Ispectrum Magazine #06


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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

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Ispectrum Magazine #06

  1. 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. 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. 3. 2 Mado Martinez Editorial Director Editorial Director Mado Martinez, Art Director Rayna Petrova Copy Editing and Proofreading Matt Loveday Jennifer James Contributing Writers Dr. Dennis K. Crawford Rob Hutchinson Mike McInnes Tania Dey Images Cover : © Billy Benavides / ,,, 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! Follow Us +44 7938 707 164 (UK)
  4. 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
  5. 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. 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. 7. 6 ByBruceBlaus(Ownwork)[CC-BY-3.0(],viaWikimediaCommons
  8. 8. 7 ByJvnkfood(Ownwork)[CC-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. 9. 8 ByBruceBlaus(Ownwork)[CC-BY-3.0(],viaWikimediaCommons
  10. 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. 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. 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. 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. 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. 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. 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. 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. 18. 17 I by Rob Hutchinson website 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. 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. 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. 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( by-sa/3.0)orGFDL(],viaWikimediaCommons
  22. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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(],viaWikimediaCommons The Hungry Retina and Dementia
  36. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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: 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: 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. 47. 46 of tissue) is...three times greater than the cerebral cor- tex...” Diamond MC, Scheibel AB, Murphy GM Jr, Harvey T. On the brain of a scientist: Albert Einstein. Exp Neurol. 1985 Apr;88(1): 198-204. Ding J, Patton N, Deary IJ, Strachan MW, Fowkes FG, Mitchell RJ, Price JF. Retinal microvascular abnormali- ties and cognitive dysfunction: a systematic review. Br J Opthalmol. 2008 Aug;92(8): 1017-25 Erejuwa OO, Sulaiman SA, Wahab MSA. Honey – A Novel Antidiabetic Agent, Int J Biol Sci 2012; 8(6):913-93. Fields R Douglas. The Other Brain. (A brilliant analysis of the growing field of glial science- MM). Simon & Schuster Paperbacks New York 2009. Fraser A, Nelson SM, Macdonald-Wallis C, Lawlor DA. Association of Existing Diabetes, Gestational Diabetes and Glycosuria with Offspring IQ, and Educational Attainment: The Avon Longitudinal Study of Parents and Children. Exp Diabetes Res. 2012: 963735 Grunstein HS, James DE, Storlien LH, Smythe GA, Kraegen EW. Hyperinsulinemia suppresses glucose uti- lization in specific brain regions: In vivo studies using the euglycemic clamp in the rat. Endocrinology. 1985 Feb;116(2):604-10. Kashyap SR, Gatmaitan P, Brethauer S, Schauer P. Bariatric surgery for type 2 diabetes: weighing the impact for obese patients. Cleve Clin J Med. 2010 Jul;77(7):468- 76. Lim SK, Park MJ, Lim JC, Han HJ, Kim GY, Cravatt BF, Woo CH, Ma SJ< Yoon KC, Park SH. Hyperglycemis induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment cells. J Cell Physiol. 2012 Feb;227(2):569-77. McCall AL, Millington WR, Wurtman RJ. Metabolic fuel and amino acid transport into the brain in experimental diabe- tes. Proc Natl Acad Sci U S A 1982 Sept;79(17):5406-10. McAuliffe Kathleen, excellent Discover Magazine article in January 2011 on the positive shrinking human brain. humans-smart-why-brain-shrinking#.UvkpXGJ_uSo Marioni RE, Strachan MWJ, Reynolds RM, Lowe GDO, Mitchell RJ, Fowkes FGR, Frier Bm, Lee AJ, Butcher I, Rumley A, Murray GD, Dreary IJ, Price JF. The Edinburgh Type 2 Diabetes Study. Association Between Raised Inflammatory Markers and Cognitive Decline in Elderly People with Type 2 Diabetes. Diabetes. 2010 March; 59(3): 710-713 Moraes W, Azevedo E, Utino A, de Mello M, Tufik S. Weight Loss Rate During Sleep and Awake Rest. Journal of Sleep and Sleep Disorders Research Vol 32 Abstract Supplement. 2009 23rd Annual Meeting of the Associated Professional Sleep societies, LLC Seattle, Washington. Ola MS, Hosova K, LaNoue KF. Influence of insulin on glutamine synthetase in the muller glial cells of retina. Metab Brain Dis 2011 Sep;26(3): 195-202. Pedersen ME, Snieckute G, Kagias K, Nehammer C, Multhaupt HA, Couchman JR, Pocock R. An epidermal microRNA regulates neuronal migration through control of the cellular glycolisation state. Science. 2013 Sep 20;341(6152): 1404-8 Peters A. The selfish brain: Competition for energy resources. Am J Hum Biol. 2011 Jan-Feb;23(1):29-34 Qui WQ, Folstein MF. Insulin, insulin-degrading enzyme and amyloid-beta peptide in Alzheimer’s disease: review and hypothesis. Neurobiol Aging. 2006 Feb;27(2):190-8 Ros S, Garcia-Rocha M, CAlbo J, Guinovart JJ. Restoration of hepatic glycogen deposition reduces hyperglycaemia, hyperphagia and gluconeogenic enzymes in a strepto- zotocin-induced model of diabetes in rats. Diabetologia. 2011 Oct;54(10):2639-48. Russell VA, Oades RD, Tannock R, Killeen PR, Auerbach JG, Johansen EB, Sagvolden T. Response variability in Attention-Deficit/Hyperactivity disorder: a neuronal and glial enegetics hypothesis. Behav Brain Function. 2006 Aug 23;2:30 Shen X, Xu G. Role of IL-1beta on the glutamine synthe- tase in retinal Muller cells under high glucose conditions. Curr Eye Res. 2009 Sep;34(9):727-36 Sherwood CC, Stimpson CD, Raghanti MA, Wildman DE, Uddin M, Grossman LI, Goodman M, Redmond JC, Bonar CJ, Erwin JM, hof PR. Evolution of increased gli-neurone ratios in the human prefrontal cortex. Proc Natl Acad U. S. A. 2006 Sep 12;103(37):13606-11. Taubes Gary. The Diet Delusion (Gary Taubes examines the entire history of diets and concludes that the low fat /high carb diet endorsed by the scientific establishment for many decades is a tragic error, and that refined car- bohydrates are the driving force of modern obesity and metabolic impairments - MM). Van Cauter E, Spieqel K, Tasali E, Leproult R. Metabolic consequences of sleep and sleep loss. Sleep Med. 2008 Sep;9 Suppl 1:S23-8. Yau PL, Castro MG, Tagani A, Tsui WH, Convit A. Obesity and metabolic syndrome and functional and structural brain impairments in adolescents. Pediatrics. 2012 Oct;130(4):e856-64.
  48. 48. by Tania Dey website 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. 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. 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. 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. 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. 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. 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. 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. 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 the News dated August 2012 on “red geopoly- mer cement”). Dr. Davidovits Dr. Davidovits
  57. 57. 56 Balanced chemical equation showing geopolymer synthesis starting with metakaolin, MK-750
  58. 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. 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. 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. 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. 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. 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. 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 ( 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: Website:
  65. 65. 64 www . ispectrummagazine . c o m “Tactility is the sensibility of the skin as surface of contact between the perceiving subject and the perceived object. Proprioception folds tactility into the body, enveloping the skin’s contact with the external world in a dimension of medi- um depth: between epidermis and viscera.“ Brian Massum