Ispectrum magazine 06

ISPECTRUM MAGAZINE

Issue 06/March - April 2014

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

CONTENTS Features

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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

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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

editorial 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 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. Thanks Tania!

Enjoy your reading!

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Mado Martinez Editorial Director

Ispectrum magazine

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 : Š Billy Benavides / neusenz.com , commons.wikimeadia.org, morguefile.com, sxc.hu

www.ispectrummagazine.com admin@ispectrummagazine.com +44 7938 707 164 (UK)

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AUTONOMIC BALANCE IS THE KEY TO HEALTH

by Dr. Dennis K. Crawford website www.crawfordnaturalhealthcenter.com

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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 differently to diet, supplements, and even exposure to pathogens and toxins.

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 testing for one’s ANS status and then utilizing therapies to bring it into homeostasis?

Perhaps because in a pharmaceutically oriented symptom based health care system as exists in the U.S and 3

The ANS is primarily two sub systems. One part is the parasympathetic 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 parasympathetic system is located in the brainstem consisting of four cranial nerves, and the sacrum consisting of three sacral nerves.

First, let’s define the ANS and explore a basic explanation of how it functions.

From there, I’ll concentrate on factors that influence the ANS, how to test for imbalances in a functional medicine paradigm, and therapies to bring it into balance.

Defining the ANS The ANS is the part of the nervous system that regulates metabolic processes beyond conscious control. It does so automatically. 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 cardiac regulation, vasomotor activity, respiration, and some reflex actions like coughing, sneezing, and swallowing. Just above the brain stem is the hypothalamus which receives ANS input and acts as the conductor for automatic functions.

There are sensory and motor components to the ANS. Sensory neurons keep track of the sugar and oxygen in the blood, arterial pressure, 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 parasympathetic components are located 4

close to organs. The enteric lies inside the digestive tube and can operate independently of the sympathetic and parasympathetic 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 functioning of the enteric system.

Functions of the ANS The divisions of the ANS are seen by many as antagonistic to each other.

What the sympathetic division does the parasympathetic does the opposite. They are in fact complementary 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 5

on course. The pilot is always adjusting to keep the plane on course and so is the body. A few of the sympathetic systems responses include constriction of sphincters, shunting blood away from the intestinal tract, inhibiting digestion and peristalsis, increasing heart rate, dilating bronchioles of the lungs, and increasing blood flow to muscles. These are all

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By BruceBlaus (Own work) [CC-BY-3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

By Jvnkfood (Own work) [CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons

part of the flight or fight response.

The parasympathetic system is calming, enhances digestion and is generally trying to restore balance.

What goes wrong that can affect people’s health?

The biggest problem is functions get stuck in one division of the ANS at the expense of the other.

For example, someone may be operating primarily from their sympathetic system and they are not being balanced by the parasympathetic system. The opposite could also be true. When this happens it throws off a myriad of functions within the body and sets the stage for illness at some point in the future. Most treatments focus on effects of this imbalance, but that is only treating symptoms of some7

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By BruceBlaus (Own work) [CC-BY-3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

thing much bigger.

Until the ANS is balanced 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 system is chronically hyperactive they can become prone to certain ailments.

A few of them are gastroesophageal reflux, colitis, insomnia, insulin dependent diabetes, high blood pressure, and in severe cases congestive heart failure, strokes, and certain psychiatric problems.

If they were to get cancer it would most likely be of the tumor type of the

breast, lung, or prostate, ovary, and pancreas. Their immune systems tend to be underactive. This person could also have

musculoskeletal pain, particularly in the low back, but it could be at any joint.

If the adrenal glands (stress glands) are exhausted due to sympathetic overload ligaments weaken affecting the integrity of joints. A simple functional test to demonstrate this is 9

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 immediately after testing its strength by having the person resist pressure.

Normal physiology would dictate that when a joint is challenged by tugging on it, it would get stronger 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 injuries occur when the individual is stressed.

the chronic parasympathetic person becomes susceptible to osteoarthritis, angina, anxieties and panic attacks, asthma, heart attacks, depression, severe allergies, skin conditions, and cardiac arrhythmias.

The cause of the stress could be anything.

Emotional stress, dietary stress and physical stress are all common and they all count. A muscle correlation to the adrenals is the sartorius muscle which connects at the pelvis and the medial knee. If it neurologically 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 contact 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 parasympathetic person becomes susceptible to osteoarthritis, angina, 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 leukemia.

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Their immune systems tend to be overactive.

Since parasympathetic people can be calcium and protein deficient, they can also experience musculoskeletal discomfort.

When they get to the point of severe back pain they will usually display bilateral sacroiliac weakness which also weakens the gluteus maximus muscles.

These are major antigravity lifting muscles.

When weak, the person will lean way forward when sitting and then push themselves up. In a grocery store they are usually leaning over their carts to take the pressure off their backs.

Diagnosing Imbalances How does one know if their imbalance 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 challenge 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 system. If weakness occurs while looking through a blue film, they are dominant on the parasympathetic side. Another simple challenge test 11

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, treatments become more obvious and can be tailored that would inhibit the dominate side and excite the weaker side. There are degrees of severity 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.

Diet and the ANS The same diet is not for everyone.

What determines why one person may get miraculous results with a particular diet and another person’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 foods that are easy to digest, and should go easy on meats, particularly 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 12

on the alkaline side.

Working to balance the ANS individualizes the treatment 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 particularly the pancreas. Processed foods also do not contain the nutrients the body needs to thrive. Consuming refined sugar products and commercial wheat foods that spike one’s insulin levels can only produce imbalance 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.

B1, B2, B3, B6, Folic acid, K, and the minerals potassium, magnesium and manganese.

Nutrients and the ANS The parasympathetic dominant person does better with Vitamins A, Just as one size does various nutrients had E, C, B12, inositol, choThis line, niacinamide, calnot fit all with diet the on the ANS. same holds true with information is invalu- cium, and pantothenic Based on this nutrients. Like foods, able when attempting acid. research if a patient nutrients can be either had a sympathetstimulatory or inhibiic disease like tory to the ANS. For breast cancer, sympathetic domit would not inant individuals a classic sympathetic be prudent it is logical that dominant person would to recit wouldn’t be do well to take Vitamins ommend the best therD, C, B1, B2, B3, B6, calcium, apy to recomFolic acid, K, and the w h i c h mend nutriminerals potassium, would furents that would magnesium and ther stimfurther enhance manganese ulate the that imbalance. sympathetNutrients that ic system for would tone down the example. sympathetic system for example, and stimulate the parasympathetic system would be most to achieve balance. beneficial. Again, the For example, a classic work of Dr. Kelley is of sympathetic dominant importance here. He person would do well researched the impact to take Vitamins D, C, 13

Treatments

I’ll briefly cover some of the ways that balance can be restored in the ANS. As previously mentioned diet and nutrients can and should be utilized to achieve that goal.

Beyond that, specific adjustments at the spinal level can be used to either stimulate or inhibit the ANS. I have found cold laser therapy to be of great value.

It can reset the ANS to a more normal setting very quickly. For example, if one has adrenal exhaustion, by gently stimulating the joint with repetitive light tugs and at the same time pointing 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 therapy. The person could look through a colored 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 frequency that balanced the body. This will be displayed by the elimi-

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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 overload would not want to do intensive exercise that enhanced the sympathetic system.

It would also be beneficial 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.

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 judgment about which remedy I think might be best. However, invariably

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after I find it and then read to the person what the remedy is for they are often shocked by how accurate it is.

Conclusion The notion that autonomic imbalance is the root cause of all disease is not new. Along with Dr. Kelley, Dr. Francis Pottenger was also in agree-

ment. Dr. Pottenger wrote two timeless 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 laboratory and clinical evidence that autonomic imbalance explains most physical and psychiatric illnesses.

Also more recently, Dr. Nicholas Gonzalez, who operates a medical clinic treating chronic degenerative disease, including cancer, uses the principles of autonomic balancing. His results with certain cancers, particularly pancreatic, are quite impressive and far superior to 16

“orthodox” cancer treatments. You would think his work would be replicated 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.

My Mind’s Eye the strange case of Ian Waterman

by Rob Hutchinson website

www.ispectrummagazine.com

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n 1971 Ian Waterman was nineteen years old and looking 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 17

the unconscious perception of movement 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

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 crippling damage a lack of proprioception 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 18

Coke. Without receptors 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.

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 orientation 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 19

By Thomas.haslwanter (Own work) [CC-BY-SA-3.0 (http://creativecommons.org/licenses/ by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons

If he was asleep at night he would not have the positional sense or the control that we have over our bodies, 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 impossible 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 proprioception we can have no inner sense of posture or limb position and cannot initiate or control movement.

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Having been admitted to hospital with what doctors thought was nothing more than gastric flu, Waterman found himself virtually 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 person to simply give-in; he started to design his own program of movement practice to reclaim

his body. Constantly repeating movement patterns and focusing on trajectories over the space of thirty years - Waterman created a new way of

controlling his body. By having constant visual contact with the environment he learned to manipulate objects and today displays little to no signs of his impediments. Every move must be calculated in advance and planned out in a vigorous, mathematical way. However, if he cannot see the 21

position of his limbs then he cannot control them, something that he will never be able to overcome.

constantly repeating movement patterns and focusing on trajectories - over the space of thirty years - Waterman created a new way of controlling his body

At Oddstock Hospital the long road to recovery 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 wheelchair 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 constantly 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 stomach muscles, which after much practice he finally tasted success and raised himself up 22

in bed. By investigating what muscles controlled which specific movement he set himself a punishing practice regime.

Without proprioception his movements would never be automatic again, but if he could start building connections between mind and muscle it started to look like he may regain some semblance of a normal life. Every action would have to be plotted. Every movement would have to a carefully thought out and executed. Waterman’s tenacious attitude was rewarded when after one year he was able to stand up for the first time.

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.

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He wanted to look and present himself as naturally as possible to others. 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

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 incredibly well honed synchronization between his hand actions and his speech, with both being presented simultaneously. This would seem to suggest that gesture is an instinctive 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 24

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.

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 suffering from any problem at all, so controlled is his movement.

Having mastered the ability to walk again we may forget how difficult 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 something with my hands I am not just looking and thinking about my hands, I am also listening to sound’ he says. ‘I can’t get anything from my pocket because I can’t feel it terribly

well…..often if someone passes me a cup I would grab it awkwardly because I don’t have the feedback of something 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’ 25

of his situation, and when asked about the time he accidentally touched a young nurses’ 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 gesture 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 people’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 telling example of how a lack of proprioception can rob a person of

any affectionate contact with another. How could anyone who cannot feel what his hands are doing be able to make love to another or demonstrate caring affection to others?

Waterman has confounded all the diagnoses of the specialists by discovering ways of performing tasks that

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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

them, and present an outward picture 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 demonstrates 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 nervous system. Often we can see people who have crippling injuries on the news or television, such as losing a limb or mental faculties, 27

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?

HOMO INSAPIENS: THE SHRINKING HUMAN BRAIN

by Mike McInnes

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he human brain is shrinking for the first time in our evolutionary 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 develop is to become smaller and smarter, a selective advantage that has been underway 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.

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Albert Einstein and the Glial Cell

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 complex roles in cerebral metabolism.

Indeed they are emerging as the real smart brain cells – they monitor and modulate neural transmission and regulate synaptic metabolism. In addition they talk with one another by calcium waves across major brain regions – a kind of cerebral broadband communication system not dissimilar to smartphones. Professor Marion Diamond at the University of Berkeley examined two vital regions in Einstein’s brain, the prefrontal cortex and the 29

inferior parietal region. She found a higher ratio of glial cells to neurones compared with other brains – an index of higher energy processing and of advanced cerebral communication. The ratio of glia to neurones, as opposed to neurone 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 degeneration.

The Glial Cell and Incipient Dementia

Short Circuiting the Brain.

The human brain has never before been presented with chronic excess energy in the circulation – its evolutionary history is one of exposure to food and energy famine.

The brain is highly efficient at preserving its energy supply during energy famines or starvation (as in anorexia nervosa), but has not evolved sophisticated mechanisms to deal with chronic systemic energy excess – it simply suppresses energy income and triggers a protracted 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 variety of neurological conditions such as Alzheimer’s disease/motor neurone disease/Parkinson’s disease and multiple sclerosis.

The human brain affords the highest rate of energy consumption known in nature. Indeed on a like for like basis the human brain consumes 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 carries only 5 grams so a fall in blood glucose concentration (hypoglycaemia) is catastrophic for the brain and will rapidly lead to a coma, if not reversed.

The cerebral glucose pump – the glutamate/glu30

I have identified 6 primary mechanisms for this suppression and there are several secondary mechanisms.

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

tamine cycle -- is housed in glial cells and is driven by the enzyme glutamine synthetase.

However it is not the threat of hypoglycaemia that is the major metabolic problem in modern humans – it is hyperglycaemia, resulting from consumption of excess refined carbohydrates and sugars. This leads in turn to chronic hyperinsulinism.

Both hyperglycaemia and hyperinsulinism trigger and suppress the cerebral glucose pump and therefore prevent glucose entry to the brain – in other words they short circuit the brain.

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Is Glucose a Cannabinoid?

the health professions). Of course the cognitive impairments that follow take years or decades to manifest after the metabolic diseases are expressed, but that in no way reflects the true sequence of causation.

One of the least understood effects of refined carbohydrates and sugar consumption is the effect on hunger. 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 pigment cells (these are classical glial cells that pump glucose into the retina – exactly as do cerebral glial cells). They found that hyperglycaemia induces apoptosis by suppressing the FAAH 1 enzyme that degrades endogenous cannabinoids, thus activating cannabis CB1 receptors that suppress the cerebral glucose pump – the glutamate/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.

The eye is an outpost of the brain and retinal glial cells provide an excellent model of the effect of hyperglycaemia and hyperinsulinism on glial cells, and of cerebral energy metabolism, via advanced magnetic resonance imaging (MRI).

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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 hyperglycaemia 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 demonstrated that insulin regulates glutamine synthetase in a time- and dose-dependent 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 insulin 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 amyloid-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.”

33

Photo;By Danny Hope from Brighton & Hove, UK (My Right Eye Uploaded by Pieter Kuiper) [CC-BY-2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

Thus the twin toxic hypers of modern excess sugar consumption, hyperglycaemia and hyperinsulinism, separately and synergistically suppress and inhibit glucose transport into the brain via suppression of the cerebral glucose pump – the glutamate/glutamine cycle, known as the iPump. Neither fats nor proteins play any part in this pathological process – indeed fats play a positive role in cerebral glucose metabolism via leptin, adiponectin and fibroblast growth factor 9 (FGF 9).

34

The Hungry Retina and Dementia

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 vulnerable 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 deficits but to chronic energy overload in the circulation, and here again we observe that the first tissue to register the suppression of the retinal glucose 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.

Sleep Deprivation and the Shrinking Brain Indeed, in Scotland, a group of endocrinology and metabolic scientists are using retinal impairment as a model for dementia associated with diabetes – retinopathy. Here again the problem is that they consider type 2 diabetes as a major risk factor for retinopathy, and not that incipient 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 universal 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 evening meal we retire to

bed with a depleted liver, with insufficient reserve energy supply (liver glycogen) to provision the brain overnight.

This does not activate quality sleep and recovery physiology, but rather chronic nocturnal metabolic stress and increased risk of metabolic syndromes – dementias/obesity/ diabetes and heart disease; note the seminal paper by Turek and Bass in 2005:

“ ... 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.

35

provision the Professor Eve brain via the van Cauter liver prior to at Chicago sleep, and University has sleep is a high energy that sleep pioneered system with respect to d e p r i studies that the human brain v a t i o n confirm poor increases quality and levels of NSE foreshortened and S-100B in sleep as one of healthy young the most potent men – indicative of driving forces of modloss of cerebral volume. ern metabolic impair- high ments and energy dys- energy system with regulation.

Professor respect to the human Christian Benedict of brain, that chronic nocUppsala University has turnal metabolic stress shown that sleep is a results from failure to 36

Metabolic Stalinism: A Century of Lost Opportunity

The tragedy of modern metabolic impairments and a rapid loss of cerebral volume over the past half century has been the direct result of influence by a small number of powerful scientists who have influenced negatively the understanding of the causes and mechanisms of a range of degenerative diseases – obesity/diabetes/heart disease, and dementias. From the 1920s through the 1970s the major figure in diabetes research was Elliot Joslin and his textbook on diabetes was mandatory. Joslin held the view that diabetes was a fat-driven condition and that sugars were not the causative agency, in spite of the knowledge that incidence of this condition dropped

K Ration Dinner Kit

dramatically during both world wars, when sugars were not readily available.

During the 1950s Ancel Keys, a brilliant American physiologist who pioneered research into nutrition and developed the famous US K-Rations for use by US servicemen during WW2, developed the 37

theory that fats and cholesterol were the driving force of cardiovascular disease, and that sugars were not significant. This double theory was then extended to include obesity and metabolic syndrome, and this remains the view to this day. Any researchers who opposed this view

were marginalised or attacked as unscientific.

A cardiologist, Robert Atkins, who, along with several other groups of researchers, had successfully treated his cardiac and obese patients with a low sugar/low carbohydrate diet, was venomously attacked; in the Senate Select Committee on Nutrition

and Human Need in April 1973, Senator Charles Percy of Illinois went on record, on behalf of Fred Stare, a nutritionist at Harvard, saying: “The Atkins diet is nonsense...the author who makes the assertion is guilty of malpractice�. Thus the theory that refined sugars may be a major cause of metabolic illness

(which has a long and illustrious history), was suppressed, and it is only now, in the second decade of the 21st century that this view has resurfaced. The period since the Senate hearing saw the inclusion of sugars in processed foods at the expense of fats, and the incidence of obesity/diabetes and dementias exploded.

Gestational Diabetes

Is it possible to refer to a condition of foetal dementia? Gestational diabetes, a growing problem, is a condition in pregnancy where the mother develops a form of type 2 diabetes in the third trimester.

The foetal circulation is then 38

subject to a combination of hyperglycaemia and hyperinsulinism.

At birth the infants are often large (macrosomic) and they are at increased risk of obesity/diabetes and metabolic syndrome.

In September 2013 a study at the University of Copenhagen showed that sugars are vital signalling cofactors in the formation of the brain via a MicroRNA system known as mir-79 (the human equivalent is mir-9). If the foetal cerebral glucose pump is suppressed, as it would be in the hyperglycaemic/hyperinsulinic environment of the foetal circulation, the outcome would be impaired formation of the new brain and incipient dementia. Recent studies point to exactly this conclusion – a study by the Universities of Bristol and Glasgow found:

formed – not so the human brain, which continues to develop and grow beyond birth and into the second decade of life.

“ ...Offspring of mothers with existing diabetes had a threefold risk of achieving no GCSEs graded A-C, whilst offspring of women with gestational diabetes had, on average, a five point lower IQ compared to offspring of women with no diabetes or glycosuria ...”

Let the alarm bells ring in every home, nursery, primary school, secondary school, college, university and all centres of learning and education. It will not be lost on the reader that the environment in which the foetus is suspended,

By the third trimester of gestational diabetes all of the organs with one exception are already fully 39

cognitive impairments in infants of gestational diabetic mothers; we also find cerebral volume and IQ deficits in childhood obesity and in ADHD.

Numerous government interventions 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.

characterized by hyperglycaemia and hyperinsulinism, the twin toxic hypers that inhibit glucose transfer 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 devastating consequence of chronic cerebral glucose deprivation is an obese infant that is cognitively impaired – a sequence that challenges the standard view of modern dementia – and that metabolic conditions such as obesity and diabetes increase risk of dementias and Alzheimer’s disease. We noted

Tragic as may be the physiological and neurological conditions that plague modern urban humanity, they may be masking un underlying and more incipient and profound degeneration, that of the shrinking human brain – the organ that makes us uniquely human and that gave rise to consciousness, language, writing, agriculture, civilisation, law, literature, art, culture, music, science, technology and philosophy. In spite of an explosion in information technology our children are advanced and advancing on the road to cognitive and neural 40

degeneration and dementia via the toxic combination of sleep deprivation and sugar-driven suppression of the cerebral glucose pump (iPump); might they become a new offshoot of Homo sapiens – Homo insapiens?

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.

What Can We Do?

Paradoxically, honey is the Gold Standard food for this purpose.

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 nutrition and health?

Bariatric Sleep

In the west we view sleep as a low energy event, a myth driven by diet gurus which is not only unscientific but positively dangerous.

As a result we retire to bed with a depleted liver, and activate not quality sleep and recovery physiology, but rather chronic nocturnal metabolic stress and increased risk of metabolic syndrome, every night of our lives. By selectively restocking the liver prior to sleep we forwardprovision cerebral energy reserves, reduce chronic nocturnal metabolic

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 41

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 exclusively sourced from adipose fat. stress, promote quality sleep and recovery physiology, reduce the risk of metabolic syndrome, and improve memory and learning during REM sleep. Sleep is a bariatric event, in so far as recovery physiology 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).

42

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 metabolic parameters correlated to weight gain and diabetes (hyperglycaemia/hyperinsulinism), are reversed in advance of weight loss.

In other words these parameters are not caused by weight gain/diabetes; they are the driving forces of these conditions.

Professor Achim Peters, leader of the Selfish Brain Group at Lubeck, has pioneered the theory that the cause of weight gain and metabolic impairments is chronic cerebral glucose deprivation – or chronic unresolved cerebral hunger.

Professor Christian Benedict at Lubeck has found that nocturnal metabolic stress is directly related to compromised cerebral energy supply. Professor JJ Guinovart at Barcelona has found that restoration of hepatic glycogen reserves reduces the conditions of modern metabolic impairment and the causative agencies of metabolic syndrome -- hyperglycaemia, hyperphagia and the enzymes of gluconeogenesis.

Why Honey?

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 physiology every night in life. This is the most neglected aspect of the Mediterranean diet; timing is a key influence in all metabolic events. Since they have recently abandoned this practice, 43

the fastest growing area for metabolic syndrome 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. Thus we can adopt the strategy enjoyed in the Southern Med by selectively replenishing the liver prior to sleep.

Honey is the Gold Standard food

for this purpose (without 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 metabolic ailments – physiological and neurological -- honey has been selected to restock the liver every night in life prior to sleep.

Honey restocks the liver via several mechanisms including fructose liberation of glucokinase/ increased glycogen synthase/reduced phosphorylase, and suppression of glucagon. Honey activates the honey/insulin/melatonin (HYMN) Cycle, promoting sleep and recovery physiology.

In addition Honey stimulates a cascade of beneficial hormones

– GLP-1/free IGF-1/ leptin. Insulin is stimulated via the HYMN Cycle, promotes melatonin and is then suppressed 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.

Nocturnal Energy Homeostasis: The Holy Grail of Modern Metabolic Impairments

It is possible to establish nocturnal global energy homeostasis, without pharmaceutical 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 44

recalibration of the glutamate/glutamine cycle (iPump), thus reducing chronic nocturnal cerebral hunger and chronic nocturnal metabolic stress. This in turn promotes quality sleep and recovery (fat burning) physiology, and improved learning and memory during REM sleep. In this sense we may state

that the optimally functioning iPump is the engine of quality sleep and recovery physiology, and therefore of nocturnal fat metabolism.

Reduced consumption of refined sugars and carbohydrates, combined with honey taken prior to sleep every night, after an early evening meal, may

constitute the single most significant and cost effective contribution 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.

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46

Pediatrics. 2012

Geopolymer research:

An interview with Joseph Davidovits

by Tania Dey website www.publicationslist.org/tania_dey

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

47

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.

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 (19831989), 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 manmade rocks, and the inventor of geopolymers and the chemistry of geopolymerization. He has authored/ co-authored more than 130 scientific papers and conference 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 conventional 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 laboratory synthesis of geopolymers and is generated by thermal activation of kaolinite clay. Geopolymers can also be made from other sources of pozzolanic materials, 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-coordinated three-dimensional aluminosilicate gel.

48

T.D. Dr. Davidovits, I have read that you went all the way to the Giza plateau 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 analysis 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 natural 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 conventional Egyptology. What prompted you to undertake this unusually remarkable study? What was the catalyzing factor?

Dr. Davidovits It was partly chance.

My work as a research chemist really started in 1972. My target was the creation of fire-resistant polymeric materials. For two years, in my laboratory 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 realized that what we were 49

producing were materials that are very close to natural cements, such as rocks based on feldspars, the feldspathoids. One day, as a joke, I asked my scientific partners, two well known French mineralogists at the MusĂŠum

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

50

d’Histoire Naturelle in Paris, what would happen if we buried in the ground a piece of the product that we were synthesizing in the laboratory at the time (our first geopolymer material), and an archaeologist discovered it

3000 years later? Their answer was surprising: the archaeologist would analyze this object disinterred from the garden of a ruin in SaintQuentin, and the analysis would reveal that the nearest natural outcrop 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 developed, it would be taken for natural stone.

T.D. Did you have to face any controversy or criticism from the scientific community, while trying to establish your point?

Dr. Davidovits I presented my ideas at several International Egyptology conferences: Grenoble, France (1979), Toronto, Canada (1982), Manchester, UK (1984), Cairo, Egypt (1988). They generated great debates, several articles in newspapers, yet no hostility. However, after the

publication of my book for the general public, (The pyramids: an enigma solved, 1988, New York), several materials scientists sent me a letter in which they asked me to stop this research because “I was jeopardizing my career”.

In 1989, an eminent American Egyptologist 51

wrote a startling review stating that I had falsified the scientific data (my chemical analysis), etc. My friends wanted me to go to court because of these insults.

I answered: “No, this is part of the game in science. A new theory is always severely challenged. This has always

been the case in the past, and remains true in our present time.â&#x20AC;?

One famous American geologist wrote a paper in 1992 that states: â&#x20AC;&#x153;... we feel it is the duty of a professional geologist to expose this egregiously absurd archeological theory before it becomes part of entrenched pseudoscience... We believe that if Davidovits had

any understanding of basic geologic principles and understood the implications of simple geological evidence at Giza, he would have realized that this geopolymer theory has no basis in fact... We have also shown how geologic common sense can destroy archaeological quackery, but not, unfortunately, before it has enjoyed widespread

publicity among the gullible and sensationminded... The geopolymer theory is defunct; we still remain in awe of the enigma of Egyptian skill and engineering.â&#x20AC;?

Ironically, his study was made on stone samples 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 sustainable cement material. But are there any shortcomings? How well does it perform in comparison to conventional cement materials?

Dr. Davidovits The only and major shortcoming is its novelty. It is too young.

Geopolymer cement was invented only 30

years ago (Portland cement, 150 years ago).

Since liability claims for construction materials require at least 20 52

years durability warranty, everybody should understand that, as far as the applications for the construction indus-

try are concerned, this is a major drawback.

This explains why geopolymer applications were first developed in other fields and niche markets, which do not require these types of codification.

Geopolymer Moulds

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?

Dr. Davidovits To understand the long-term durability issues on geopolymers we may make a parallel with glass technologies and science. It has been recognized for a long time that there is at least a rough correlation between the dura-

bility of glasses and the number of non-bridging oxygens (-Si-OH or -SiOâ&#x2C6;&#x2019; Me+ groups). The results of this study reveal several points that may be transferred to geopolymer structures. One is that the addition of aluminum 53

to a silicate framework generally increases durability. The importance of non-bridging oxygens on glass durability is that non-bridging oxygens provide a point of attack on a molecular scale for protons or water mole-

cules. Similarly in geopolymers, it is the highly polymerized regions that are resistant to

chemical attack and offer long-term stability, whereas the less polymerized regions

with Al-OH or Si-O-AlO-Si- species are prone to shrinkage and leachability.

T.D. In the context of durability of geopolymer materials, how well characterized are the gel pores, cement hydration and alkali-aggregate reaction? What improvements can we, the scientists, make in order to further optimize the product?

Dr. Davidovits Pore solution analysis is worthwhile for monomeric/dimeric gels like those found in Portland cement or alkali-activated slag for example.

It is not valid for the investigation of any fully condensed geopolymer matrix. It may be used to show that geopolymerization, i.e. networking of the framework, is not complete.

Instead of pore solution analysis, we measure

the pH of the material and perform Nuclear Magnetic Resonance spectrometry (NMR) for silicon (Si) and aluminium (Al).

As for alkali-aggregate reaction, I published my first study on this topic 20 years ago, in Ceramic Transactions, Vol. 37, (1993), CementBased Materials: Present, Future, and Environmental Aspects. pp 165-182, titled: 54

Geopolymer Cements to Minimize Carbondioxide GreenhouseWarming. The demonstration was clear.

Geopolymer material does not generate any deleterious alkaliaggregate reaction.

T.D. What do you consider to be some of the greatest challenges in this field of research?

Dr. Davidovits To get those scientists working in the field of geopolymer cement and who had a Portland cement chemistry back-

ground to shift away from hydration-based reasoning towards geopolymer terminology and chemistry.

This is not easy because it requires from them that they go back to school.

T.D. What, in your opinion, are some of the emerging applications that will gain interest in the next few years?

Dr. Davidovits 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 applications, high-tech ceramics, paints and coatings, and heat-resistant composite materials. As for the cement field, I guess that the newly discovered ferro-sial55

ate geopolymer cement type will provide the solution for mass production worldwide (see at www.geopolymer.org the News dated August 2012 on â&#x20AC;&#x153;red geopolymer cementâ&#x20AC;?).

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

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T.D. One North American geopolymer application is a blended Portlandgeopolymer cement known as Pyrament速 (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?

Dr. Davidovits I once visited a cement plant in South Africa and was struck by the local conditions ruling the manufacture of Portland cement there.

The plant was located very close to the market (the cities of Pretoria

and Johannesburg) but the geological resources, 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, geopolymer cement is a complementary material to Portland cement.

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?

Dr. Davidovits Well, you should con- the presence of a poly- weight molecules. This sider the geopolymeric meric network or, at is not the case for reguterminology that implies least, of high molecular lar calcium phosphate 57

hydrates such as brushite, CaHPO4.2H2O, which results from the reaction of phosphor-

ic acid, and wollastonite, CaSiO3. On the other hand, aluminum phosphate cements

and binders are genuine geopolymers, with high-macromolecular networks.

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 attributes of geopolymers make them attractive for use in high-cost, severeenvironment applications such as bridges. Can you name a few industries that are actively producing geopolymers for construction?

Dr. Davidovits 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 development of new materials.

For example, one million geopolymer pavement bricks (roughly 3,000 tons) were manufactured 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 companies such as Tata Steel.

They are planning to have 10 commercial installations in India in the coming 5 years.

An Australian company ROCLA, one of the pioneers in geopolymer precast concrete for commercial production, claimed in Dec. 2011 58

to have achieved “the ‘world first’ production run of geopolymer concrete”. It was undertaken in Canberra, involving the production of 3,000 components, totaling 2,500 tons. I had visited ROCLA in 1999.

In 2011, in Germany, France and the UK, the global chemical company BASF launched a geopolymer joint grout named PCI-Geofug®.

Another Australian com-

Prof. Joseph Davidovits visiting India in 2010, to expand research collaboration

pany, Rockwool, a manufacturer of insulating material, has found a way to capture, recycle and re-use tons of waste generated from the manufacturing process, using a geopolymer to bind the waste

into briquettes. The briquettes of geopolymer material are fed back into the furnace and made into fibers for Rockwool insulation.

The plant has been running this geopolymer process since 2007, yet 59

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 geopolymer concrete.

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 networking that you have established to date. Any upcoming events that you would like to make us aware of?

Dr. Davidovits My archaeological research is attracting a lot of interest in some developing countries.

We are presently preparing a partnership with the major building institution in Egypt,

namely HBRC, Cairo, the Egyptian Housing & Building National Research Center. The target is to transfer our knowledge of ancient building materials (pyramid stone and the like)

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for the development of sustainable construction 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.

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 overwhelming; they asked thought-provoking questions and became more and more interested. What message do you have for student researchers like them?

Dr. Davidovits Although geopolymerization does not rely on toxic organic solvents but only on water, it needs strong alkalis such as sodium hydroxide (NaOH) that may be dangerous, and therefore requires some safety precautions. Because I was a chemist, when I started the research on geopolymers I decided to select alkaline conditions that could be classified as “mild”, i.e. userfriendly. Unfortunately,

this was not followed by other engineers and scientists involved in the development of geopolymeric systems.

Apparently, these scientists never put their finger into their reaction mixture, which has a SiO2:Na2O ratio of 0.20 or 0.60. The problem is that practically all papers dealing with “alkali-activated” cements describe recipes that are not userfriendly. To recommend 61

them for regular building and civil engineering operations, where people are working with bare hands, is nonsense.

This could explain why geopolymer cement technology has not reached mass applications and remains confined to high-tech niche markets. So my message is: develop “userfriendly” systems.

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: â&#x20AC;&#x153;Geopolymers, more than just cementâ&#x20AC;?.

Indeed, when, in 1979, I introduced the geopolymer concept and the related terminology, I had no idea about cement. But in the mind of cement scientists, geopolymer is only cement and therefore they try to understand its material properties with their Portland cement background, replacing calcium (Ca) with sodium (Na), which is not appropriate. To better

Dr. Tania Dey posed with her lab students during Instron compressive strength measurement of geopolymer moulds

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explain these chemical processes and the resultant 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 practitioners in the field of alkali-activated cements who still tend to explain such reaction chemistry in Portland cement terminology. On the other hand, materials scien-

tists working on hightech ceramics and composites understand the importance of the geopolymer terminology and use it with success in numerous scientific projects worldwide.

T.D. Dr. Davidovits, many thanks for your time and for this insightful discussion. 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 application potential. The author can be reached at: taniadey.asp@hotmail.com Website: http://publicationslist.org/tania_dey

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