Issue number #6 is here and that means that we have been with you for a whole year! That’s right. We started this dream last March! And here we come again with spring, and a new edition full of fascinating contents. Doctor Crawford, from California, contributes with an article that illustrates to us the importance of autonomic balance; the key to health. I am sure you will find it very useful. Rob Hutchinson writes about the strange case of Ian Waterman, who at 19 caught a virus that destroyed half of his nervous system. Since then, he has been unable to mentally sense the relative positions of his limbs in space and whether or not they are in motion. The human brain is shrinking for the first time in our evolutionary history. If modern humans are so smart, why are our brains shrinking? There are some leading theories about why the human brain has been getting smaller since the Stone Age. Mike McInnes, a retired Scottish pharmacist and author of The Honey Diet has some information about it to share with us. Joseph Davidovits is a French materials scientist known for the invention of geopolymer chemistry. He posited that the blocks of the Great Pyramid are not carved stone but mostly a form of limestone concrete or man-made stone. Tania Dey has had the honour of interviewing him for us

1. AUTONOMIC BALANCE
IS THE KEY TO HEALTH
HOMO INSAPIENS:
THE SHRINKING HUMAN BRAIN
Geopolymer research:
An interview with
Joseph Davidovits
My Mind’s Eye
the strange case of
Ian Waterman
ISPECTRUMMAGAZINE
Issue 06/March - April 2014

2. 1
Features
03
AUTONOMIC BALANCE
IS THE KEY TO HEALTH
04 Defining the autonomic nervous
system (ANS)
05 Functions of the ANS
11 Diagnosing Imbalances
13 Nutrients and the ANS
14 Treatments
17
My Mind’s Eye
the strange case of Ian
Waterman
19 Proprioception
21 The strange case of Waterman
23 Fighting to Control what cannot
be felt
24 Visualization and movement
28
HOMO INSAPIENS:
THE SHRINKING HUMAN BRAIN
30 The Glial Cell and Incipient
Dementia
32 Is Glucose a Cannabinoid?
35 Sleep Deprivation and the
Shrinking Brain
41 Bariatric Sleep
43 Why Honey?
47
Geopolymer research:
An interview with Joseph
Davidovits
48 What is a Geopolymer?
49 The Great Pyramids
58 Geopolymers for construction
28
3
13 47
17
CONTENTS

3. 2
Mado Martinez
Editorial Director
Editorial Director
Mado Martinez,
madomartinez@ispectrummagazine.com
Art Director
Rayna Petrova
raynapetrova@ispectrummagazine.com
Copy Editing and Proofreading
Matt Loveday
mattloveday@ispectrummagazine.com
Jennifer James
Contributing Writers
Dr. Dennis K. Crawford
Rob Hutchinson
Mike McInnes
Tania Dey
Images
Cover : © Billy Benavides / neusenz.com ,
commons.wikimeadia.org,
morguefile.com,
sxc.hu
editorial
Ispectrum
magazine
Dear readers,
Issue number #6 is here and that means
that we have been with you for a whole
year! That’s right. We started this dream
last March! And here we come again with
spring, and a new edition full of fascinat-
ing contents.
Doctor Crawford, from California, con-
tributes with an article that illustrates to
us the importance of autonomic balance;
the key to health. I am sure you will find
it very useful.
Rob Hutchinson writes about the strange
case of Ian Waterman, who at 19 caught
a virus that destroyed half of his nervous
system. Since then, he has been unable
to mentally sense the relative positions
of his limbs in space and whether or not
they are in motion.
The human brain is shrinking for the
first time in our evolutionary history. If
modern humans are so smart, why are
our brains shrinking? There are some
leading theories about why the human
brain has been getting smaller since
the Stone Age. Mike McInnes, a retired
Scottish pharmacist and author of The
Honey Diet has some information about
it to share with us.
Joseph Davidovits is a French materi-
als scientist known for the invention of
geopolymer chemistry. He posited that
the blocks of the Great Pyramid are not
carved stone but mostly a form of lime-
stone concrete or man-made stone. Tania
Dey has had the honour of interviewing
him for us. Thanks Tania!
Enjoy your reading!
www.ispectrummagazine.com
Follow Us
admin@ispectrummagazine.com
+44 7938 707 164 (UK)

4. W
3
hen it comes to health
issues the autonomic
nervous system (ANS) rules.
If the ANS were to remain
balanced it would be almost
impossible to get sick. If
that is the case, why isn’t
more emphasis put on test-
ing for one’s ANS status and
then utilizing therapies to
bring it into homeostasis?
Perhaps because in a phar-
maceutically oriented symp-
tom based health care sys-
tem as exists in the U.S and
AUTONOMIC BALANCE
IS THE KEY TO HEALTH
elsewhere, it simply has no
place. To ignore it however,
is to miss maybe the most
important diagnostic picture
we could currently obtain
from a patient. Correcting
this imbalance is what allows
the body to heal itself as it
is designed to do and is also
true prevention against future
diseases. Autonomic balance
explains why people react dif-
ferently to diet, supplements,
and even exposure to patho-
gens and toxins.
by
Dr. Dennis K. Crawford
website
www.crawfordnaturalhealthcenter.com

5. 4
The ANS is the part of the ner-
vous system that regulates meta-
bolic processes beyond conscious
control. It does so automatical-
ly. Digestion, circulation of blood,
secretion of hormones, and the rate
of metabolism are all examples of
the ANS at work. The ANS in the
brain is located in the medulla
oblongata at the lower brainstem.
The major functions here are car-
diac regulation, vasomotor activity,
respiration, and some reflex actions
like coughing, sneezing, and swal-
lowing. Just above the brain stem
is the hypothalamus which receives
ANS input and acts as the conduc-
tor for automatic functions.
First, let’s define the ANS and
explore a basic explanation
of how it functions. From
there, I’ll concentrate on fac-
tors that influence the ANS,
how to test for imbalances in
a functional medicine para-
digm, and therapies to bring
it into balance.
The ANS is primarily two sub sys-
tems. One part is the parasym-
pathetic nervous system and the
other is the sympathetic nervous
system. These two systems work
independently in some functions
and interdependently in others.
They usually have opposite actions.
If one excites, the other inhibits.
The sympathetic system is more of
a quick acting system whereas the
parasympathetic system is slower.
The location of the sympathetic
system is from the first thoracic
vertebra to the second and third
lumbar vertebra. The parasym-
pathetic system is located in the
brainstem consisting of four cranial
nerves, and the sacrum consisting
of three sacral nerves.
There are sensory and motor com-
ponents to the ANS. Sensory neu-
rons keep track of the sugar and
oxygen in the blood, arterial pres-
sure, and gut and stomach contents.
Taste and smell, although they are
conscious functions, are controlled
by sensory neurons. The motor
component of the ANS is part of
sympathetic, parasympathetic, and
enteric functions. The sympathetic
components (ganglia) reside close
to the spinal cord. The parasym-
pathetic components are located
Defining the ANS

6. 5
close to organs. The
enteric lies inside the
digestive tube and can
operate independent-
ly of the sympathetic
and parasympathet-
ic branches. This is
why it has been called
“the second brain.” An
excellent book by that
name came out a few
years ago that does a
great job describing
the anatomy and func-
tioning of the enteric
system.
The divisions of the ANS are seen by
many as antagonistic to each other.
What the sympathetic division does
the parasympathetic does the oppo-
site. They are in fact complementa-
ry because they both have the same
goal which is to keep the body in
homeostasis. It is rare however, for
one’s state of balance to be perfect,
just as an airplane is never exactly
on course. The pilot is always adjust-
ing to keep the plane on course and
so is the body. A few of the sym-
pathetic systems responses include
constriction of sphincters, shunting
blood away from the intestinal tract,
inhibiting digestion and peristalsis,
increasing heart rate, dilating bron-
chioles of the lungs, and increasing
blood flow to muscles. These are all
Functions of the ANS

7. 6
ByBruceBlaus(Ownwork)[CC-BY-3.0(http://creativecommons.org/licenses/by/3.0)],viaWikimediaCommons

8. 7
ByJvnkfood(Ownwork)[CC-BY-SA-3.0(http://creativecommons.org/licenses/by-sa/3.0)],viaWikimediaCommons
part of the flight or fight
response. The para-
sympathetic system
is calming, enhances
digestion and is gener-
ally trying to restore
balance.
What goes wrong that
can affect people’s
health? The biggest
problem is functions
get stuck in one divi-
sion of the ANS at the
expense of the other.
For example, someone
may be operating pri-
marily from their sym-
pathetic system and
they are not being bal-
anced by the parasym-
pathetic system. The
opposite could also be
true. When this hap-
pens it throws off a
myriad of functions
within the body and
sets the stage for ill-
ness at some point in
the future. Most treat-
ments focus on effects
of this imbalance, but
that is only treating
symptoms of some-

9. 8
ByBruceBlaus(Ownwork)[CC-BY-3.0(http://creativecommons.org/licenses/by/3.0)],viaWikimediaCommons

10. 9
thing much bigger.
Until the ANS is bal-
anced there will always
be symptoms to treat.
Here’s an important
point; you can never
treat enough
symptoms to
fix the cause!
If someone’s
sympathetic
nervous sys-
tem is chroni-
cally hyper-
active they
can become
prone to cer-
tain ailments.
A few of them
are gastro-
esophageal reflux, coli-
tis, insomnia, insulin
dependent diabetes,
high blood pressure,
and in severe cases
congestive heart fail-
ure, strokes, and cer-
tain psychiatric prob-
lems. If they were
to get cancer it would
most likely be of the
tumor type of the
breast, lung, or pros-
tate, ovary, and pan-
creas. Their immune
systems tend to be
underactive. This per-
son could also have
musculoskeletal pain,
particularly in the low
back, but it could be
at any joint. If the
adrenal glands (stress
glands) are exhaust-
ed due to sympathet-
ic overload ligaments
weaken affecting the
integrity of joints. A
simple functional test
to demonstrate this is
to challenge any joint
and test its integrity to
oppose the challenge.
That can be achieved
by doing a light tug on
the joint and immedi-
ately after
testing its
s t r e n g t h
by having
the per-
son resist
pressure.
N o r m a l
p h y s i o l -
ogy would
d i c t a t e
that when
a joint is
challenged
by tug-
ging on
it, it would get stron-
ger to resist the stress
and prevent injury.
When the ligaments
are weakened due to
adrenal exhaustion the
opposite happens.
The same result will
happen with any joint.
This is why more inju-
ries occur when the
individual is stressed.

11. 10
The cause of the stress
could be anything.
Emotional stress,
dietary stress and
physical stress are all
common and they all
count. A muscle cor-
relation to the adre-
nals is the sartorius
muscle which connects
at the pelvis and the
medial knee. If it neu-
rologically weakens the
sacro-iliac joint on the
affected side will go
posterior and medial
knee stability will be
compromised. If that
is the case all it takes is
a twisting or rotation of
the joint and it could be
injured. Even in a con-
tact sport like football,
most knee injuries are
not contact induced,
but rather the wrong
movement creating the
injury. In other words,
when the body is in a
stress response it is an
accident looking for a
place to happen.
The chronic para-
sympathetic person
becomes susceptible
to osteoarthritis, angi-
na, anxieties and panic
attacks, asthma, heart
attacks, depression,
severe allergies, skin
conditions, and cardiac
arrhythmias. If this
person got cancer it
would be of the non
solid type like leuke-
mia.
Their immune
systems tend to
be overactive.
Since parasym-
pathetic people
can be calci-
um and protein
deficient, they
can also expe-
rience musculo-
skeletal discomfort.
When they get to the
point of severe back
pain they will usually
display bilateral sacro-
iliac weakness which
also weakens the glu-
teus maximus muscles.
These are major anti-
gravity lifting muscles.
When weak, the per-
son will lean way for-
ward when sitting and
then push themselves
up. In a grocery store
they are usually lean-
ing over their carts to
take the pressure off
their backs.
the chronic parasympathetic person
becomes susceptible to osteoarthritis,
angina, anxieties and panic attacks,
asthma, heart attacks, depression,
severe allergies, skin conditions, and
cardiac arrhythmias.

12. 11
How does one know if their imbal-
ance is toward the sympathetic or
parasympathetic sides? Knowing
the duties of each, the symptoms
one is presented with is the first
clue. There also some simple chal-
lenge tests that can reveal one’s ANS
status. For example, the color red
stimulates the sympathetic system.
If one looks through a red film and
it weakens their nervous system as
exhibited by muscle testing, chances
are good they are on sympathetic
overload. Conversely, the color blue
stimulates the parasympathetic sys-
tem. If weakness occurs while look-
ing through a blue film, they are
dominant on the parasympathetic
side. Another simple challenge test
is to have the person take a deep
breath in and hold it and monitor
for reflexive changes, which would
display as a postural shift, or again
a muscle test could be done. Once
this imbalance is revealed, treat-
ments become more obvious and
can be tailored that would inhibit the
dominate side and excite the weaker
side. There are degrees of sever-
ity of imbalances. Questionnaires
could also be utilized. Years ago Dr.
William Kelley, who did much of the
pioneering work on ANS imbalances,
developed extensive questionnaires.
He identified ten different states of
imbalance.
Diagnosing Imbalances

13. 12
The same diet is not for everyone.
What determines why one person
may get miraculous results with
a particular diet and another per-
son’s health would deteriorate
following exactly the same diet?
The answer is in the state of the
ANS. That is what determines what
foods are best digested, and what
foods best balance the autonomic
state of the person. For example,
a sympathetic dominant type is
the person who tends to have slow
digestion and is
on the acidic
side. They
do better
with more
p l a n t
foodsthat
are easy
to digest,
and should
go easy on
meats, particu-
larly fatty red meats. Rich foods
should also be avoided. Conversely,
the parasympathetic person would
do well with more meat in the diet.
Their digestive systems are also
more efficient. They tend to be more
on the alka-
line side.
W o r k i n g
to bal-
ance the
ANS indi-
v i d u a l i z -
es the treat-
ment protocol.
Eating with conscious
awareness to balance the ANS is
the goal. Eating deficient processed
foods cannot bring about balance
because of the stress they bring to
the digestive system and particu-
larly the pancreas. Processed foods
also do not contain the nutrients the
body needs to thrive. Consuming
refined sugar products and com-
mercial wheat foods that spike one’s
insulin levels can only produce imbal-
ance in the ANS. High fructose corn
syrup is the main source of calories
to the average American. Besides
being produced from GMO corn,
this “food” is a shocker to the ANS.
Along with the physical ramifications
of consuming these items, there
are proven connections to diet and
behavior and the state of the ANS
and behavior.
Diet and the ANS

14. 13
Nutrients and the ANS
Just as one size does
not fit all with diet the
same holds true with
nutrients. Like foods,
nutrients can be either
stimulatory or inhibi-
tory to the ANS. For
sympathetic dom-
inant individuals
it is logical that
it wouldn’t be
the best ther-
apy to recom-
mend nutri-
ents that would
further enhance
that imbalance.
Nutrients that
would tone down the
sympathetic system for
example, and stimulate
the parasympathetic
system would be most
beneficial. Again, the
work of Dr. Kelley is of
importance here. He
researched the impact
various nutrients had
on the ANS. This
information is invalu-
able when attempting
to achieve balance.
For example, a classic
sympathetic dominant
person would do well
to take Vitamins D, C,
B1, B2, B3, B6, Folic
acid, K, and the miner-
als potassium, magne-
sium and manganese.
The parasympathetic
dominant person does
better with Vitamins A,
E, C, B12, inositol, cho-
line, niacinamide, cal-
cium, and pantothenic
acid. Based on this
research if a patient
had a sympathet-
ic disease like
breast cancer,
it would not
be prudent
to rec-
o m m e n d
calcium,
w h i c h
would fur-
ther stim-
ulate the
sympathet-
ic system for
example.
a classic sympathetic
dominant person would
do well to take Vitamins
D, C, B1, B2, B3, B6,
Folic acid, K, and the
minerals potassium,
magnesium and
manganese

15. 14
Treatments
I’ll briefly cover some
of the ways that bal-
ance can be restored
in the ANS. As pre-
viously mentioned
diet and nutrients can
and should be utilized
to achieve that goal.
Beyond that, specific
adjustments at the spi-
nal level can be used
to either stimulate or
inhibit the ANS. I have
found cold laser thera-
py to be of great value.
It can reset the ANS
to a more normal set-
ting very quickly. For
example, if one has
adrenal exhaustion,
by gently stimulating
the joint with repeti-
tive light tugs and at
the same time point-
ing the laser light at
the brain stem, there
will be a rapid reset
of the adrenals. This
is from the work of
Dr. George Gonzalez,
DC,QN. Color therapy
is also very powerful.
By monitoring reflexes,
I find the color that
balances the body and
incorporate that color
into the person’s ther-
apy. The person could
look through a col-
ored film, use colored
glasses, cover a lamp
with the color, and so
on. Sound can also
work very nicely. If
I’m using tuning forks
I would test each one
until I found the fre-
quency that balanced
the body. This will be
displayed by the elimi-
nation of the postural
distortion one displays
on my treatment table.
Specific exercises can
be of value tailored to
the imbalance of the
individual. Someone
on sympathetic over-
load would not want
to do intensive exer-
cise that enhanced the
sympathetic system.
It would also be ben-
eficial to monitor heart
rate. After establishing
a base line, if the heart
rate is up 10 points or
more in the morning it
would be best not to
train that day.

16. Conclusion
Essential oils are powerful ANS
modulators. I test by having the
person sniff each until I find the one
that balances the body. If there is
emotional stress going on I often
employ Bach Flower Remedies. I
utilize the testing procedures from
Dr. Scott Walker’s N.E.T. system
then find which remedy balances the
body. The body tells me the correct
remedy. I am not making a judg-
ment about which remedy I think
might be best. However, invariably
after I find it and then read to the
person what the remedy is for they
are often shocked by how accurate
it is.
The notion that autonomic imbal-
ance is the root cause of all disease
is not new. Along with Dr. Kelley, Dr.
Francis Pottenger was also in agree-
15

17. 16
ment. Dr. Pottenger wrote two time-
less classics, Nutrition and Physical
Degeneration and Symptoms of
Visceral Disease. More recently, Dr.
Ernst Gellhorn, M.D.,Ph.D. Professor
of Physiology at the University of
Minnesota provided both labora-
tory and clinical evidence that auto-
nomic imbalance explains most
physical and psychiatric illnesses.
Also more recently, Dr. Nicholas
Gonzalez, who operates a medical
clinic treating chronic degenera-
tive disease, including cancer, uses
the principles of autonomic balanc-
ing. His results with certain can-
cers, particularly pancreatic, are
quite impressive and far superior to
“orthodox” cancer treatments. You
would think his work would be rep-
licated all across the country. It’s
not for reasons that will be a topic
for another day, but isn’t it about
time that results are put at the top
of medicine’s priority list? There are
just too many people dying and a
lot of them unnecessarily so.

18. 17
I
by
Rob Hutchinson
website
www.ispectrummagazine.com
My Mind’s Eye
n 1971 Ian Waterman was
nineteen years old and look-
ing forward to the future and all life
had to offer. However, he was to be
cruelly robbed of any sort of future
he could have imagined. Suddenly
he lost all sense of touch and spatial
positioning of his body from the neck
down, despite his motor systems
being unimpaired. Proprioception is
the unconscious perception of move-
ment and spatial orientation arising
from stimuli within the body itself,
and without this ability Waterman
found himself unable to walk, use
objects or go to the bathroom by
himself. Despite going from being
a healthy teen to bedridden in a
matter of days however, he was
determined to fight back and try
the strange case of
Ian Waterman

19. 18
to live as normal a life as possible.
His courageous determination to
carry on led to many studies into
his condition, books being written
about him and an illuminating BBC
documentary of his struggles - The
Man Who Lost His Body.
Being an unconscious function of the
body it is hard to imagine what crip-
pling damage a lack of propriocep-
tion can cause. Proprioception comes
from the nervous system as a whole,
with the input from nerves inside the
body. Even if we close our eyes we
have a sense of body position. Lying
in bed we know where exactly we
are in the bed. All our muscles and

20. 19
tendons, amongst many other parts
of the body, contain proprioceptors
which send positional information to
the brain. The brain then provides
us with a sense of our bodily orien-
tation and movement.
To give you an idea of how vital a
function proprioception is, without
proprioception we would be unable
to keep our eyes on the road as we
drive as we would need to focus
our attention on the position of our
arms on the steering wheel and feet
on the pedals. Such a simple task
as driving would become virtually
impossible. Take an even simpler
example; that of holding a can of
Coke. Without recep-
tors to help us feel
how much of a grip we
have on the can we
could easily crush it
by exerting too much
force.
The problem for
Waterman was that
although he could see
where his body was
and could instruct his
body to move, he was
unable to control it.

21. 20
If he was asleep at night he would
not have the positional sense or the
control that we have over our bod-
ies, purely because he could not see
the position of his limbs. Even when
the lights were on and he could see
where his body was, learning how
to control his muscles again using
only sight seemed like an impos-
sible task.
Proprioception is like a sixth sense
in that it is so vitally important for
our capacity to move and function in
the world. Without this propriocep-
tion we can have no inner sense of
posture or limb position and cannot
initiate or control movement.
ByThomas.haslwanter(Ownwork)[CC-BY-SA-3.0(http://creativecommons.org/licenses/
by-sa/3.0)orGFDL(http://www.gnu.org/copyleft/fdl.html)],viaWikimediaCommons

22. 21
Having been admit-
ted to hospital with
what doctors thought
was nothing more than
gastric flu, Waterman
found himself virtual-
ly cut off from his
own body. He
had contracted a
disease so rare
that the doctors
in Jersey, where
he lived, couldn’t
even diagnose it.
The future looked
grim, with doctors
expecting him to
need the use of
a wheelchair for
the rest of his
life. Even though
he wasn’t paralyzed as
such, he had no control
over his limbs and so
had no chance of being
able to walk.
However, Waterman’s
story is one of courage
in the face of adversity
and, not the type of per-
son to simply give-in;
he started to design his
own program of move-
ment practice to reclaim
his body. Constantly
repeating movement
patterns and focus-
ing on trajectories -
over the space of thir-
ty years - Waterman
created a new way of
controlling his body. By
having constant visual
contact with the envi-
ronment he learned to
manipulate objects and
today displays little to
no signs of his impedi-
ments. Every move
must be calculated in
advance and planned
out in a vigorous, math-
ematical way. However,
if he cannot see the
position of his limbs
then he cannot control
them, something that
he will never be able to
overcome.

23. 22
At Oddstock Hospital
the long road to recov-
ery started. Upon being
admitted Waterman
was full of anger at his
situation. But from this
anger sprang his great
determination.
Although he could
hardly stand up and
walk he was dogged
in his desire to not be
confined to a wheel-
chair for the rest of his
life. With his nerves
so badly damaged the
doctors had no real
way of helping him,
and if he wanted to
move again he would
have to bypass these
nerves and create a
new link between his
mind and his muscles.
Sitting up was the first
major problem, and he
likened it to falling over
as a child as he con-
stantly practiced how
to keep himself upright.
After these difficulties
he turned to a different
method.
Waterman began to
think that if he could
visualize moving his
muscles in his mind this
might have some affect
on his body. He tried
sitting up by controlling
and tensing his stom-
ach muscles, which
after much practice he
finally tasted success
and raised himself up
in bed. By investigat-
ing what muscles con-
trolled which specific
movement he set him-
self a punishing prac-
tice regime.
Without propriocep-
tion his movements
would never be auto-
matic again, but if he
could start building
connections between
mind and muscle it
started to look like
he may regain some
semblance of a nor-
mal life. Every action
would have to be plot-
ted. Every movement
would have to a care-
fully thought out and
executed. Waterman’s
tenacious attitude was
rewarded when after
one year he was able
to stand up for the first
time.
constantly repeating movement patterns and focusing on
trajectories - over the space of thirty years - Waterman
created a new way of controlling his body

24. 23
He realised that to have control
over his movements his eyes would
have to tell his brain what his limbs
were doing. Seeing his hands he
could control them, but if his gaze
wandered then his hands had a
mind of their own, knocking glasses
off tables or clumsily knocking into
things. With his resolute and serious
willpower he began learning to walk
again, looking at his feet all the time
to see their exact location. Most of
us might have been overjoyed at
this and start to build a new life
around our newly reacquired skills
of movement. But not Waterman.
He wanted to look and present him-
self as naturally as possible to oth-
ers. To do this, he would have to
master gesture. When we talk with
friends our body language and our
gestures are an integral part of the
conversation even though we may
not realise it. Waterman wanted
this back. It took years of practice
for him to capture gestures again,
although for the rest of his life they
would be more staged than natural.
Waterman’s ability to take control of
his gestures once more had piqued
the interest of numerous scientists

25. 24
and researchers, including Professor
David McNeil, who met Waterman
to find out if there was still any
kind of automatic process that was
enabling him to use gestures again.
McNeil asked Waterman to watch
a cartoon and later asked him to
describe it. During his description
Waterman used gestures to signal
some of the events in the cartoon.
After studying the video recording
of this description McNeil pointed
out that Waterman had an incred-
ibly well honed synchronization
between his hand actions and his
speech, with both being presented
simultaneously. This would seem to
suggest that gesture is an instinc-
tive part of language, controlled by
a part of the brain separate to that
of movement. To prove this McNeil
then asked Waterman to report the
events of the cartoon again, but
this time without being able to see
his body. If McNeil was right and
gesture is controlled by a different
area of the brain to movement then
Waterman should still be able to
present a synchronized description
using speech and gesture, regardless
of the fact he cannot see his hands.
Sure enough, Waterman’s timing
of gesture was still there, backing
McNeil’s theory. But without seeing
his hands his movements became
imprecise. Waterman’s visualizing
the gesture in his head helps him
express himself better, although not
perfectly. In gesture it seems that
there is a link between visualization
and movement, which helps link
our speech and our gestures, which
contributes to how Waterman has
recaptured his use of them.

26. 25
Ian Waterman speaks
very eloquently about
his condition, and in the
many interviews and
documentaries you can
find online, it is hard to
realise that he is suf-
fering from any prob-
lem at all, so controlled
is his movement.
Having mastered the
ability to walk again
we may forget how dif-
ficult it remains for him
to do everyday tasks as
he has no receptors to
help signal to him what
his hands are doing.
‘Whenever I do some-
thing with my hands
I am not just looking
and thinking about my
hands, I am also listen-
ing to sound’ he says. ‘I
can’t get anything from
my pocket because I
can’t feel it terribly
well…..often if some-
one passes me a cup I
would grab it awkward-
ly because I don’t have
the feedback of some-
thing coming from the
fingertips saying you’ve
actually picked up the
cup incorrectly.’
Waterman seems to
have retained a sense of
humour about aspects
‘Whenever I do something with my hands I am not
just looking and thinking about my hands, I am also
listening to sound’

27. of his situation, and
when asked about the
time he accidentally
touched a young nurs-
es’ breast he replied
smiling ‘I’ve only just
got over the litigation!
I was in hospital…. and
I’d made one of my bold
gestures…. I sat on the
edge of my bed and the
nurse was next to me
and I was making a ges-
ture pointing to another
part of the ward….and
my hand touched her
breast and she slapped
my face. I said what
was that all about and
she said well you just
don’t do that….you just
don’t go touching peo-
ple’s breasts like that!
Well I didn’t know that
I had! I didn’t notice
that was what I’d done.
I wouldn’t have mind
getting a slap around
the face if I’d gone for
it but I hadn’t!’ Perhaps
this is the most tell-
ing example of how a
lack of proprioception
can rob a person of
any affectionate con-
tact with another. How
could anyone who can-
not feel what his hands
are doing be able to
make love to another
or demonstrate caring
affection to others?
Waterman has con-
founded all the diag-
noses of the specialists
by discovering ways of
performing tasks that
should be impossible
for him. Something
as simple as holding
a fork to eat a meal,
which we do with ease
and no thought, was
a million miles away
from Waterman after
his diagnosis. But, with
years of single minded
effort he has regained
the use of his limbs
through his eyes. As
long as he can see
the limbs he wants to
move he can control
26

28. 27
them, and present an outward pic-
ture to those who don’t know him
that there is absolutely nothing
wrong with him. A huge amount
of conscious effort is required for
every movement but I am sure that
for Waterman it is worth it.
His amazing story not only dem-
onstrates courage in the face of
extreme adversity but also how
adaptive the mind and body can
be, with Waterman developing an
entirely new way of using his ner-
vous system. Often we can see
people who have crippling injuries
on the news or television, such as
losing a limb or mental faculties,
and we may pause to think how we
would cope if that injury befell us.
Usually, however, this brief moment
of contemplation passes and we
move on with our daily lives. But
having read Ian Waterman’s story,
can any of us really consider being
in his position? Would we have the
determination to tirelessly fight on
and on, or would we slump onto the
bed, cursing how unfair life is and
accept that we will never move our
body again?

29. 28
he human brain is shrinking for
the first time in our evolution-
ary history – for 2 reasons, one
positive and one wholly negative. In an
upright bipedal species with a narrow
pelvis (Homo sapiens), the brain has
reached its limit of size, because a larger
brain would not exit the pelvic canal at
birth. Therefore the only way that the
brain may continue to evolve and devel-
op is to become smaller and smarter, a
selective advantage that has been under-
way for around 15,000 years. In this very
short time span the human brain has lost
around 150mls – that is around 10% of its
volume.
HOMO INSAPIENS:
THE SHRINKING HUMAN
BRAIN
by
Mike McInnes
T

30. 29
Neurones constitute only about
15% of the human brain – the rest
of the brain’s volume is taken up by
cells known as glial cells. The word
‘glia’ derives from ‘glue’ - they were
until quite recently thought to be
simply a form of structural material
supporting neurones, or a form of
neural glue.
Recent science has discovered
that glial cells play major roles in
providing neurones with energy,
and have a large number of com-
plex roles in cerebral metabolism.
Indeed they are emerging as the
real smart brain cells – they moni-
tor and modulate neural transmis-
sion and regulate synaptic metabo-
lism. In addition they talk with one
another by calcium waves across
major brain regions – a kind of
cerebral broadband communication
system not dissimilar to smart-
phones. Professor Marion Diamond
at the University of Berkeley exam-
ined two vital regions in Einstein’s
brain, the prefrontal cortex and the
inferior parietal region. She found
a higher ratio of glial cells to neu-
rones compared with other brains
– an index of higher energy pro-
cessing and of advanced cerebral
communication. The ratio of glia
to neurones, as opposed to neu-
rone number, is now known to be
an index of evolutionary advance.
It seems there may be a selective
advantage to having a smaller,
smarter brain, and that Einstein
expressed this. However, modern
humans are now rapidly shrinking
the brain. This process has been
underway for at least a century
and has dramatically accelerated
in the past half century – since
we increased our consumption of
refined carbohydrates and sugars.
The glial cell is at the centre of
this toxic and devastating degen-
eration.
Albert Einstein and
the Glial Cell

31. 30
Short Circuiting the Brain.
The human brain has never before
been presented with chronic excess
energy in the circulation – its evo-
lutionary history is one of expo-
sure to food and energy famine.
The brain is highly efficient at pre-
serving its energy supply during
energy famines or starvation (as
in anorexia nervosa), but has not
evolved sophisticated mechanisms
to deal with chronic systemic ener-
gy excess – it simply suppresses
energy income and triggers a pro-
tracted short circuit (chronic/not
acute).
The key to understanding a range
of modern metabolic diseases, both
physiological and neurological, is to
be found in the glial cell. That is to
say that this cell, for which there
are around 6 for every neurone, is
ground zero in obesity/diabetes/
cardiovascular disease and a vari-
ety of neurological conditions such
as Alzheimer’s disease/motor neu-
rone disease/Parkinson’s disease
and multiple sclerosis.
The human brain affords the high-
est rate of energy consumption
known in nature. Indeed on a like
for like basis the human brain con-
sumes 22 times the energy of a
muscle cell (The Expensive Tissue
Hypothesis). At any moment there
is only around 1 gram of glucose
in the brain – sufficient for only a
few minutes. The circulation car-
ries only 5 grams so a fall in blood
glucose concentration (hypoglycae-
mia) is catastrophic for the brain
and will rapidly lead to a coma, if
not reversed. The cerebral glu-
cose pump – the glutamate/glu-
The Glial Cell and
Incipient Dementia

32. 31
tamine cycle -- is housed in glial
cells and is driven by the enzyme
glutamine synthetase. However
it is not the threat of hypoglycae-
mia that is the major metabolic
problem in modern humans – it
is hyperglycaemia, resulting from
consumption of excess refined car-
bohydrates and sugars. This leads
in turn to chronic hyperinsulinism.
Both hyperglycaemia and hyperin-
sulinism trigger and suppress the
cerebral glucose pump and there-
fore prevent glucose entry to the
brain – in other words they short
circuit the brain.
I have identified 6 primary mech-
anisms for this suppression and
there are several secondary mech-
anisms. This leads to chronic
cerebral glucose deprivation, to
increased cerebral hunger and to
consumption of the same foods
with the same result, and so the
cycle repeats again and again and
again...leading to increased risk of
obesity/diabetes and heart disease.
Note that the initiating and driving
influence is chronic cerebral glucose
deprivation or hunger, and that can
cause incipient dementia (not the
reverse as is usually assumed by

33. 32
the health professions). Of course
the cognitive impairments that fol-
low take years or decades to mani-
fest after the metabolic diseases
are expressed, but that in no way
reflects the true sequence of cau-
sation.
The eye is an outpost of the brain
and retinal glial cells provide an
excellent model of the effect of
hyperglycaemia and hyperinsulin-
ism on glial cells, and of cerebral
energy metabolism, via advanced
magnetic resonance imaging (MRI).
One of the least understood effects
of refined carbohydrates and sugar
consumption is the effect on hun-
ger. Indeed these foods make us
hungrier shortly after consumption
than before. Why?
In 2011 Seul Ki Lim and team
at Chonnam National University,
South Korea, examined the effect
of hyperglycaemia on retinal pig-
ment cells (these are classical glial
cells that pump glucose into the
retina – exactly as do cerebral
glial cells). They found that hyper-
glycaemia induces apoptosis by
suppressing the FAAH 1 enzyme
that degrades endogenous canna-
binoids, thus activating cannabis
CB1 receptors that suppress the
cerebral glucose pump – the glu-
tamate/glutamine cycle. In other
words, glucose as hyperglycaemia
acts as a cannabinoid and replicates
cannabinoid-driven ‘munchies’. In
this sense hyperglycaemia acts as
a cannabinoid signalling system,
deprives the brain of energy, and
upgrades the orixegenic (appetite)
hormones.
Is Glucose a
Cannabinoid?

34. 33
A 1985 study published in the journal Endocrinology by HS Grunstein et al
showed that hyperinsulinaemia suppresses glucose utilization in specific brain
regions.
In 2012 Lim and team in the Journal of Cell Physiology showed that hyper-
glycaemia induces apoptosis via CB1 activation through the decrease of FAAH 1
in retinal pigment cells.
In 1982 AL McCall et al, in the journal Proceedings of the National Academy
of Sciences, found that hyperglycaemia reduces glucose transport into the brain
by 45% by reduction of the GLUT hexose transporters: “... These results suggest
that chronic hyperglycaemia decreases the number of hexose carrier molecules
available at the blood-brain barrier. Such an adaptation could operate to decrease
the net flux of glucose into the brain during sustained hyperglycaemia...”
In 2011 in the journal Metabolic Brain Disease, MS Ola and others demon-
strated that insulin regulates glutamine synthetase in a time- and dose-depen-
dent fashion -- increase in insulin suppresses glutamine synthetase in retinal
glial cells.
In 2009 X Shen and G Xu in a study in the journal Current Eye Research
showed that the cytokine IL-1beta (which is increased by pathological microbiota
during excess glucose in the gut) suppresses glutamine synthetase in retinal glial
cells during conditions of high glucose concentration.
Hyperinsulinism is a major risk factor for Alzheimer’s disease via the insu-
lin degrading enzyme (IDE), which degrades both insulin and the amyloid-beta
peptide (a significant contributing influence in this degenerative disease). Excess
insulin would monopolise IDE and reduce the clearance and degradation of amy-
loid-beta peptide. In the absence of the ApoeE4 gene the mechanism would be
exclusively sugar driven. A 2006 study by WQ Qui and MF Folstein examined
this relationship and found: “It is intriguing to notice that both hyperinsulinaemia
and IDE gene variations are related to the risk of AD when the ApolipoproteinE4
(ApoE4) allele, the major risk factor of late-onset AD, is not present. Further
studies of the role of IDE in the pathogenesis of AD, which may uncover potential
treatment targets, are much needed.”

35. 34
Thus the twin toxic hypers of mod-
ern excess sugar consumption,
hyperglycaemia and hyperinsulin-
ism, separately and synergistically
suppress and inhibit glucose trans-
port into the brain via suppression
of the cerebral glucose pump – the
glutamate/glutamine cycle, known
as the iPump. Neither fats nor pro-
teins play any part in this patho-
logical process – indeed fats play
a positive role in cerebral glucose
metabolism via leptin, adiponectin
and fibroblast growth factor 9 (FGF
9).
The human retina consumes even
greater energy on a cell for cell
basis than does the human brain,
which is why it is the most vulner-
able tissue in any decrement in
energy supply. We know this from
any attack of hypoglycaemia; the
retina cells are the first cerebral
energy cells to respond – vision
is blurred and stars appear in the
visual field. Modern humans are
subject not to chronic energy defi-
cits but to chronic energy over-
load in the circulation, and here
again we observe that the first
tissue to register the sup-
pression of the retinal glu-
cose pump are the retinal
glial cells; glutamate, the
cerebral (retinal) hunger
signal, is not converted to
glutamine, and glutamate
is the most excitotoxic
amino acid in the brain;
excess accumulation of toxic
glutamate and damage to the
retina is expressed many years
before visual loss manifests.
Photo;ByDannyHopefromBrighton&Hove,UK(MyRightEyeUploadedbyPieterKuiper)
[CC-BY-2.0(http://creativecommons.org/licenses/by/2.0)],viaWikimediaCommons
The Hungry Retina
and Dementia

36. 35
Indeed, in Scotland,
a group of endocrinol-
ogy and metabolic sci-
entists are using reti-
nal impairment as a
model for dementia
associated with diabe-
tes – retinopathy. Here
again the problem is
that they consider type
2 diabetes as a major
risk factor for retinopa-
thy, and not that incip-
ient dementia of the
brain is the initiating
and driving causative
influence. They seem
to miss the correct
sequence of events –
from chronic cerebral
and retinal glucose
deprivation (hunger) to
increased consumption
of more high-energy
carbohydrate foods, in
a repeating cycle.
One of the most uni-
versal and pernicious
influences on modern
metabolic impairment
is that driven by the
myth that sleep is a low
energy protocol. This
has led to the notion,
promoted by diet gurus
and not opposed by
the health professions,
that it is unhealthy to
eat late. The impact of
this on metabolic health
has been profoundly
negative – it means
that after an early eve-
ning meal we retire to
bed with a depleted
liver, with insufficient
reserve energy supply
(liver glycogen) to pro-
vision the brain over-
night.
This does not acti-
vate quality sleep and
recovery physiology,
but rather chronic noc-
turnal metabolic stress
and increased risk of
metabolic syndromes
– dementias/obesity/
diabetes and heart dis-
ease; note the semi-
nal paper by Turek and
Bass in 2005:
Sleep Deprivation and
the Shrinking Brain
“ ... However, while there is a growing awareness
among some sleep, metabolic, cardiovascular,
and diabetes researchers that insufficient sleep
could lead to a cascade of disorders, few in the
general medical profession or in the lay public
have yet made the connection ...”: Sleepless in
America: A Pathway to Obesity and Metabolic
Syndrome.

37. 36
provision the
brain via the
liverpriorto
sleep, and
that sleep
d e p r i -
v a t i o n
increases
levels of NSE
and S-100B in
healthy young
men – indicative of
loss of cerebral volume.
Professor Eve
van Cauter
at Chicago
University has
p i o n e e r e d
studies that
confirm poor
quality and
foreshortened
sleep as one of
the most potent
driving forces of mod-
ern metabolic impair-
ments and energy dys-
regulation. Professor
Christian Benedict of
Uppsala University has
shown that sleep is a
high
energy system with
respect to the human
brain, that chronic noc-
turnal metabolic stress
results from failure to
sleep is a high energy
system with respect to
the human brain

38. 37
The tragedy of mod-
ern metabolic impair-
ments and a rapid loss
of cerebral volume over
the past half century
has been the direct
result of influence by a
small number of power-
ful scientists who have
influenced negatively
the understanding of
the causes and mecha-
nisms of a range of
degenerative diseases –
obesity/diabetes/heart
disease, and demen-
tias. From the 1920s
through the 1970s the
major figure in diabe-
tes research was Elliot
Joslin and his textbook
on diabetes was man-
datory. Joslin held the
view that diabetes was
a fat-driven condition
and that sugars were
not the causative agen-
cy, in spite of the knowl-
edge that incidence of
this condition dropped
dramatically during
both world wars, when
sugars were not read-
ily available. During
the 1950s Ancel Keys,
a brilliant American
physiologist who pio-
neered research into
nutrition and devel-
oped the famous US
K-Rations for use by
US servicemen during
WW2, developed the
theory that fats and
cholesterol were the
driving force of cardio-
vascular disease, and
that sugars were not
significant. This dou-
ble theory was then
extended to include
obesity and metabol-
ic syndrome, and this
remains the view to this
day. Any researchers
who opposed this view
Metabolic Stalinism: A Century of
Lost Opportunity
K Ration Dinner Kit

39. 38
(which has a long and
illustrious history), was
suppressed, and it is
only now, in the second
decade of the 21st cen-
tury that this view has
resurfaced. The period
since the Senate hear-
ing saw the inclusion
of sugars in processed
foods at the expense of
fats, and the incidence
of obesity/diabetes and
dementias exploded.
were marginalised or
attacked as unscien-
tific. A cardiologist,
Robert Atkins, who,
along with several other
groups of research-
ers, had successfully
treated his cardiac and
obese patients with
a low sugar/low car-
bohydrate diet, was
venomously attacked;
in the Senate Select
Committee on Nutrition
andHumanNeedinApril
1973, Senator Charles
Percy of Illinois went
on record, on behalf of
Fred Stare, a nutrition-
ist at Harvard, saying:
“The Atkins diet is non-
sense...the author who
makes the assertion
is guilty of malprac-
tice”. Thus the theo-
ry that refined sugars
may be a major cause
of metabolic illness
Is it possible to refer
to a condition of foetal
dementia?Gestational
diabetes, a growing
problem, is a condition
in pregnancy where
the mother devel-
ops a form of type 2
diabetes in the third
trimester. The foe-
tal circulation is then
subject to a combina-
tion of hyperglycaemia
and hyperinsulinism.
At birth the infants are
often large (macroso-
mic) and they are at
increased risk of obesi-
ty/diabetes and meta-
bolic syndrome.
Gestational Diabetes

40. 39
In September 2013 a study at the
University of Copenhagen showed
that sugars are vital signalling co-
factors in the formation of the brain
via a MicroRNA system known as
mir-79 (the human equivalent is
mir-9). If the foetal cerebral glu-
cose pump is suppressed,
as it would be in the
hyperglycaemic/hyper-
insulinic environment
of the foetal circulation,
the outcome would be
impaired formation of the
new brain and incipient
dementia. Recent stud-
ies point to exactly this
conclusion – a study by
the Universities of Bristol
and Glasgow found:
“ ...Offspring of moth-
ers with existing diabe-
tes had a threefold risk
of achieving no GCSEs
graded A-C, whilst off-
spring of women with
gestational diabetes had,
on average, a five point lower IQ
compared to offspring of women
with no diabetes or glycosuria ...”
By the third trimester of gesta-
tional diabetes all of the organs
with one exception are already fully
formed – not
so the human
brain, which
continues to
develop and
grow beyond
birth and into
the second
decade of
life.
Let the alarm bells ring in every
home, nursery, primary school,
secondary school, college, univer-
sity and all centres of learning and
education. It will not be lost on
the reader that the environment
in which the foetus is suspended,

41. 40
characterized by hyperglycaemia
and hyperinsulinism, the twin toxic
hypers that inhibit glucose trans-
fer into the brain, is not radically
different to the diobesic food and
carbohydrate charged matrix which
all of us modern urban humans
inhabit. The foetus of gestational
diabetes shows us that the dev-
astating consequence of chronic
cerebral glucose deprivation is an
obese infant that is cognitively
impaired – a sequence that chal-
lenges the standard view of mod-
ern dementia – and that metabolic
conditions such as obesity and dia-
betes increase risk of dementias
and Alzheimer’s disease. We noted
cognitive impairments in infants of
gestational diabetic mothers; we
also find cerebral volume and IQ
deficits in childhood obesity and in
ADHD.
Numerous government interven-
tions into the crises of obesity/
diabetes and heart disease over
the past half century have failed
to induce any significant behaviour
changes in the general population,
in spite of huge media interest and
coverage. Indeed the incidence of
dementia/diabetes and obesity is
rapidly growing.
Tragic as may be the physiologi-
cal and neurological conditions that
plague modern urban humanity,
they may be masking un underlying
and more incipient and profound
degeneration, that of the shrink-
ing human brain – the organ that
makes us uniquely human and that
gave rise to consciousness, lan-
guage, writing, agriculture, civili-
sation, law, literature, art, culture,
music, science, technology and phi-
losophy. In spite of an explosion
in information technology our chil-
dren are advanced and advancing
on the road to cognitive and neural

42. 41
degeneration and dementia via the
toxic combination of sleep depri-
vation and sugar-driven suppres-
sion of the cerebral glucose pump
(iPump); might they become a new
offshoot of Homo sapiens – Homo
insapiens?
Perhaps now, at last, we have the
opportunity to promote a public
discussion around the question of
whether our excess consumption of
sugars and refined carbohydrates
is shrinking the human brain in
ourselves, in our children, and in
the offspring of our children. May
we open a new era in human nutri-
tion and health?
There are two very simple and cost
effective strategies that may halt
or reverse this process.
We reduce consumption of refined
sugars and carbohydrates, an
opportunity that is now available
since a new public discourse, led by
researchers such as Robert Lustig
and Gary Taubes, has opened about
the true role of sugars in metabolic
impairments.
We forward-provision the brain in
the period prior to sleep after
an early evening meal, reducing
chronic nocturnal metabolic stress
and the risk of all the metabolic
conditions.
Paradoxically, honey is the Gold
Standard food for this purpose.
In the west we view sleep as a
low energy event, a myth driven by
diet gurus which is not only unsci-
entific but positively dangerous.
As a result we retire to bed with a
depleted liver, and activate not qual-
ity sleep and recovery physiology,
but rather chronic nocturnal meta-
bolic stress and increased risk of
metabolic syndrome, every night of
our lives. By selectively restocking
the liver prior to sleep we forward-
provision cerebral energy reserves,
reduce chronic nocturnal metabolic
What Can We Do?
Bariatric Sleep

43. 42
stress, promote quality sleep and
recovery physiology, reduce the
risk of metabolic syndrome, and
improve memory and learning dur-
ing REM sleep. Sleep is a bariatric
event, in so far as recovery physi-
ology utilises adipose fats drawn
from the circulation; exercise uses
a mix of adipose and muscle fat.
Eight hours of quality sleep and
recovery physiology may oxidise 5
times the body fat of a 90-minute
exercise session (Dr Michael Mosley
in a BBC study – 49 grams versus
9.5 grams).
In a study presented in 2009
at the 23rd Annual Meeting of
the Associated Professional Sleep
Societies, LLC Seattle, Washington,
a group led by Professor Sergio
Tufik at the University of Sao Paulo,
Brazil, measured weight loss in
healthy young men, and found
that weight loss during sleep was 3
times that of awake bed rest, and
that the highest level measured
was during slow wave (recovery)
sleep. No explanation was offered
for the significant differences, but
recovery physiology during sleep is
an energy expensive enterprise, is
dependent on sleep, and is exclu-
sively sourced from adipose fat.
This important study seems to
have slipped below the radar of the
metabolic science community, but
underpins the perspectives of this
project.
Post bariatric surgery, the met-
abolic parameters correlated to
weight gain and diabetes (hyper-
glycaemia/hyperinsulinism), are
reversed in advance of weight loss.
In other words these parameters
are not caused by weight gain/dia-
betes; they are the driving forces
of these conditions.

44. 43
Professor Achim
Peters, leader of the
Selfish Brain Group at
Lubeck, has pioneered
the theory that the
cause of weight gain
and metabolic impair-
ments is chronic cere-
bral glucose depriva-
tion – or chronic unre-
solved cerebral hunger.
Professor Christian
Benedict at Lubeck
has found that noctur-
nal metabolic stress is
directly related to com-
promised cerebral ener-
gy supply. Professor JJ
Guinovart at Barcelona
has found that restora-
tion of hepatic glyco-
gen reserves reduces
the conditions of mod-
ern metabolic impair-
ment and the causative
agencies of metabolic
syndrome -- hypergly-
caemia, hyperphagia
and the enzymes of
gluconeogenesis.
In the Southern
Mediterranean, for
thousands of years,
the population retired
to bed after a healthy
evening meal, around
10-11pm, with a
restocked liver, and
activated quality sleep
and recovery physi-
ology every night in
life. This is the most
neglected aspect of the
Mediterranean diet;
timing is a key influ-
ence in all metabol-
ic events. Since they
have recently aban-
doned this practice,
the fastest growing
area for metabolic syn-
drome is in that region.
They (unconsciously)
practiced the principle
of forward-provisioning
the brain via the liver
prior to sleep. In the
west it is not likely that
the universal culture of
the early evening meal
will be altered any time
soon. Thuswecanadopt
the strategy enjoyed
in the Southern Med
by selectively replen-
ishing the liver prior
to sleep. Honey is
the Gold Standard food
Why Honey?

45. 44
for this purpose (with-
out digestive burden),
after an early evening
meal. Honey is a potent
anti-diabetic food, and
since it is the twin toxic
hypers (glycaemia/
insulin) associated with
a pre-diabetic state
that drive our meta-
bolic ailments – physi-
ological and neurologi-
cal -- honey has been
selected to restock the
liver every night in life
prior to sleep.
Honey restocks the
liver via several mecha-
nisms including fructose
liberation of glucoki-
nase/ increased glyco-
gen synthase/reduced
phosphorylase, and
suppression of gluca-
gon. Honey activates
the honey/insulin/mel-
atonin (HYMN) Cycle,
promoting sleep and
recovery physiology.
In addition Honey
stimulates a cascade
of beneficial hormones
– GLP-1/free IGF-1/
leptin. Insulin is stim-
ulated via the HYMN
Cycle, promotes mela-
tonin and is then sup-
pressed and controlled
via melatonin and
growth hormone – a
lovely poetic negative
feedback mechanism
available only during
the dark phase of the
circadian cycle. No
other food can match
honey in this respect.
It is possible to estab-
lish nocturnal global
energy homeostasis,
without pharmaceu-
tical intervention, by
forward-provisioning
cerebral energy in the
liver via honey; this
leads to activation of
the HYMN Cycle and the
promotion of a cascade
of nocturnal hormones
that facilitate cerebral
uptake of glucose via
recalibration of the
glutamate/glutamine
cycle (iPump), thus
reducing chronic noc-
turnal cerebral hunger
and chronic nocturnal
metabolic stress. This
in turn promotes qual-
ity sleep and recov-
ery (fat burning) phys-
iology, and improved
learning and memory
during REM sleep. In
this sense we may state
Nocturnal Energy
Homeostasis:
The Holy Grail of Modern
Metabolic Impairments

46. 45
that the optimally func-
tioning iPump is the
engine of quality sleep
and recovery physiol-
ogy, and therefore of
nocturnal fat metabo-
lism.
Reduced consumption
of refined sugars and
carbohydrates, com-
bined with honey taken
prior to sleep every
night, after an early
evening meal, may
constitute the single
most significant and
cost effective contribu-
tion to public health
and learning in several
generations.
(c). Mike McInnes
Mike McInnes is a retired Scottish pharmacist with a special interest in cerebral
energy metabolism and its modern impairments.
Mike, who lives in Edinburgh, has written The Honey Diet – a popular book on weight
control that introduces the public to the glial cell and to chronic cerebral glucose
deprivation as the driving force of obesity, via suppression of the cerebral glucose
pump (iPump), and to sleep deprivation as a cofactor in weight gain.
The Honey Diet is published by Hodder and Stoughton, Imprint of Hachette. January
2nd 2014.
Aiello LC, Wheeler P. The Expensive Tissue Hypothesis:
The Brain and the Digestive System in Human and Primate
Evolution. Current Anthropology, Vol.36, No 2(Apr.,1995),
pp. 199-221
Baker LD, Cross DJ, Minoshima S, Belongia D, Watson
GS, Craft S. Insulin resistance and Alzheimer’s-like
reductions in regional cerebral glucose metabolism for
cognitively normal adults with prediabetes or early type 2
diabetes. Arch Neurol. 2011 Jan;68(1):51-7.
Bass J, Turek FW. Sleepless in America: A Pathway to
Obesity and the Metabolic Syndrome? Arch Intern Med/
Vol 165, Jan 10, 2005.
Bellisle F. Infrequently asked questions about
the Mediterranean Diet. Public Health Nutr. 2009
Sep;12((A):1644-7
Benedict C, Kern W, Schmid SM, Schultes B, Born J,
Hallschmid M. Early morning rise in hypothalamic-pitu-
itary-adrenal activity: a role for maintaining the brain’s
energy balance. Psychneuroendocrinology. 2009 Apr;
34(3):455-62.
Convit A Excellent PP on impact of obesity and type
2 diabetes on brain structure and function. Again the
causation is posited as from obesity/type 2 diabetes to
cognitive impairment – the reverse of the true sequence
of events in modern sugar driven suppression of the cere-
bral glucose pump: http://www.iom.edu/~/media/Files/
Activity%20Files/Children/NeuroEffectsChildren/Convit.
pdf
Denton M. University of Otago, New Zealand Excellent
description of the colossal metabolic rate and energy
demand of the retina – 3 times that of the cerebral
cortex: http://www.arn.org/docs/odesign/od192/invert-
edretina192.htm
“...The mammalian photoreceptor is capable of generat-
ing electrical response to a single photon of light -- the
minimal bundle of light energy. This remarkable capacity
is dependent on a complex catalytic cascade consisting
of a series of enzymes in the photoreceptor cell which
massively amplifies the initial signal -- the absorption
by a single rhodopsin molecule of a single photon. This
amplification process requires vast quantities of metabolic
energy and consequently the photoreceptor layer has one
of the highest metabolic rates of any known tissue. The
oxygen consumption of the mammalian retina (per gram
REFERENCES

47. 46
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Ding J, Patton N, Deary IJ, Strachan MW, Fowkes FG,
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Oct;130(4):e856-64.

48. by
Tania Dey
website
www.publicationslist.org/tania_dey
An interview with
Joseph Davidovits
Geopolymer research:
G eopolymer is a sustainable cement
material. It is amazing how geopolymer
research has evolved and advanced in the
last several years. Joseph Davidovits is a
pioneer in this area. It is interesting to note
that his work was inspired by archeological
specimens. This interview-based article will
throw some light on his research work and
obstacles, the state-of-the-art progress in
geopolymer technology, and the thoughts
and suggestions that he has to offer.
47

49. 48
Professor Joseph Davidovits
is famous for his pioneering work on geopolymers.
He is an internationally renowned French Materials
Scientist and Archeologist, who was honored by
French President Jacques Chirac with one of France’s
two highest awards, the “Chevalier de l’Ordre National
du Mérite”, in November 1998. Davidovits has a
French Degree in Chemical Engineering and a German
Doctorate Degree (PhD) in Chemistry, is professor
and founder of the Institute for Applied Archaeological
Sciences in Barry University, Miami, Florida (1983-
1989), Visiting Professor in Penn State University,
Pennsylvania (1989-1991) and Professor and Director
of the Geopolymer Institute, Saint-Quentin, France
(1979-present). He is a world expert in modern and
ancient cements, as well as in geosynthesis and man-
made rocks, and the inventor of geopolymers and the
chemistry of geopolymerization. He has authored/
co-authored more than 130 scientific papers and con-
ference reports, holds more than 50 patents and has
written the first reference book on geopolymer science,
“Geopolymer Chemistry and Applications”.
What is a Geopolymer?
A geopolymer is a sustainable alternative to conven-
tional Portland cement, having lower carbon dioxide
emissions during manufacture, greater chemical and
thermal resistance, and better mechanical properties
both at ambient and extreme conditions. Metakaolin
is commonly used as a starting material for the labo-
ratory synthesis of geopolymers and is generated by
thermal activation of kaolinite clay. Geopolymers can
also be made from other sources of pozzolanic materi-
als, such as volcanic ash, fly ash, slag, pumicite etc.
Geopolymerization is a multi-step process and the final
product is an inorganic polymer network of highly-coor-
dinated three-dimensional aluminosilicate gel.

50. 49
It was partly chance.
My work as a research
chemist really start-
ed in 1972. My tar-
get was the creation of
fire-resistant polymer-
ic materials. For two
years, in my labora-
tory in Saint-Quentin,
Picardie, France, I
worked essentially on
the chemical reactions
with clay minerals.
Nobody took any notice
of us and with my team
we developed the first
applications, for the
building industry. But
in June 1974, I real-
ized that what we were
producing were materi-
als that are very close
to natural cements,
such as rocks based
on feldspars, the feld-
spathoids. One day, as a
joke, I asked my scien-
tific partners, two well
known French miner-
alogists at the Muséum
T.D. Dr. Davidovits, I have read that you went all the way to the Giza pla-
teau to study the Egyptian pyramids and in your books Why the pharaohs
built the Pyramids with fake stones and The Pyramids: an enigma solved
you have presented a captivating and surprising view of how the pyramids
were built, supported by archeology, hieroglyphic texts, scientific analy-
sis and religious and historical facts. Your theory was that the stones of
the Great Pyramid were not quarried or carved from huge blocks hauled
on fragile ramps, but made on site from re-agglomerated stone (a natu-
ral limestone treated like a concrete) cast in moulds, somewhat similar to
modern cement and other artificial building techniques. You first aired this
intriguing theory, which made you famous, in 1974, crippling the conven-
tional Egyptology. What prompted you to undertake this unusually remark-
able study? What was the catalyzing factor?
Dr. Davidovits

51. 50
Joseph
Davidovits
posited that
the blocks
of the Great
Pyramid are
not carved
stone but
mostly a form
of limestone
concrete or
man-made
stone

52. 51
T.D. Did you have to face any controversy or criticism from the scientific
community, while trying to establish your point?
I presented my ideas
at several International
Egyptology conferenc-
es: Grenoble, France
(1979),Toronto,Canada
(1982), Manchester, UK
(1984), Cairo, Egypt
(1988). They generat-
ed great debates, sev-
eral articles in news-
papers, yet no hostil-
ity. However, after the
publication of my book
for the general public,
(The pyramids: an enig-
ma solved, 1988, New
York), several materials
scientists sent me a let-
ter in which they asked
me to stop this research
because “I was jeop-
ardizing my career”.
In 1989, an eminent
American Egyptologist
wrote a startling review
stating that I had falsi-
fied the scientific data
(my chemical analysis),
etc. My friends want-
ed me to go to court
because of these insults.
I answered: “No, this is
part of the game in sci-
ence. A new theory is
always severely chal-
lenged. This has always
d’Histoire Naturelle in
Paris, what would hap-
pen if we buried in the
ground a piece of the
product that we were
synthesizing in the lab-
oratory at the time (our
first geopolymer mate-
rial), and an archae-
ologist discovered it
3000 years later? Their
answer was surprising:
the archaeologist would
analyze this object dis-
interred from the gar-
den of a ruin in Saint-
Quentin, and the analy-
sis would reveal that
the nearest natural out-
crop of the stone was
in Egypt in the Aswan
region! It was on that
day that I realized that
if I did not reveal the
synthetic nature of the
product we had devel-
oped, it would be taken
for natural stone.
Dr. Davidovits

53. 52
The only and major
shortcoming is its nov-
elty. It is too young.
Geopolymer cement
was invented only 30
years ago (Portland
cement, 150 years ago).
Since liability claims for
construction materi-
als require at least 20
years durability war-
ranty, everybody should
understand that, as far
as the applications for
the construction indus-
been the case in the
past, and remains true
in our present time.”
One famous American
geologist wrote a paper
in 1992 that states:
“... we feel it is the
duty of a profession-
al geologist to expose
this egregiously absurd
archeological theory
before it becomes part
of entrenched pseudo-
science... We believe
that if Davidovits had
any understanding of
basic geologic prin-
ciples and understood
the implications of sim-
ple geological evidence
at Giza, he would have
realized that this geo-
polymer theory has no
basis in fact... We have
also shown how geolog-
ic common sense can
destroy archaeologi-
cal quackery, but not,
unfortunately, before it
has enjoyed widespread
publicity among the
gullible and sensation-
minded... The geopoly-
mer theory is defunct;
we still remain in awe of
the enigma of Egyptian
skill and engineering.”
Ironically, his study was
made on stone sam-
ples taken from natural
limestone that was part
of the bed-rock upon
which the pyramid was
constructed.
T.D. There is an increasing trend in science and technology to go for
greener materials, and geopolymer is certainly an example of a sustain-
able cement material. But are there any shortcomings? How well does it
perform in comparison to conventional cement materials?
Dr. Davidovits

54. 53
T.D. Volume change is the most detrimental property of cement, causing
shrinkage which affects long-term strength and durability. Any suggestions
specific to geopolymers, about how to overcome this problem?
To understand the
long-term durability
issues on geopolymers
we may make a paral-
lel with glass technolo-
gies and science. It has
been recognized for a
long time that there is
at least a rough correla-
tion between the dura-
bility of glasses and the
number of non-bridging
oxygens (-Si-OH or -Si-
O− Me+ groups). The
results of this study
reveal several points
that may be transferred
to geopolymer struc-
tures. One is that the
addition of aluminum
to a silicate framework
generally increases
durability. The impor-
tance of non-bridging
oxygens on glass dura-
bility is that non-bridg-
ing oxygens provide
a point of attack on
a molecular scale for
protons or water mole-
Dr. Davidovits
try are concerned, this
is a major drawback.
This explains why geo-
polymer applications
were first developed in
other fields and niche
markets, which do not
require these types of
codification.
Geopolymer Moulds

55. cules. Similarly in geo-
polymers, it is the high-
ly polymerized regions
that are resistant to
chemical attack and
offer long-term stabil-
ity, whereas the less
polymerized regions
with Al-OH or Si-O-Al-
O-Si- species are prone
to shrinkage and leach-
ability.
Pore solution analysis
is worthwhile for mono-
meric/dimeric gels like
those found in Portland
cement or alkali-acti-
vated slag for example.
It is not valid for the
investigation of any fully
condensed geopolymer
matrix. It may be used
to show that geopo-
lymerization, i.e. net-
working of the frame-
work, is not complete.
Instead of pore solution
analysis, we measure
the pH of the materi-
al and perform Nuclear
Magnetic Resonance
spectrometry (NMR) for
silicon (Si) and alumini-
um (Al).
As for alkali-aggregate
reaction, I published
my first study on this
topic 20 years ago, in
Ceramic Transactions,
Vol.37,(1993),Cement-
Based Materials:
Present, Future, and
Environmental Aspects.
pp 165-182, titled:
Geopolymer Cements
to Minimize Carbon-
dioxide Greenhouse-
Warming. The dem-
onstration was clear.
Geopolymer materi-
al does not generate
any deleterious alkali-
aggregate reaction.
54
T.D. In the context of durability of geopolymer materials, how well char-
acterized are the gel pores, cement hydration and alkali-aggregate reac-
tion? What improvements can we, the scientists, make in order to further
optimize the product?
Dr. Davidovits

56. 55
T.D. What do you consider to be some of the greatest challenges in this
field of research?
T.D. What, in your opinion, are some of the emerging applications that will
gain interest in the next few years?
To get those scien-
tists working in the field
of geopolymer cement
and who had a Portland
cement chemistry back-
ground to shift away
from hydration-based
reasoning towards geo-
polymer terminology
and chemistry.
This is not easy because
it requires from them
that they go back to
school.
I always make a
clear distinction
between Geopolymer
Technologies and
Geopolymer Cement
applications. With
respect to Geopolymer
Technologies, we should
see the commercial-
ization in the field of
pharmaceutical applica-
tions, high-tech ceram-
ics, paints and coat-
ings, and heat-resistant
composite materials. As
for the cement field, I
guess that the newly
discovered ferro-sial-
ate geopolymer cement
type will provide the
solution for mass pro-
duction worldwide (see
at www.geopolymer.org
the News dated August
2012 on “red geopoly-
mer cement”).
Dr. Davidovits
Dr. Davidovits

57. 56
Balanced chemical equation showing geopolymer synthesis starting with
metakaolin, MK-750

58. 57
I once visited a cement
plant in South Africa
and was struck by the
local conditions rul-
ing the manufacture of
Portland cement there.
The plant was located
very close to the market
(the cities of Pretoria
and Johannesburg) but
the geological resourc-
es, namely limestone,
had to be extracted ca.
100 km up north and
transported by train to
the plant. On the other
hand, the local geology
was perfectly adapted
for the manufacture of
geopolymer cement.
Other regions in the
world are experiencing
the same situation. In
other words, geopoly-
mer cement is a com-
plementary material to
Portland cement.
Well, you should con-
sider the geopolymeric
terminology that implies
the presence of a poly-
meric network or, at
least, of high molecular
weight molecules. This
is not the case for regu-
lar calcium phosphate
Dr. Davidovits
Dr. Davidovits
T.D. One North American geopolymer application is a blended Portland-
geopolymer cement known as Pyrament® (patented in 1984) for rapid
pavement repair. Shall we consider geopolymer as a supplementary or
rather a complementary material to cements and concretes, or does it
really have the potential to replace the conventional Portland cements on
a large scale?
T.D. As a research scientist, I have worked on calcium phosphate cement
(another sustainable cement material) derived from calcium silicate-based
natural minerals, but not having aluminium as a primary constituent.
Would you classify this kind of material as a geopolymer?

59. 58
Yes, there are several.
Most of them needed
several years in R&D
before being ready for
commercialization and
industrialization. This is
typical for any develop-
ment of new materials.
For example, one million
geopolymer pavement
bricks (roughly 3,000
tons) were manufac-
tured in 2012 in India
under the supervision of
Dr. Sanjay Kumar from
the Council of Scientific
& Industrial Research,
Jamshedpur, India. I
met with Dr. Kumar in
2005. The development
involved major compa-
nies such as Tata Steel.
They are planning to
have 10 commercial
installations in India
in the coming 5 years.
An Australian compa-
ny ROCLA, one of the
pioneers in geopolymer
precast concrete for
commercial production,
claimed in Dec. 2011
to have achieved “the
‘world first’ production
run of geopolymer con-
crete”. It was undertak-
eninCanberra,involving
the production of 3,000
components, totaling
2,500 tons. I had vis-
ited ROCLA in 1999.
In 2011, in Germany,
France and the UK, the
global chemical com-
pany BASF launched a
geopolymer joint grout
named PCI-Geofug®.
Another Australian com-
hydrates such as brush-
ite, CaHPO4.2H2O,
which results from the
reaction of phosphor-
ic acid, and wollaston-
ite, CaSiO3. On the
other hand, aluminum
phosphate cements
and binders are genu-
ine geopolymers, with
high-macromolecular
networks.
Dr. Davidovits
T.D. It seems that none of the potential applications has advanced beyond
the development stage (correct me if I am wrong), but the durability attri-
butes of geopolymers make them attractive for use in high-cost, severe-
environment applications such as bridges. Can you name a few industries
that are actively producing geopolymers for construction?

60. 59
pany, Rockwool, a man-
ufacturer of insulating
material, has found a
way to capture, recy-
cle and re-use tons of
waste generated from
the manufacturing pro-
cess, using a geopoly-
mer to bind the waste
into briquettes. The
briquettes of geopoly-
mer material are fed
back into the furnace
and made into fibers
for Rockwool insulation.
The plant has been run-
ning this geopolymer
process since 2007, yet
the company made it
public only in December
2011, 4 years later. But
you are right in stating
that no bridge has, so
far, been built in geo-
polymer concrete.
Prof. Joseph Davidovits visiting India in 2010, to expand research collaboration

61. T.D. I know you are very much active with a range of events in the
Geopolymer Institute. Your institute regularly organizes tutorials, camps,
conferences and so on, not to speak of the widespread research network-
ing that you have established to date. Any upcoming events that you would
like to make us aware of?
My archaeological
research is attracting a
lot of interest in some
developing countries.
We are presently pre-
paring a partnership
with the major build-
ing institution in Egypt,
namely HBRC, Cairo,
the Egyptian Housing
& Building National
Research Center. The
target is to transfer our
knowledge of ancient
building materials (pyr-
amid stone and the like)
for the development of
sustainable construc-
tion materials. We have
a timing problem due to
the political situation in
that country. We hope
to be able to start in
the coming year.
Dr. Davidovits
60

62. 61
T.D. As a lab instructor, recently I got a chance to introduce the topic of
geopolymers and ceramics to an international group of students. Students
made their own geopolymer samples from fly-ash, prepared moulds and
characterized them by FTIR using KBr pellets (for structural composition),
by DSC of fresh mixture (to obtain heat of hydration), by Instron machine
using ASTM standards, after wet, dry and wet-dry processing (to measure
compressive strength) and so on. The student feedback was overwhelm-
ing; they asked thought-provoking questions and became more and more
interested. What message do you have for student researchers like them?
Although geopolymer-
ization does not rely on
toxic organic solvents
but only on water, it
needs strong alkalis
such as sodium hydrox-
ide (NaOH) that may be
dangerous, and there-
fore requires some safe-
ty precautions. Because
I was a chemist, when I
started the research on
geopolymers I decided
to select alkaline condi-
tions that could be clas-
sified as “mild”, i.e. user-
friendly. Unfortunately,
this was not followed
by other engineers
and scientists involved
in the development of
geopolymeric systems.
Apparently, these sci-
entists never put their
finger into their reac-
tion mixture, which
has a SiO2:Na2O ratio
of 0.20 or 0.60. The
problem is that practi-
cally all papers dealing
with “alkali-activated”
cements describe reci-
pes that are not user-
friendly. To recommend
them for regular build-
ing and civil engineer-
ing operations, where
people are working with
barehands,isnonsense.
This could explain why
geopolymer cement
technology has not
reached mass applica-
tions and remains con-
fined to high-tech niche
markets. So my mes-
sage is: develop “user-
friendly” systems.
Dr. Davidovits

63. 62
T.D. Any other aspect that you would like to address for the scientific
reader community, something that may not have been covered in my
questionnaire?
Dr. Davidovits
My friend Dr.
Waltraud Kriven from
Illinois University
once proclaimed:
“Geopolymers, more
than just cement”.
Indeed, when, in 1979,
I introduced the geo-
polymer concept and
the related terminol-
ogy, I had no idea
about cement. But in
the mind of cement
scientists, geopolymer
is only cement and
therefore they try to
understand its materi-
al properties with their
Portland cement back-
ground, replacing cal-
cium (Ca) with sodi-
um (Na), which is not
appropriate. To better
Dr. Tania Dey posed with her lab students during
Instron compressive strength measurement of
geopolymer moulds

64. 63
explain these chemical
processes and the resul-
tant material properties
requires a major shift in
perspective, away from
the classical crystalline
hydration chemistry of
conventional cement
chemistry. To date this
shift has not been well
accepted by practitio-
ners in the field of alka-
li-activated cements
who still tend to explain
such reaction chemistry
in Portland cement ter-
minology. On the other
hand, materials scien-
tists working on high-
tech ceramics and com-
posites understand the
importance of the geo-
polymer terminology
and use it with success
in numerous scientific
projects worldwide.
T.D. Dr. Davidovits, many thanks for your time and for this insightful discus-
sion. I hope the scientific community will greatly benefit from your work,
thoughts, and suggestions. Interested readers may wish to go through
your books and website (www.geopolymer.org) for further details.
The author, Dr. Tania Dey, is a research scientist by profession. She earned her PhD
in 2002 and since then has worked in the area of colloids, polymers, nanostructures
and advanced materials. Her work has been multi-disciplinary with diversified appli-
cation potential. The author can be reached at: taniadey.asp@hotmail.com
Website: http://publicationslist.org/tania_dey

65. 64
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