of external irradiation.

8.2 Molecular temperature

The molecular temperature can be assessed using Raman

and measuring the Stokes-Anti-Stokes ratio either side of
the exciting laser frequency. Does this vary in a mixture
depending upon specific irradiation with infra-red
frequencies associated with only one of the components?
Thermochromic molecules might also be usefully
employed here.

8.3 Pond life/ bacteria; use of microscopes.

The most effective detector of the efficiency of a

perturbing infra-red communication is a living creature
that can be monitored for behavioural changes. Thus we
may experiment with a simple or unicellular organism
like Amoeba or Stentor and observe its behaviour or life
process whilst being irradiated with infra-red radiation of
different frequencies emitted from a monochromator (or
more recent laser beam devices) to see if there are

100

frequencies that upset it or cause measurable effects.
Thus we can build (and I have) a living detector
spectrometer. We can also make emitters involving a
range of heated biological molecules or possible
pharmacological molecules. We can use a heated calcium
phosphate or hydroxyapatite emitter using an electrically
core heated apatite sample placed at the focus of a
parabolic reflector made of silver or copper sheet. Plant
germination under differential conditions of low levels of
specific emitters might show effects.

In all these we have to measure the total energy absorbed

and the qualitative effect it has on the animal or bacteria
sample. Note that these experiments are technically
challenging since the optical systems have to be
transparent, which means directing the beams down on
the biological samples from above and using an inverted
microscope. Windows would have to be capable of
contact with water without dissolving, Caesium Iodide or
KRS5, but their effects on living systems being examined
would have to be checked as a control. A chopped beam
can be detected with a synchronous detector from
anomalous movements and the frequency output rectified
and taken to a recorder.

8.4 Two beam or crossed beam experiments

Molecular characteristics, as measured by one set of

criteria, may be examined with and without irradiation at
specific infra-red frequencies or by sets of frequencies
associated with various elements of the processes being
examined. For example, does irradiation with infra-red at

101

specific frequencies affect the rotatory dispersion or
other spectroscopic or optical characteristics of peptides
or proteins and if so what is the variation of the effect
with infra-red frequency? Other molecular probes may
be devised.

One such experiment might involve examining the

infrared absorption spectrum of a protein or enzyme in
aqueous solution whilst irradiating the solution in a
direction perpendicular to the absorption spectrum beam.
If there is an effect, what is its relaxation time? Can the
protein “remember” being irradiated by the crossing
perturbation beam?

What is the effect of apatite radiation upon a

phospholipid film? On the excised cell membrane?

8.5 Urey experiments

The attempt to create more complex molecules and

sustain their existence and “growth” may be carried out
in a version of the Urey primitive Earth experiments, the
molecular soup, but over a substrate of apatite or other
mineral rocks or stones which are externally irradiated
with synthetic sunlight. The spectrum of products in the
presence and absence of the apatite (or any other mineral
base) can be compared using chromatography, mass
spectrometry or other analytical methods to see what
effect the substrate has relative to control substrates with
no powerful absorption/ emission bands in the infrared.

102

8.6 DNA mutation experiments

There are many systems available to measure genetic

damage. One such would be to expose germinating
seedlings to low level infra-red radiation of specific or
bundled frequencies and compare chromosome damage
in the meristem. Other methods could be devised.

8.7 Warning

When ionizing radiation was discovered, many

researchers developed cancer and died because the
effects of ionizing radiation on the DNA: the mutation
effects were not appreciated. If I am correct, irradiation
experiments at infrared frequencies could in principle
cause serious genetic damage or might even initiate
biological processes which are unstoppable. Here I am
suggesting that phosphate radiation may have been the
initial source of energy for life. It is also clear however
that key molecular processes in eukaryotic complex life
including genetic and cell copying processes involve
phosphates. The key energy molecule is a tri-phosphate.
Phosphate radiation will penetrate deeply into tissue and
will resonantly energise a whole spectrum of key
biological molecules. I would suggest that anyone
carrying out experiments in this area takes great
precautions and experiment on animals behind infra-red
blocking shielding until it is clear that dangers do not
exist. Most important, recall that cancer induction is not
an easily measurable effect until several years have
passed. Happily it is fairly easy to block infra-red
radiation.

103

8.5 Summary

What has been presented is a hypothesis that the key

processes in living systems involve transfer of energy at
infrared frequencies. It is this energy exchange that is the
vis viva, the life force. The chemical components of the
cell and the strategies that living creatures evolved to
increase their efficiency and complexity, derive from an
evolutionary development of the best chemical
components, the hardware, necessary to improve the
electromagnetic energy transfer processes. The question
raised by Schrödinger relating to thermodynamics of
living processes, the negative entropy question raised by
life, is answered by the way that quantum exchanges of
energy separate molecules in terms of the individual
molecular energies. Living creatures are first and
foremost hotter than their surroundings and it is this
quality which is the common necessity for life to borrow
energy from the decay of sequences of energy exchanges
until background temperature is attained. This energy is
created and sustained by infrared radiation which
ultimately originates in the solar or other heating of the
earth and in more advanced creatures from the
metabolism of various carbon based materials created by
photosynthesis. But in the first instance, the start of life
itself, the energy was supplied, in my scenario, by a
conversion of short wave energy to specific long
wavelengths through intermediates. This specific energy
could then be “eaten” by molecules which have the
correct quantum absorption appetite, and the reactions
and progress of these molecular reactions in the presence

104

of the radiative “food” provided the stage for the
development of life through molecular natural selection.
These early molecules, which are hotter than their non-
absorbing neighbours, their environment, I say are alive:
they eat, they grow, they divide. This division is fairly
random at first but natural selection will produce ever
more efficient molecular species.

I have discussed some of the experiments that support

this idea, and have suggested others. In a final Chapter I
will turn to intercellular effects and to cancer, which is at
least in part, a breakdown of intercellular signalling. It
may be that we can reverse cancer by altering the weight
of intercellular infrared signalling, and this is an exciting
prospect.

105

 106

 9

Molecular Communication and Cancer

9.1 Intra and intercellular signalling

Both the maintenance of morphology and the

development from fertilisation to adult in complex
creatures must be controlled by intercellular signalling.
The cessation of development of normal cell cultures at
boundaries (glass sides of containers) must also involve a
cell signalling process. I read somewhere of some
Eastern European guy who put cancer cells one side of a
cover slip and normal cells the other side and the cancer
cells reverted; but only when the slide was made of
silica; glass was no good. Can this be true? One reads so
much weird stuff. But it certainly might be predicted by
what I am proposing. Recent discoveries in the field of
genomic instability and the radiation bystander effect
make it quite clear that cells communicate with each
other over significant distances and therefore may be
considered as “communities” with a common or
somehow agreed response to stimuli. The bystander
effect is where a single cell is targeted by an alpha
particle track which causes ionizing radiation damage to
that cell. However, it has been shown that cells quite
remote from the attacked cell respond by increasing
genetic damage as measured by a whole range of
objective indicators e.g. chromosome damage.

Rupert Sheldrake pointed out the bankruptcy of current

explanations for developmental morphology and had

107

recourse to a novel concept of a morphological field, a
kind of memory, but his idea, though fascinating, is
ultimately only an arm-waving transfer of ignorance to a
name, and is little better than a religious explanation.
Though his attack on Science I am all in agreement with
and hooray for having the nerve to do all that mad stuff.

Conventional Science on the big questions is now

arrested in its development by a Holy Mother Church
system of black boxes, guys who think they are scientists
because they support each other in their group tanks, and
guys who work for industry or the military. The black
boxes give explanations that are unpersuasive but few
have the time, energy or funding to open the boxes up,
also because what evidence there is suggests that to do so
will be very bad for business. Also the Emperor’s New
Clothes effect is very powerful. No one looks to be
accused of stupidity. Physics is par excellence the place
where the priests are terribly insecure about their
cleverness. I have opened up the radiation black box and
I have subsequently been kicked out of 4 universities one
after another following representations (if we can call
them that) from the nuclear industry and its running dogs
(I always wanted to use that phrase). I am not saying my
explanation here will be more than slightly better but at
least I am stepping outside the paradigm, and then also it
is experimentally accessible and may even be right.

The implied current theory of cellular signalling as a

basis for morphological development assumes that the
signalling occurs through contact, thus one cell is in

108

contact with four or six cells and somehow there is a
message passed between these cells that tells a cell at the
eventual periphery of the growing system to stop. This
seems extremely unlikely. Where is the master template
held? In the first cell? If this is copied to the second and
subsequent cells how do they know that they are the
second and subsequent cells and in particular, how does
the final cell know that it has to stop there? But if we are
dealing with electromagnetic resonances, the final copy
is available to all the cells which share the data. The
amplification by resonance of the electromagnetic data
coded on the DNA is available to all the cells as a
resonant field, rather like Sheldrake’s Morphic Field. It
ought to be possible, if this is the case, to disrupt this
with electromagnetic fields from a different species.

But let’s think about the nature of these interactions. If

such intercellular signals exist, there should be
amplification mechanisms, damping mechanisms and
memories. There has to be (for obvious reasons)
feedback control on common mode rejection or the
whole system would fly apart. Elena Burlakova, invited
me to talk about all this stuff in Moscow in 2008, at a
conference on ultra-low dose effects. She has carried out
a large number of experiments with living systems which
show effects at doses which seem unbelievable; where
stochastically no molecules of the effector substance can
be present at a single cell which is nevertheless switched.
We are here in the realm of homeopathy. Nevertheless,
results in research on the “memory of water” and similar
oddities, are only dismissed by those with a rationalist

109

addiction to current science. We just do not know what
is happening here. Water itself has a very plastic
structure and can form ordered domains, what I see as
liquid snowflakes. Such domains may be ordered in
particular ways by incident infra-red radiation or perhaps
even longer wavelengths. Pollack has shown the proton
separation effects associated with infra-red absorption for
a flat or black body distribution. But what about a more
specific distribution? How long can these ordered
domains persist? And if water alone can do this, how
much more possible is the absorption of specific infrared
frequencies by a molecule as large as a universal protein
like serum albumen? And once such a memory is
embedded, will it not be also resonant with other
memory protein molecules within the range to the set of
frequencies being remembered? This is an amplification
system for low levels of initial perturbation.

What Burlakova found was fascinating. She carried out

the usual experimental determination of a number of
dose responses. She reduced the concentration to very
low but non-zero levels and obtained the linear or
monotonic response (which others draw straight lines
through, aiming at the origin, zero dose/ zero effect). But
then she lowered the dose again. The effect increased. At
very very low dose, the effect went up. So she pursued
this at lower and lower doses. The effect decreased. But
she was not content with this and lowered the doses
again. The effect went up. She told me that there was an
oscillation of effect with dose at extraordinary low levels.
In some experiments the concentrations where the effect

110

ran out of steam were 10-15M. That is 600,000 molecules
in one cubic centimetre or solution. That is one molecule
in 3000 cells. How can this work? But the same question
was asked about insect pheromone detection by Wright
with similar relative levels of pheromone molecule per
moth. These are data! This is what Elena Burlakova
found.

The genomic bystander effect has been studied by my

friend (and global authority on the effect) Carmel
Mothersill. She looks at fish. She irradiates one sample
of fish and then the radiation damage effect appears in a
second un-irradiated group. There are various theories
about the mechanisms of transfer of the signals, but no-
one knows.

9.2 Cancer

I have written two books about cancer, Wings of Death

1995 and Wolves of Water 2007. I have studied cancer as
an epidemiologist and the relation between cancer and
ionising radiation and other causes. I have acted as an
expert witness in more than 20 cancer radiation cases and
nearly all were successful. If you want to know more
then read these books. There is a cancer epidemic which
began in the 1980s and shows little sign of decreasing.
What was a disease of no-one in primitive tribes
unaffected by pollution has become a one in 5 persons
disease in the 1990s and is now a 1 in 3 person disease.
By 2020 it will be a one in 2. This is not because of an
ageing population: it is an age standardised phenomenon.
The increases are a result of the contamination of the

111

biosphere by radioisotopes like Strontium-90, Caesium-
137, Uranium-239 and so forth. Initially the nuclear
atmospheric test fallout and later the releases from civil
nuclear power and then Uranium. The trend of increased
child leukemia exactly follows the trend in world radium
production that followed the discovery of the element by
Marie Curie. Marie Curie has become an icon for a
cancer charity but the woman herself died from
leukemia.

The cancer research organisations pay scant attention to

radiation, or indeed pay much attention to the causes
altogether. They take your money and pursue treatments.
The main treatments continue to be slash and burn:
chemotherapy, radiation, and surgery. This is not very
effective.

Cancer is a genetic disease expressed at the cellular level

and by now we all know that the disease begins with
genetic lesions in the cellular DNA. Mutations. It is like
a Bingo Card but the prize is cancer: you get the correct
numbers of oncogenes and the cell runs away to become
a tumour. That explains the trend with age and also risks
in those who have contact with mutagens. I won’t go on,
you can read my earlier books. This is called the Somatic
Mutation Theory and even now it dominates thinking
about cancer. Its message is this: cancer is a consequence
of accumulated errors in genes on the cellular control
DNA.

But this is not the whole picture. The cells may become
genetically altered so that they believe they need to

112

replicate unchecked. And from a host of epidemiological
and experimental evidence this seems to be a correct
explanation for part of the process. But it is clear now
that this is not the whole picture. In some way, the cells
around them, the community, stop the unchecked
replication, at least when the proto-tumour is small.
Transplant a tumour cell to healthy tissue it fails to
develop. There are some fascinating mouse radiation
breast cancer chimera experiments that have been
published and were explained to me in Paris by the
researcher Mary-Ellen Barcellos-Hoff who did all this
bizarre stuff: swapping breasts between mice. You need,
she said, the seed and the soil both. It is clear that the
community of cells controls the behaviour of rogues. The
idea was presented by Carlos Sonnenschein at a meeting
I was invited to contribute to in Kos several years ago.
Sonnenschein and Soto have written about their idea that
cancer is a disturbance of the community of cells which
interact with one another by some kind of signalling
process. This idea, which seems to be catching on, is now
called the Tissue Field Organisation Theory TOFT.
There is currently much argument between the
proponents of the two, TOFT and SMT. But of course it
is both, though it may well be that cancer can develop
independent of pre-existing genetic damage if the field
breaks down. There are examples of field cancerization
where many tumours independently appear at many
different primary development sites in the same tissue.

113

There will be more rogues, or more likelihood of rogues
if the DNA has been previously damaged (by radiation,
by oxidative stress, by methylating agents) but if the
surrounding cells are healthy they can somehow switch
off the tumour, communicate with the bad cells and ask
them to commit suicide. Muir Gray was on the UK
military Depleted Uranium Oversight Board the DUOB,
when I was a member. The board was discussing the idea
of ultrasound scanning the Uranium-exposed soldiers for
kidney cancer. He said that you would find tumours. But
that wasn’t the whole answer, since they had done some
pilot studies and a most of the tumours regressed and
disappeared. Maybe I’m not supposed to write this: it
raises some interesting ethical issues. It is true that
autopsies show up a lot of occult cancer. Cancers that do
not develop and kill you. Something is keeping them in
check. It is currently believed to be the “immune system”
that catch-all for observations that cannot be explained.

Another story supports this. I was interviewing a GP in

Carlingford, County Louth, Ireland, Andy McDonald in
Greenore. He is dead now. But he had a database of his
patients which he shared with me. I was interested in
cancer rates in those living near the mud banks in
Carlingford Lough, a sea inlet on the east coast of the
republic of Ireland which is contaminated with
radioactive particles from Sellafield. I write about this is
Wolves of Water and what I found. But he told me an
interesting tale. A patient, a woman came to see him
about some trivial matter. He examined here and noticed
a hard lump on her breast, about the size of a penny (say

114

a Euro coin). He asked her about this. Oh sure I have had
this for 10 years doctor, it’s no problem, it doesn’t hurt at
all, at all. But it may be a cancer, he said? We should
check it. What for? It might kill you. But I have been
alright for the 10 years it was here, she says. So they
check it out. It is a cancer. They operate. She dies of
metastatic breast cancer within 6 months after
chemotherapy, radiation, mastectomy, the whole works.
What’s going on there then?

The picture that emerges from this for me is that you may
be able to reverse cancer, to cause regression, by either
increasing the magnitude of the signal from the larger
cell community surrounding the tumour or else
increasing the ability of the tumour cells to recognise the
signal from surrounding cells.

9.3 Hyperthermia

A friend of mine developed kidney cancer. He was

relatively young, in the early 50s. It was detected by
ultrasound; it was quite small. Big panic: it was removed
surgically from the kidney at one of the most prestigious
(and expensive) cancer hospitals in the USA. The cancer
nevertheless metastasized. Over the following six months
or so he was treated with a drug that had frightful side
effects. This seemed to hold the situation but then he
developed secondary tumours in the lung, and bones of
the shoulder and arm. One of the new experimental
immune system potentiator drugs was prescribed. A
tumour on his back was removed. It did not look good.
Another friend who has prostate cancer suggested that he

115

forget the US treatment and go to Germany to try
hyperthermia. We visited a number of clinics where this
treatment was offered and I persuaded him to check in
for treatment. He was treated with hyperthermia, where
they raise your core temperature. Later scans after his
treatment showed the tumours were shrinking. So it
works; and indeed the doctors at the clinics we visited
provided a lot of evidence that hyperthermia works.

Hyperthermia is a treatment where the tumour (if

accessible and localised) or the patient (if not) are heated
up. The local heating is carried out either with a
microwave generator (like a cooker) or for whole-body
the patient is placed in a tent and subjected to infra-red
heating from electric incandescent lamps. In the more
advanced versions, these lamps are water jacketed and so
the water wavelengths are blocked (absorbed by the
water jacket). This means that the infrared radiation
penetrates deeper into the body, otherwise it is mainly
absorbed by surface tissue water and doesn’t heat the
deep tissue. Obviously it is uncomfortable, and core
temperatures are carefully monitored with a rectal
thermometer. Above a core temperature of about 43
degrees life systems are threatened. In the ultimate
version of this hyperthermia, the patient is anaesthetized
and immersed in a water bath: the temperature is raised
to the limit that the body can stand for as long as the
body can stand it but the patient has to be healthy to
begin with.

116

Those who began this treatment (which apparently
originated in Russia, the Latvians say Latvia) followed
observations that sometimes an individual with cancer
who became infected with a virus and developed a high
temperature found that the cancer had regressed. It was
(and is still) believed that it was the “immune system”
that was potentiated by the fever and the immune system
destroyed the tumour. One treatment was to infect the
cancer patient with an otherwise harmless virus. In
Latvia, where I live, they use “virotherapy” which
involves an enterovirus which is harmful in children but
less so in adults. I spoke with the clinic in Riga who use
this treatment. Others in Germany employ a chicken
virus, Newcastle Disease, to cause a temperature increase
(or as they think, potentiate the immune system).

There is another clue. One doctor in Germany who I was

discussing this with told me that the cancer patients he
treated all had low normal temperatures. The normal
temperature is about 37 degrees but in the cancer patients
it was less, about 36 degrees. I saw this in the graph of
one poor chap who was being heated up in the infra-red
tent; the plot on the computer screen of his rectal
temperature showed it increasing from less than 36
degrees.

So what is going on here? This is a real phenomenon. If

we view this through the lens of those who administer
the treatment, what is happening is the sequence—
artificial fever—immune system switches on—cancer is
attacked. They know that the immune system has been

117

switched on because they do blood tests. But if we look
at it through the lens of the molecular communication
idea what is happening is the sequence: increased
temperature—increased signal ratio from surrounding
cells—tumour cell death—immune system clears up the
debris.

My explanation is different. The reason that the increased

temperature kills the tumour cells is that the cell
community surrounding the tumour has a larger volume:
there are more cells, and heating up the tumour and the
surrounding layer causes more signals from the more
remote tissue in the normal cell community without
changing the signal resonance from the tumour
community.

If this is the correct explanation it suggests a

development of the treatment using selected frequencies.

9.4 Proposed targeted or resonant hyperthermia for

cancer treatment

The immune system potentiation theory is based on

temperature. If you increase the temperature, they say,
the immune system starts to increase its surveillance and
floods the body with immune system cells. The
wavelength (frequency) is irrelevant: what you are doing
is heating the tissue up. And this may be true. But what if
it is not the “tissue” you are heating up, but some critical
molecules. If this is the case, these molecules will also
increase their molecular energy, their molecular
temperature, their bond vibrational energy. But instead

118

of broad band (called black-body spectrum) infra-red we
could devise lamps which emitted specific frequencies or
a specific set of frequencies. In one version of this I have
built a phosphate apatite infra-red emitter. This is a piece
of apatite heated internally electrically and placed at the
focus of a silver parabolic reflector. In the molecular
communication experiment I used a similar emission
source to show that only resonant absorbers responded
by heating up. Infrared laser devices are now available
for specific frequencies. What if we use specific sets of
frequencies or specific frequencies to heat up the patient
or the tumour. Before you run away and try this out,
please read the warning message I have written in
Chapter 7. After all, DNA can be specifically heated with
apatite radiation, and DNA can mutate and this results in
cancer many years later. The phosphate emission band at
around 1000cm-1 will theoretically penetrate deep into
tissue and energise the phosphate backbone of DNA and
RNA, will energise the mitochondrial energy molecules
and will disrupt the cell membrane. So watch out.

9.5 Koch and Morré

I will write a few words about William Koch. Koch

developed a treatment for cancer which by all accounts
was very successful. However he was attacked by the US
Federal Drug Administration and fled to Brazil. A friend
of mine, Roger Coghill once showed me a sheaf of
documents from hospitals in the USA which gave before-
and-after medical reports about patients with terminal
cancers, written off by the hospitals, who unexpectedly

119

recovered and were cancer free after receiving Koch’s
treatment. You can find Koch on the internet, and I have
a copy of his book, which is hard to find. Koch believed
that cancer was a metabolic disease in which the cancer
cell had reverted to anaerobic metabolism and had
therefore digested parts of the cell membrane. This, he
believed prevented signalling. His treatment was a single
injection of small quantities of chemical substances he
believed would catalyse a reversion to oxidative
phosphorylation, to oxygen-based metabolism. There
were a number of different molecules he employed. The
early ones were D-unsaturated ketones and aldehydes.
Later he employed quinones, the most accessible of these
being p-benzoquinone.

This is an interesting molecule both chemically and

energetically. The structure is:

The infrared spectrum is shown in Fig 9.1. Notice that it

swamps all the regions where living systems absorb. The
spectrum of a mouse oocyte is shown for comparison in
Fig 9.2. I have had to import these spectra so sometimes
(as in this case) they are presented “upside down” but
notice the way in which the p-benzoquinone absorption

120

mirrors the range of signals which, if I am correct, must
include the key intercellular signals.

Quite recently, it has been shown though various elegant

experiments by Morré and Morré that proteins associated
with cell surface metabolism are key to understanding
cancer expression, and indeed these discoveries allow
cancer and pre cancer cells to be diagnosed long before
clinical expression merely by employing 2-way
electrophoresis to locate proteins which are flags for
specific cancers. The very latest cancer treatments
involve targeting the cell surface with tailored immune
system active drugs. What this suggests to me is that it is
the intercellular signalling that is key. In the case of p-
benzoquinone, we are perhaps interfering with these
signals in some way, rather than, as Koch thought,
catalysing a change from anaerobic to aerobic
metabolism.

I suggested to my friend, the kidney cancer man, that he

try out Koch’s benzoquinone. So he did; and whether it
was the hyperthermia or the Koch treatment, it worked.
He is still alive now about 18 months since the tumour
metastasized and about 6 months after it looked like he
would die.

I should finally point out that all these spectra I have

shown are of the pure compounds. The spectra in
solution will be different, and in some cases perhaps
quite different. There are big, though not insuperable,
problems obtaining infra-red data from aqueous

121

solutions, and usually spectra are of the compounds in
melts or paraffin mulls or sodium bromide pressed discs.

Fig 9.1 Infra red spectrum of p-benzoquinone

Fig 9.2 Murine oocyte full infrared spectrum with

assignments to bands

122

 10

Endnote

Allow me to return to the question of evolution. If

communication is through infra-red signalling then the
integrity of DNA becomes less certain. It is entirely
possible that DNA is maintained in cell communities by
resonance, rather like Sheldrake’s idea of a
morphogenetic field. It is also possible that, though
pretty bomb-proof as a molecule, the expression of DNA
may be perturbed by external infra-red signals. This is a
new possible component of evolutionary directionality.

One of the reasons I have been impelled into writing

this, apart from all the others, is that I was giving a paper
at a Breast Cancer conference in Birmingham in August
of this year. I met and got talking with Peter Weightman
of the University of Liverpool, one of the universities I
have been kicked out of over my nuclear radiation and
health work. To my astonishment (since I work in an
intellectual vacuum as far as this thesis of life is
concerned) Weightman turned out to also have an
interest in life and electromagnetic radiation. Indeed he
seemed to have some funding to look at the interaction
between Terrahertz radiation and living systems.
Terrahertz radiation is at the long wavelength end of the
IR spectra I have been discussing. The wavelengths are
between 1mm and 100P cm-1 to 100cm-1). I seem to
recall he said there is evidence that THz irradiation can
cause DNA changes. I outlined my work to him and said
I thought those wavelengths were too long. They might

123

affect gross low frequency molecular modes and thus
shake the molecule apart, but they would not have the
resolution to make specific changes. Anyway, he told me
that there was a whole community of scientists out there
trying to figure this stuff out. So I thought, right, I will
put down what I think is happening and see what
happens.

As I wrote in the introduction, I have made almost no

attempt to examine the literature in this area, so what you
have read is what I have figured out, and also there are,
for the same reasons, as well as time pressure and
laziness, no references. I will however add a select
bibliography at the end.

Finally, because I think it important, I repeat my warning

to those intending to tinker around in this area.

Warning

When ionizing radiation was discovered, many

researchers developed cancer and died because the
effects of ionizing radiation on the DNA: the mutation
effects were not appreciated. If I am correct, irradiation
experiments at infrared frequencies could in principle
cause serious genetic damage or might even initiate
biological processes which are unstoppable. I am
thinking here of “spontaneous human combustion”. You
may laugh, but there have been too many reports by
unimpeachable witnesses of the existence of this
phenomenon. Here I am suggesting that phosphate
radiation may have been the initial source of energy for

124

life. It is also clear however that key molecular processes
in eukaryotic complex life including genetic and cell
copying processes involve phosphates. The key energy
molecule is a tri-phosphate. Phosphate radiation will
penetrate deeply into tissue and will resonantly energise
a whole spectrum of key biological molecules. I would
suggest that anyone carrying out experiments in this area
takes great precautions and experiment on animals
behind infra-red shielding until it is clear that dangers do
not exist. Most important, recall that cancer induction is
not a measurable effect until several years have passed.
Happily it is fairly easy to block infra-red radiation and
so the weapons development concerns can I think (hope)
be laid aside.

125

 Select Bibliography

Baker SG (2015) A cancer theory kerfuffle can lead to

new lines of research. J.Natl.Cancer.Inst. 1-8

Barlow R.B. (1964) Introduction to chemical

pharmacology. London: Methuen

Barlow R.B. (1980) Quantitative aspects of chemical

pharmacology. London: Croom Helm

Bellamy L J (1975) The infrared spectra of complex

molecules. Vol I London: Chapman and Hall

Bellamy L J (1980) The infrared spectra of complex

molecules. Vol II advances in infrared group frequencies.
London: Chapman and Hall

Bernal JD (1951) The physical basis of life London:

Routledge and Kegan Paul

Busby Chris (2007) Wolves of Water. Aberystwyth:

Green Audit

Butler JAV (1949) Chemical Thermodynamics. London:

Macmillan

Colthup NB, Daly LH and Wiberley SE ((1975)

Introduction to infrared and Raman spectroscopy. New
York: Academic Press

Dawkins R (1986) The blind watchmaker London:

Longmans

126

Feyerabend Paul (1975) Against Method. London: New
Left Books.

Goodman and Gilman’s Pharmacological basis of

therapeutics 11th Edn (2006). Ed—Laurence L Brunton,
John S Laszo and Keith L Parker. San Francisco:
McGraw Hill.

Koch WF (1961) The survival factor in neoplastic and

viral diseases. Detroit: Vanderkloot Press

Kwang W Jeon (1973) The biology of the amoeba. New

York: Academic Press

Lahav Noam (1999) Biogenesis. Oxford University Press

Latour B (1987) Science in Action Cambridge MT:

Harvard University Press

Midgeley Mary (2002) Evolution as a Religion.

Routledge

Morre J and Morre DM (2013) ECTO-NOX proteins,

Growth, Cancer and Ageing. New York: Springer

Nakamoto K (1963) The infrared spectra of inorganic

and coordination compounds New York: Wiley

Oparin AI (1957) The origin of life on the earth New

York: Academic Press

Pollack G H, Cameron IC and Wheatley DN (2006)

Water and the Cell. New York: Springer

127

Pollack GH (2014) The fourth phase of water. Beyond
Solid, liquid and vapour. Publ. Ebner and Sons

Schneider ED and Sagan D (2005) Into the cool. Energy

flow, thermodynamics and life. University of Chicago
Press.

Schrödinger (1943) What is Life? Cambridge: University

Press

Sonnenschein C and Soto AM (1999) The society of

cells. Oxford: Bios

Turin Luca (2007) The secret of scent. Adventures in

perfume and the Science of Smell. London: Faber and
Faber.

Urey Harold (1952) On the early chemical history of the

earth and the origin of life. Proc.Nat.Acad.Sci.38: 351-
363

128

 129

 130