We have all heard about the 'Fight or Flight' response in the Neanderthal context.  This basically refers to the hormonal changes  triggered when a caveman met a wild beast.  It was designed to preserve the species.  He, or she, was suddenly forced to fight the beast or leg it out and out-run or out-climb the more powerful animal.  The response being referred to involves the activation of a set of neuro-endocrine pathways designed to enhance performance in what was usually a short term yet very intense struggle.

Another, possibly more precise way of describing these neuro-endocrine responses is to characterize them as sympatho-adrenal.  'Sympatho' refers to activation of the sympathetic nervous system.  Activation of the sympathetic nervous system (SNS) causes the release of epinephrine (adrenalin) and norepinephrine into the bloodstream.  These have a panoply of metabolic actions including the elevation of blood pressure and blood glucose.  Increased propensity of the blood to coagulate is another indirect effect which would act to stem bleeding from an artery that might be injured.  Activation of the SNS also produces a rise in serum triglyceride levels.  Triglyceride-rich particles facilitate the neutralization of multiple hostile invaders such as bacteria, viruses and protozoans.  As is apparent, these responses are designed to maximize outcomes in the field of battle. 

The 'adrenal' part of the sympatho-adrenal response refers to release of the stress hormone cortisol into the bloodstream from the adrenal gland.  Because of this, serum cortisol levels rise.  Cortisol is in the category of 'glucocorticoid' hormones.  'Gluco' refers to the link with sugar and  the subsequent elevation of blood sugar levels caused by cortisol.  The benefit of enhanced blood glucose availability is that the muscles (those organs necessary for transporting you away from an angry tiger) will then have an uninterrupted supply of the fuel source they rely on.

In the past, most serious threats were usually resolved one way or another relatively rapidly.  However, in modern times the typical triggers of this primordial hormonal response are chronic in nature and thus produce a prolonged activation of the hormonal responses just described. They were never designed for chronic use.  Modern day stressors are the primary triggers of the fight or flight hormonal response.  In most circumstances stress develops not from crossing paths with a wild animal, but from the unremitting demands at home or at work, financial pressures, lack of sleep and trying to cram too much into too little time.  The hormonal responses are then activated in a continuous fashion.  The persistence of these hormonal responses is at the root of many modern day illnesses including high blood pressure, weight gain, weak bones and heart disease.  This observation is especially germane for the brain.  When exposed to persistently elevated cortisol levels, neurons suffer.  They lose contacts with their neighbors, shrink, and are less resistant to the daily insults all cells are continuously exposed to.  In rodent studies, when infused for just three weeks with the rat equivalent of cortisol, brains wither and memory suffers.  This is in only three weeks!  Imagine how many of us are exposed to chronic stress lasting for months or years.  In the animal studies, the amazing observation is that if the stress hormone infusion is stopped, the brain atrophy reverses!  If this didn't happen, there would be little more to discuss.  However, because it does reverse the question remains, "What can be done about modern brains exposed to chronic stress?"

This is where complete understanding of the flight or fight response is important.  As it evolved over millions of years, it consisted of two related phases. The first phase involves the stress response and subsequent hormonal activation.  It is followed almost immediately by the second phase, the flight response-the most likely reaction to the (generally) physical stressor.  The flight response involves running, jumping, climbing or other similar strenuous activities.  These are identical to what we refer to today as exercise!  When we exercise we trigger the same physiological responses.  They tend to counteract the effects of the stress inducer.  That is the beauty of the combination of stress and vigorous physical activity.  As a result, blood pressure falls, glucose levels fall and triglycerides fall after exercise.  Exercise even reverses the hormonal changes.  It appears to provide the best and most natural antidote for stress.  When the two phases of the fight or flight response are dissociated, or uncoupled, and one is engaged without the other (the situation occurring in most of us today) we experience only the bad effects and it takes its toll on our health. Hence, the optimal way to reverse the ill effects of our stressful lives and the associated adverse impact on our health is to exercise vigorously on a daily basis.  By understanding our ingrained physiology (the fight or flight response) and what goes awry when it is only partially turned on (especially in a continuous fashion), it is clear what the best approach is to address the problem.  Daily exercise is Mother Nature's solution to one aspect of our modern day lifestyles.        

Sounds pretty healthy at first blush, doesn't it?  How could anything having to do with fruit be anything but healthy?  After all, it is recommended that we consume five to eight servings of fruits and vegetables each day.  They contain many healthy nutrients such as antioxidants-the compounds that counteract the harmful effects of 'free radicals', those damaging compounds that age cells, injure the genetic material they depend on, and cause clumping of our functional proteins and lipids- those fatty compounds that enhance function in each cell in the body.  For example, grapes contain resveratrol, a unique ingredient that has been purported to lengthen the life span of various organisms.  I believe there are many healthy nutrients in fruits and veggies.  However, try to imagine in your mind's eye how these foodstuffs might have appeared in the distant past.  For example, take an apple.  It would clearly not have been the large, succulent type of fruit that appears on today's grocery shelves.  It would have been small, tough, and shriveled.  Nothing resembling what is eaten today.  The major difference is that the current varietals are aptly described as tasting sweet, for good reasons.  They are large and starchy; full of sugar. The typical apple contains approximately 1.5 grams of glucose, 6 grams of fructose (fruit sugar), and 3 grams of sucrose (read table sugar).  

 As our gene pool evolved over the past several million years, one of the major influences shaping genetic alterations is the diet.  Of note is the observation that, aside from the past 10,000-20,000 years, we have been exposed to food that included essentially no rapidly absorbed carbohydrates (other than for seasonal honey-like substances).  The rapid absorption of the glucose in starchy foods such as potatoes and bread has been studied along with the related rapid rise in blood insulin levels (associated with the Glycemic Index concept).  Books have been written discussing the Glycemic Index and what it implies.  However, in my opinion, equal emphasis has not been given to the impact that fruit sugar, or fructose, as it is otherwise called, has upon our health.  As an example, the GI (Glycemic Index) of white bread is 100.  That represents the exaggerated rate of rise in blood glucose, and with it the tightly correlated rise in blood insulin levels.  If you consume the same number of carbohydrates in the form of table sugar (or sucrose, which consists of a molecule of glucose and fructose linked together), the GI is only about 60, roughly two-thirds as high as the white bread.  This makes it seem like eating sugar is healthy because its GI is much lower than that of bread.  This couldn't be further from the truth.... for reasons other than those reflected by their glycemic index.

Sugars, such as glucose and fructose, have the uncanny ability to bind to functional proteins, fats and DNA particles.  When this occurs, they dramatically degrade the vital activity of these molecules.  This forms the basis for a commonly requested lab test called HBA1c that measures the average blood sugar level for the past couple of months.  This is a test that represents adequacy of blood sugar regulation over a long period of time and is important in diabetic control.  It reflects the innate ability of these sugars to bind to the hemoglobin protein that is naturally present in the bloodstream.

What is important to note is that the propensity of fructose to bind to these important biological molecules is ten-fold greater than that of glucose even though glucose has a much higher GI.  This is a shortcoming of the GI.  There are many reasons why this distinction is important, but the one I am most concerned about is the relationship between binding of these sugars to delicate proteins in the body and the correlation with brain atrophy.  Brain atrophy may be viewed as brain shrinkage, which is not a good thing to have going on in your brain.  Clinical investigations have documented the close correlation between brain atrophy and level of HbA1c in the blood-a proxy for the degree of binding of these sugars to functional compounds in the body.  One study even found it to be the most significant indicator of brain atrophy. 

The take home message is to avoid foods that contain high amounts of fructose, or fruit sugar.  In this context it is not necessarily the apple I am referring to, but HFCS (high-fructose corn syrup) and table sugar (sucrose).  Numerous foods contain 20 to 40 or more grams of these ingredients.  Be careful to read labels because they even sneak into ketchup and other condiments.   

Athletes who compete at the highest level are able to do so because they train the muscles they depend on to maintain their competitive edge.  For example, basketball players are required to get high off the court to lob a pass or perform a jump shot over the outstretched arms of an opponent.  The extensor muscles in the leg such as the quadriceps and gastronemius/soleus groups are the ones that must perform. The same principle applies for each sport.  To maximize performance, attention must focus on the appropriate muscle groups.  Brain training follows similar rules .... to a degree.

When the brain performs a task, we see no external movement or activity associated with the neurons that were firing during a particular thought process.  To visualize what parts of the brain were activated, scientists use very sophisticated types of brain scanning devices.  The two most popular are PET scanning, for Positron Emission Tomography, and functional MRI scanning, which is a type of magnetic scan.  When a subject is required to perform a mental function such as an arithmetic calculation in one of these machines, specific regions of the brain 'light up.'  This is a reflection of the increased metabolic activity in the requisite areas of the brain necessary for the particular function required.  If the muscles of an athlete were imaged in a scanner while exercising, we would see analogous findings.

The optimal training for an athlete mandates a training regimen designed to work out specific muscle groups under competitive conditions.  The optimal training regimen for the brain is somewhat different.  The cognitive demands of modern day life necessitate a flexible thinking machine, not a robot that performs one thing well time and time again.  This observation mandates quite a different training approach.  What seems to work best is a program that turns on, activates, or lights up, large regions of the cerebral cortex-the surface of the brain which is the part of the brain most densely packed with nerve-to-nerve connections.

Going back to the lab for a moment, when asked to perform a unique task that has not been done before, it is common to see large areas of the brain turned on when visualized via a functional MRI scan.  This is not unexpected.  What is surprising, however, is when that same task is performed a second time or a third time, there is much less response on the scan.  Much smaller areas light up.  An athlete excels by repetitive training and the enhanced ability to maximally fire certain muscles.  The brain seems to 'learn' how to do something in a way that the second time around it functions better and faster with less work.  However, to get to this point it needs to start out performing a unique task.  Hence, it seems like novel situations are what the brain was built to handle and what it should be trained for and with.

What is the take home message from all of this science-speak?  It is that 'the brain loves novelty.'  Translated into modern living circumstances this means if you want to train your brain most effectively you should choose tasks that are out of the ordinary for your daily circumstances.  Simple examples include such basic chores as using the computer mouse with your left hand if you are right-handed, walking on an irregular surface with bare feet, going backwards up the stairs, or in a non-physical example, approaching a common problem in a unique way.  All of these are brain-training exercises.  What is worth noting is that as you activate, or engage, large regions of the brain for one task, these same regions may be required for the performance of other, possibly more complex and unrelated, demands.  Yet, you have trained them and thus enhanced their connectivity with neighboring neurons with these seemingly simple training tools. 

So, each day it would be a good idea to try and activate your brain in new, novel and different ways in challenging circumstances.  It will also be fun and exciting.  Enjoy your new brain workouts!

I was reading the reviews of Gary Taubes' new book Good Calories, Bad Calories on the Amazon.com website and was amused to see that for the most part the reviewers gave him either 1 Star or 5 Stars.  He was either loved or hated.  There must be many good reasons for such a polarized reception to what he had to say but my impression was that the line in the sand was drawn based on his discussion of the "fat vs carbohydrate" hypothesis.

Much of the literature studying the impact of various subcategories of macronutrients (such as saturated fat, trans fat, starch, and rapidly absorbed or refined carbohydrates) on vascular disease has been limited by the tools available for evaluating their propensity to modulate specific lipid parameters or other biological endpoints.  Variances in these variables are then related to heart attack rates, strokes, Alzheimer's disease or other cardiovascular endpoints.  As technology advances, the tools become available to more intimately dissect and measure physiologic indicators that will ultimately be found to reliably predict desired clinical outcomes of interest.  Until appropriate tools are available, scientists must often rely on inadequate metabolic measurements and opine about their prognostic implications.

In his review of the science behind the 'fat' hypothesis of heart disease, Mr. Taubes starts with the parameter of choice at the time, that being TC (Total Cholesterol).  He describes how it was quantitated in thousands of persons in numerous large studies designed to prove that TC was a predictor of future heart disease in broad population groups (as opposed to those subjects with familial hyperlipidemia).  Since the distribution of TC was almost superimposable between the groups with and without heart disease, it clearly was a poor discriminator between the two.

Following TC as the preferred indicator was LDL cholesterol (a. k. a.-the 'bad' cholesterol).  This was a bit better.  The latest, and hopefully most discriminating parameter thus far is the subclass determination of LDL cholesterol as measured by gradient gel electrophoresis.  This is a blood test that identifies the component particles that are the purported 'bad actors' in the heart disease saga-the small, dense LDL particles located in subfraction IVb.  Levels above 10% appear to identify those individuals who are at greatest risk of undergoing invasive cardiac surgeries such as angioplasty, stenting, and bypass procedures. 

This parameter is directly related to serum triglyceride levels and inversely related to HDL cholesterol (the 'good' cholesterol) levels.  The small, dense LDL particles are those that studies have shown are the most likely to damage blood vessels.  Because they vary as the HDL and TG levels do, they are intimately related to the action of insulin and insulin and blood sugar levels.  They are also linked to inflammatory mediators such as CRP (C-reactive protein), an indicator of inflammation throughout the body and a well-established predictor of future cardiac events.

Hopefully as measurement of LDL subclasses become more commonplace, discourses on heart disease will become less divisive.

Alzheimer's disease is a chronic disease frequently associated with age.  It is the most common dementing illness and affects 50% of those who reach age 85. Type II diabetes, insulin resistance and the Metabolic Syndrome are all considered risk factors for this disorder because they double or triple the chances of developing it and may also accelerate disease progression.  Based on this observation, it is reasonable to conclude that abnormalities of either blood sugar or insulin metabolism play a pivotal role.  If that is true, then it is likely that refined and other rapidly digested carbohydrates are important factors as well.

The characteristic brain tissue findings associated with Alzheimer's disease, senile plaques and neurofibrillary tangles , were identified by Alois Alzheimer about 100 years ago.  The 1990s were called the "Decade of the Brain" and with this designation research on Alzheimer's disease was put in the cross hairs of neurological investigators.  While this helped, what really was instrumental in facilitating an improved understanding of what caused the disease was the recognition that aberrations of glucose and insulin metabolism were associated with increased incidence. 

Among the vanguard of scientists pursuing this approach is Dr. Suzanne Craft at the University of Washington.  She has documented numerous abnormalities of glucose and insulin metabolism in Alzheimer's disease and has observed associations between these metabolic changes and the physiology of the beta-amyloid peptide found in the senile plaques that accumulate in the brains of afflicted patients.  Additional investigators pursuing this lead have found aberrations in the insulin signaling pathway in the brain,  while other neuroscientists have identified a link between the degradation of beta-amyloid and IDE (Insulin Degrading Enzyme-the enzyme responsible for recycling the hormone insulin).  When researchers inject a compound into the brains of mice that blocks the insulin receptor in the brain, or separately blocks the insulin signaling pathway, the animals develop plaque-like deposits and become demented.  Doctors from Brown University Medical School have coined the phrase "Type III Diabetes" to refer to the inability of the brain to properly use glucose in Alzheimer patients, akin to what happens in the bodies of diabetics.

To evaluate whether such findings have clinical merit, Dr. Craft conducted a study in patients suffering from Alzheimer's disease.  There are pharmaceutical compounds on the market that are able to improve the body's sensitivity to insulin.  She asked the question, if insulin resistance (the metabolic abnormality linked with diabetes and the Metabolic Syndrome) truly does play a seminal role in this form of dementia, then a drug that is able to improve insulin sensitivity should be a beneficial treatment.   That is exactly what she found!  Such observations serve to open the door for new pharmaceutical approaches.

The most exciting news is that factors other than drugs can improve insulin sensitivity.  They are diet and lifestyle choices including good nutrition, weight maintenance and exercise-all easily within our purview.  The new book Good Calories, Bad Calories by Gary Taubes provides novel nutritional recommendations to help in this regard. 

Just remember, the time to get started on such a brain-healthy program is now.

The prognosis for most patients with malignant brain tumors is poor.  Surgical resection followed by radiation therapy is the standard therapy.  Chemotherapy is often used in an adjuvant fashion.  Of potential interest in this area are several papers that have appeared in the medical literature over the past 10-15 years evaluating potential dietary approaches to these devastating, and frequently poorly responsive, neoplasms.  Interestingly, they didn't seem to make the radar screen of most oncologists and other physicians treating these patients.  Recently there has been renewed interest in the possible beneficial effects of a nutritional program to assist in the treatment of various cancers. 

The basis for such an approach arises from the metabolic inflexibility shown by brain tumor cells.  Having arisen from the same basic cell type, brain tumor cells share many common traits with normal brain cells.  However one of the key differences, and one that is shared by many other types of cancer cells, is that as they make the normal to cancerous transition they lose some of the properties of the normal brain cells.  In the case at hand, we will contrast how normal and cancer cells produce the large amount of energy that allows them to proliferate.  Brain cells depend almost exclusively on glucose they receive from the blood stream as the ultimate fuel source they generate their energy from.  Somewhere during their evolutionary history they learned a neat trick.  Famine and starvation were common occurrences and were usually associated with a fall in glucose availability.  This was because the body can only store enough glucose (mostly in the liver) to last about 24 hours.  After this reserve is exhausted, protein is broken down and converted to glucose to provide a continuing fuel supply for the brain cells.  It is not surprising that if this continues unabated our lean tissues including the heart and muscles would eventually start to malfunction.  In order to prevent this from occurring, we tap into our fat stores.  Yet, the brain can't burn fat so how does this help?  The fats in the blood are transported to the liver where they are partially burned.  The remaining partially burned fats are called ketone bodies, or ketones.  They are released into the blood and carried to the brain where they may be used as an alternative fuel source by the brain cells.  This preserves our lean tissue and gives the brain an additional source of energy.

Thus, normal brain cells can burn a mixture of glucose and ketone bodies and are very happy to do so.  They actually feel no difference because the energy is all they require whatever the source.  Stick with me, this is where it gets interesting.  Brain cancer cells usually lose the sophisticated metabolic machinery required to burn both glucose and ketones.  They still depend solely on glucose.  When they are faced with less glucose and more ketone bodies, they can only use the former.  Hence they react as if they were being starved.  When this happens, they can't produce the energy required to sustain their rapid growth rate, at least this is what should happen theoretically.  But does it really occur this way.  That is what several fascinating studies suggest.

In an article published in the Journal of the American College of Nutrition (1995;14:202-208) the impact of a diet that decreased serum glucose levels and increased ketone levels in two patients with advanced malignant astrocytomas (brain tumors) was studied.  To determine the effect on the metabolic rate of the tumors a special type of scanning technique was used.  It is called positron emission tomography, or PET.  Since tumors can't burn ketones, their metabolic rate is determined by how much glucose they burn.  That is precisely what PET scans measure.  After only one week on the diet these patients had their PET scans.  Amazingly, the metabolic rate of the tumors was cut by 20%.  This was the end of the study. 

What we really want to know is what effect this type of diet will have on the growth of the tumor.  This information can only be provided by controlled clinical trials.  To make sure they are comparing apples with apples, scientists need to perform the experiment in identical animals with identical tumor types.  When this was done they observed a 35-65% decrease in tumor growth and a marked increase in function and survival.  If confirmed in humans, this would be extraordinary indeed.      

The type of diet used was a calorically-restricted ketogenic diet.  One version of the diet was enhanced by the provision of MCT oil (medium chain triglyceride) which is rapidly converted to ketones in the body.  For information in how the diet was configured you can see the published results in the Journal of the American Dietetic Association (1995;95:693-697).    

I recently received an email questioning whether mental illness might in whole or in part be related to diet and nutrition.  It is clear to me that the two are intimately related.  Around the turn of the prior century the mental asylums of the southern United States were filled with patients suffering from dementia, melancholy, psychosis and a host of related ailments.  The disease responsible for this malady became known as pellagra.  The prevailing view of the medical profession at this time was that such an epidemic could only be caused by an infectious agent.  It took the knowledge and willpower of Dr. Joseph Goldberger to convince his colleagues that pestilence was not the cause.  He proved that the deficiency of a single nutrient from the diet, niacin (nicotinic acid) in this case, was the causative factor.  To change the mindset of the medical establishment he and his associates held 'filth fests' where they, acting as human guinea pigs, injected themselves with blood and ingested the excreta from patients severely afflicted with pellagra.  Other than for squeamishness in several of the study participants, no symptoms of disease developed over the ensuing six months.  This served to dispel any further investigations into the 'germ' theory of pellagra (niacin, or nicotinic acid, deficiency disease).  Nicotinic acid therapy produced miraculous results.  In spite of this discovery, it still took five years to cure the large number of patients suffering from the disorder.  Part of the problem was the persistence of poor dietary habits.  Poor nutrition remains a major health problem today.

Because of sporadic food fortification, pellagra has become a relic of the past.  However, the broad role of nutrition, and more specifically the impact of prolonged, less severe, dietary deficiencies appears to be playing an increasing role in the production of an array of illnesses.  Mental diseases are no exception.  This is being recognized in the clinic and in the laboratory.  Based on such insights physicians have started recommending dietary interventions alone, or in addition to pharmaceutical treatments to help their patients.  A Harvard-based psychiatrist, Dr. Andrew Stohl, thought one reason responsible for the increase in depressive disorders he was seeing was related to changes in the essential fatty acid content in the modern diet.  There are two essential fats required by the body.  They are the groups of omega 3 and omega 6 fatty acids.  We are consuming much more omega 6 fatty acids than required, and much less omega 3 fat.  Not only is the absolute amount of each class of fats important, their  ratio is also key.  Today we are experiencing an absolute deficiency of the omega 3 fats and a dramatic increase in the omega 6/omega 3 ratio in our diet.  When persistent, these alterations produce inflammation and cause changes in cellular attributes of neuronal function. 

To test his theory, he studied the response to essential fatty acid (EFA) therapy in a group of depressed patients.  Using pharmacological doses of the omega 3 EFAs (meaning about 5-10 times the amount required on a daily basis), he noted a marked improvement in their depressive symptoms.  Additional studies documented improvement in patients with Bipolar Disorder.  He also observed that in a number of his patients he was able to lower the dosage of medication when he incorporated omega 3 EFAs to the treatment regimen.  Obviously this is something that should not be considered without the input of your personal physician.  It does show the power of nutrition to beneficially impact brain function specifically in the arena of mood disorders.

When provided in amounts in excess of the RDI, other nutrients such as folic acid have been shown to beneficially impact depressive symptomatology.  This suggests that they have functional utility beyond their established role in basic metabolic processes. 

Mental illness clearly also has a genetic component, but the clinical phenotype-meaning if, when, and how it expresses itself- is clearly modulated by nutritional factors.  This reasoning even applies in the realm of ADD/ADHD (attention-deficit disorder/attention-deficit-hyperactivity disorder) where symptomatic improvement has coincided with EFA therapy.  This suggests to me there are intimate links between brain function, diet and mental illness and one component in the prevention and/or treatment of these devastating conditions should involve dietary recommendations.

There are millions of Americans who require insulin for the medical treatment of diabetes.  Doctors who direct the therapy of these patients often recommend what is referred to as 'tight' glucose control.  Such a regimen necessitates multiple injections of insulin throughout the day designed to keep blood sugar levels within normal limits at all times.  The purpose of this approach is to minimize the chances of developing cardiovascular complications (such as heart attack and stroke) that are associated with poor blood sugar regulation.  This requires frequent blood sugar testing throughout the day, calculation of insulin doses based upon the blood sugar level, and frequent injections of insulin.  One of the most troubling complications of this type of therapy is hypoglycemia (low blood sugar).  These hypoglycemic episodes are directly related to the injection of an excess of insulin.  When this occurs, symptoms may develop that include tremulousness, jittery feelings, dysphoria, and slowed mentation.  In the presence of even lower glucose levels confusion, somnolence and coma may ensue.  These constitute medical emergencies.  Whether these episodes are mild, or more severe, they are not good for the health of the brain.  Yet, for diabetics they are an unfortunate fact of life.  They may develop slowly, or more rapidly.  With a gradual onset the patients are trained to eat or drink something containing a rapidly digestible source of glucose to counteract the falling sugar level.  This frequently is sufficient to mitigate symptoms of hypoglycemia, but may generate an associated surge, or overshoot, of blood sugar-an undesirable result.  Such is the life of a person grappling with diabetes.  

Anything that would alleviate the occasionally serious signs and symptoms arising from these episodes would be helpful for a large segment of the population and would save many neurons.  A clever study, published in the medical journal Diabetes (1994;43:1311-1317), provided clues to this dilemma.  The brain usually depends almost exclusively on glucose to supply its substantial energy requirements.  During hypoglycemia associated with prolonged fasting or strenuous exercise, circulating ketone body levels increase many-fold.  Ketone bodies (acetoacetate and beta hydroxybutyrate) are products of partial fat metabolism which are generated in the liver and are secreted into the circulation.  They constitute a fuel source that is easily burned by the brain and is able to provide the energy the falling blood glucose can't.  This study was designed to investigate whether ketones would provide similar protection under insulin-induced hypoglycemia.  The experimental conditions were chosen to model what happens when diabetics become hypoglycemic due to injection of too much insulin.

Infusion of precise amounts of insulin was performed in two groups of subjects, one who had shortly before received an infusion of ketone bodies, and one group who had received a placebo (inactive infusion containing no ketone bodies).  Blood samples were then drawn and cognitive function testing was performed. 

Compared to the group that received insulin plus placebo (no ketones), the group that had insulin plus ketone bodies had reduced signs and symptoms of hypoglycemia.  They remained asymptomatic until blood glucose levels fell to the 40 mg/dl range compared to the production of symptoms in the more typical 50 mg/dl range of blood sugar in the other group.  These remarkable findings suggest that ketones help protect neurons from severe hypoglycemia.  While such therapy may not be useful in all circumstances, it is expected to expand the safety margin of tight glucose control in a large number of diabetic patients. 

Ketone body therapy is not currently available.  However,  when taken as a supplement to the diet MCT oil (medium chain triglyceride) is rapidly turned into ketone bodies which would be expected to produce the same beneficial effect.