Saturday, October 10, 2009











2. Why are These Deficiencies Present in America?

Unfortunately, intuitive, yet compelling arguments can be made as to why sun exposure and fat consumption might be unhealthy: the sun's UV rays can cause cancer by introducing errors in DNA transcription; heart disease is strongly associated with fatty deposits in the coronary artieries, fatty acids in the blood, and obesity. It is too easy to imagine that these correlates would likely be related to fat consumption. But does research support these intuitions?

It has been well established that vitamin D and calcium deficiencies are at epidemic proportions in America today. Calcium is known for its role in building strong bones and teeth, but it also plays a critical role in food metabolism. The best source of calcium is milk; however, today people prefer sugar-laden beverages over milk. It has been estimated that 75% of Americans are deficient in calcium. A recent study showed an alarming increase in broken bones in today's children compared to those in the 1970's [16]. Rickets is now reappearing among children [12], and teenagers are being diagnosed with osteoporosis, something that was unheard of in the last two generations.

It has been estimated that 70% of America's children are currently deficient in vitamin D [20] (Details) . This is not surprising, given current medical advice. The sunscreen industry lobby has convinced most Americans, including medical experts, that the sun should be aggressively avoided to prevent skin cancer. This, in spite of the fact that the sun is an excellent source of vitamin D, allowing the skin to manufacture it directly from cholesterol. Moreover, vitamin D is protective against all cancers (Details) a characteristic which, in my view, more than compensates for any extra skin cancer risk incurred by sunbathing. Vitamin D deficiency is also associated with an increased risk of high blood pressure and diabetes [35]. In order to get vitamin D from food, it is necessary to eat animal fats; animals manufacture vitamin D, a fat-soluble vitamin, and store it in their fat cells.

The American medical establishment is heavily entrenched in the idea that dietary fat is unhealthy. People are encouraged to adopt low fat diets, which inevitably lead to an increase in their intake of carbs and sugars, as much of the fat removed in foods is replaced with sugars to make them palatable. Many foods are also often highly processed and easily digested, leading to a rapid rise in blood sugar. At the same time, foods containing vitamin D are avoided, due to their universally high fat content.

Vitamin D is crucial to the absorption of calcium from the gut into the blood stream, and both vitamin D and calcium are important catalysts in crucial biological processes. Fats also promote the vuptake of calcium in the gut, whereas dietary fiber, touted as being healthy, impedes it [38] (Details) . These three nutrients, fats, vitamin D, and calcium, have intricate mutual dependiencies that make it important to consume them together. Americans are deficient in these important nutrients because of their perceived need to pursue a low fat diet and avoid sun exposure.

3. The Basic Problem: Impaired Glucose Uptake

My research on homeostasis, the process by which the body manages its energy needs, leads me to conclude that a person who suffers from calcium and vitamin D deficiency is operating under an unusual set of rules for energy management. Energy management is a crucial component of all cell metabolism. Any work that a cell does consumes energy, and this energy is supplied by either fatty acids, in the form of triglycerides (derived from dietary fat or supplied by fat cells on the body) or from glucose (derived from carbohydrates and proteins or supplied from temporary stores in the liver). While muscle cells can typically store a small amount of fuel locally, these local stores are quickly depleted during intense exercise. New supplies of nutrients are then extracted from the blood stream. The levels of glucose and triglycerides in the blood are constantly monitored and adjusted based on complex chemical signaling, to maintain sufficient supplies to all the body's cells.

The basic problem that a person with metabolic syndrome faces is an impaired ability for glucose to enter muscle cells [13] (Details) . Critically, this includes the heart muscle. Glucose transport is inhibited because the cell has an inadequate supply of calcium [27] and vitamin D [2][3][28] (Details) . These two nutrients are both critical for the pancreas to release insulin into the blood. Insulin in turn stimulates glucose uptake in the muscle cells [7]. Calcium is also critical for the migration of the catalyst GLUT4 to the membrane of the cell [21][36], where it orchestrates the transfer of glucose across the membrane, providing energy to the cell.

The muscle cell consumes energy when it contracts. The source of this energy is adenosine triphosphate (ATP), which releases energy through a chemical process that converts it to adenosine monophosphate (AMP). The energy that is released when the ATP is converted to AMP fuels muscle contraction. The cell's mitochondria are able to convert AMP back to ATP (to be recycled) by consuming either glucose or fat. When there is not enough fuel to convert AMP back to ATP, the ratio of AMP to ATP builds up. The ratio of AMP to ATP within the cell is a measure of its energy state, and is used by many different types of cells in the body to detect energy shortages and trigger corrective measures.

As the muscle cell exhausts its internal stores of energy, it attempts to draw in more glucose from the blood. An impaired glucose transport mechanism inhibits this process. As a consequence, the ratio of AMP to ATP in the cell steadily rises, activating a powerful regulating peptide secreted by the cell, known as AMPK. AMPK in the muscle cell promotes the movement of GLUT4 to the membrane, even in reduced insulin contexts [33]. With GLUT4 at the cell membrane the cell can now begin to draw upon the glucose and insulin supplies in the blood.

At this point, several things happen to counteract the falling level of blood glucose, which is detected by the pancreas and hypothalamus. They emit hormones and peptides that signal the body to replenish glucose levels in the blood. The alpha cells in the pancreas react by secreting glucagon, a hormone that triggers the liver to convert its stores of glycogen into glucose and release it into the blood stream. Similar glucose-sensing cells in the hypothalamus increase the appetite and stimulate the person to consume food, in order to replenish the supplies being drawn down in the liver.

Both of these glucose sensing mechanisms (in the hypothalamus and in the pancreas) depend on AMPK, and both involve a rush of calcium into the cell as part of their signaling cascade [27] (Details) . I hypothesize that deficiencies in calcium cause these glucose sensing mechanisms to detect low glucose levels internally even when glucose levels in the blood are still reasonably high. This is in fact an intelligent design, to tie their glucose-sensing mechanisms to those of the muscle cells, because, if the muscle cells can't absorb glucose efficiently, it is in some sense equivalent to having low blood glucose.

Thus, due to poor glucose uptake, the set point for the blood levels of glucose is maintained at an artificially high level. This is because poor uptake can be somewhat compensated for by elevating the concentration in the blood. Eating easily processed sugars and starches is the most effective way to quickly satisfy the cravings caused by poor glucose uptake. While the higher levels of glucose help to satisfy the muscles' needs, the glucose is also available to the fat cells, which feed on the excess sugars and store them as fats. Over time, sustained high blood sugar leads to chronic weight gain, diabetes, and heart disease.

Correcting the underlying glucose uptake problem will require long-term dietary changes which I will later describe. But first, I would like to explain some of the biological processes involved in food metabolism and weight, and show how the body tries to compensate for malfunctioning glucose uptake.

4. Fat Cells to the Rescue

The fat cells play a fascinating role in attempting to compensate for glucose uptake deficiencies. Fat cells are now considered by experts to be an essential part of the endocrine system, in that they can orchestrate energy management by many organs of the body by releasing hormones into the blood [8][11][26]. Fat cells are able to absorb excess sugar from the blood and convert it into fat. The fat will later be released into the blood stream as fatty acids and triglycerides, which offer an alternative energy source to the muscle cells (and most other cells of the body) - an alternative that does not suffer from the problem of membrane transport, which is specific to glucose.

In a situation where glucose transport is defective, the fat cells appear to: (1) program the muscle cells to consume fats rather than sugars, and (2) take upon themselves the task of converting as much of the incoming sugar as possible to stored fats. The fat cells accumulate fat whenever the blood sugar levels are high, and then release it into the blood stream whenever blood sugar levels are low enough. Thus they strive to maintain in the blood stream a steady supply of an alternative and more efficient source of fuel (fats) for the muscles to consume instead of sugar.

Through signaling involving a peptide released into the blood stream by fat cells, called leptin, fat cells are able to redirect the muscle cells to obtain most of their energy needs from fats instead of from glucose. However, as a consequence, the fat cells then become burdened with the task of of converting as much as possible of the incoming glucose to fats.

The fat cells must thus buffer up a reserve store of fats, and release fats into the blood to provide nutrition for the muscle cells during fasting conditions, when glucose is not available. After meals, when glucose levels are high, the fat cells are preoccupied with extracting glucose from the blood, and therefore are unable to release fats. Thus, they must provide additional triglycerides in advance of a meal, so that the muscle cells will continue to have food while the glucose is being taken up by the fat cells and converted to a renewed supply of fat. This safety buffer of triglycerides is what is responsible for the observed high fasting triglyceride levels of the obese.

If more dietary fats were consumed, fat from food sources would be available to the muscles while the fat cells are distracted with taking up glucose, and there would be correspondingly less glucose to convert. But because so much fat is needed to feed the muscles, and because so much excess sugar is going to waste, the fat cells find themselves unable to meet the demand, so they end up proliferating -- and the person becomes obese.

The fat cells also suffer from an impairment of glucose transport, as they rely on the same mechanism involving GLUT4 and insulin to transport sugar across their cell walls (Details) . Fat cells however are able to internally hoard both vitamin D [5] and calcium [40], so that they can improve somewhat their own abilities to transport glucose across their cell membrane. But this also leaves the muscles more vulnerable to glucose uptake inefficiencies, because it further depletes the availability of calcium and vitamin D in the blood. As long as the muscle cells use up fats as their energy source instead of glucose, and as long as the fat cells can maintain a good supply of fats in the blood, all will be well. This is the scheme that the fat cells are trying to perpetuate.

5. How does the Heart Cope?

The heart is similar to the skeletal muscles in that it too faces glucose deprivation when calcium and vitamin D supplies are inadequate. Like the skeletal muscles, it can utilize both fat and sugar as fuel, and it uses the same GLUT4 peptide to usher the glucose across the cell walls [31]. As long as the fat cells in the rest of the body are able to release a steady stream of triglycerides into the blood stream, the heart can simply use these for most of its energy needs. But it is likely that, especially after a high-carb, low-fat meal, there will be intervals when the heart is fuel deficient.

I propose that the heart adopts two different coping mechanisms: (1) grow bigger, and (2) develop its own "private" supply of nutrients, in the form of fat deposits. By becoming enlarged, the heart is using the strategy of "strength in numbers." Imagine that six children are competing against three adults in a tug-of-war. The children may win, even though they are weaker, simply because there are more of them. Likewise, the heart, by increasing the number of muscle cells, may be able to beat as strongly as a smaller heart, but each independent muscle cell carries a lesser burden, and therefore can get by on a reduced fuel supply.

The second strategy, creating an internal supply of fats, begins with fatty deposits in the linings of the arteries supplying the heart, known familiarly as arteriosclerosis. These deposits, with time, become "hardened," i.e, associated with calcium deposits; calcium that has been hoarded by the fat cells over the years, just as is done in the abdominal fat cells. The calcium is hoarded because it enables the fat cells to absorb glucose and convert it into fats. As a further strategy, the heart develops a layer of "pericardial fat," [9] fatty deposits, typically just outside of the major arteries feeding into the heart. These deposits supply additional fats directly to the heart, to supplement those lining the artery walls.

One problem with encasing the heart with fats is that it becomes susceptible to bacterial infection. The highly oxygenated blood, coming directly from the lungs, may easily become contaminated with bacteria that have entered the body through the lungs. These bacteria may find it attractive to feed off of the fatty deposits lining the arterial walls. As a consequence, cholesterol must infiltrate the artery walls, as a first line of defense in the immune system, to attack the bacteria (Details) . The cholesterol also draws upon white blood cells to assist in the battle. Furthermore, the fat cells encasing the heart, as contrasted with fat cells elsewhere in the body, are especially primed to release cytokines [9], which are also infection-fighting agents. Thus the presence of fat in the heart's arterial walls and encasing the heart is associated with high levels of cholesterol and cytokines in the blood.

6. Hormones and Enzymes that Control Appetite

The fat cells are able to influence the muscles to preferentially take up fats rather than glucose by releasing certain hormones into the blood, hormones that also have a powerful influence over appetite. One of these hormones is leptin. While leptin influences the muscle cells indirectly through its signaling in the hypothalamus, it also stimulates the muscle cells directly, and influences them to oxidize fatty acids in their mitochondria [26]. Leptin also encourages the fat cells to release their fats through lipolysis [24]. All of these actions work in concert to redirect fuel usage away from glucose. The programming of the muscles to preferentially consume fats aligns well with the fat cells' infusion of fats into the blood and absorption of sugars through their fat-producing factories.

Leptin also has the effect, via the hypothalamus and pituitary gland, of suppressing appetite. Adiponectin is another hormone released by fat cells, and it is generally agreed that adiponectin induces hunger. Leptin and adiponectin levels would ordinarily fluctuate throughout the day, with leptin levels rising at night to encourage a switch from glucose-based to fat-based energy management. However, in the obese person, the leptin levels are typically high all the time, and the adiponectin levels are kept very low [41]. High levels of leptin in the blood signal to the appetite center in the brain a sense of being full [8], whereas high levels of adiponectin are hunger-inducing. This means that the obese are being informed both that they are full, and that they are not hungry. You would think that this would protect them from overeating. However, it is likely that the observed insensitivity to leptin as an appetite suppressant in the obese is also related to calcium depletion, because the signaling mechanisms that respond to leptin in both the hypothalamus (Details) and the pituitary gland (Details) depend on changes in internal calcium concentrations.

So, why does the obese person overeat? I have reached the almost inescapable conclusion that the culprit is over-sensitized AMPK, as is also suggested by several other researchers [15][17][18]. AMPK operates not only in muscle cells, but in just about all cells of the body [15]. In particular, it plays a critical role in sensors in specialized cells in the brain: in the hypothalamus and the pituitary gland. These cells release chemicals into the blood that influence the liver, the pancreas, and the appetite, in terms of turning on or turning off mechanisms that will provide further fuel into the system, in the form of either fats or glucose.

As was said before, whenever the muscles exert themselves for sustained periods, they soon reach a critical point where large amounts of ATP have been converted to AMP, in the process of releasing energy to drive muscle contraction. The AMP:ATP ratio rises sharply. This activates AMPK, which then reprograms the muscle to both increase the levels of calcium inside the cell and consume more sugar [30][32][37], a very bad idea since calcium and insulin are in short supply. Certain GI or "Glucose Inhibited" cells in the hypothalamus, as well as alpha cells in the pancreas, are programmed to respond to low glucose levels by instructing the liver to release more sugars and increasing the appetite for foods with a high glycemic index. They essentially broadcast the urgent message to the brain that more glucose is desperately needed. The person is compelled to consume sugars and carbs that will digest very quickly and further raise the already high blood sugar levels.

7. The Body Grows Larger

Ironically, the arguments made above suggest that aerobic exercise is ill-advised for those who suffer from this impaired glucose-uptake syndrome. While many have speculated that our more sedentary lifestyle is likely a contributing factor toward obesity, I believe that instead physical fatigue itself is a predictable outcome of defective glucose metabolism, The inability to obtain sufficient fuel from glucose on the part of both the muscles and the heart simply saps us of the energy to move around [22] (Details) .

The effect of sustained aerobic exercise is to switch the muscle back into a glucose-uptake modus operandi for energy acquisition, which, however, is malfunctioning due to calcium and insulin insufficiency. Exercise is able to induce GLUT4 to migrate to the membrane even in the absence of calcium [13] . The insulin/glucose levels fall to possibly dangerously low values, which induces the appetite center in the hypothalamus to sound the alarm bells. The subsequent appetite stimulation induced by AMPK in the hypothalamus overrules all of the other appetite regulating signals and compels the person to overeat the very foods they should be avoiding.

As a consequence of further increases in the already high levels of sugar in the blood, the fat cells are compelled to squirrel away as much of the excess sugar as they can. Particularly susceptible to this urge to make fats will be the abdominal fat, since it is situated in close proximity to both the pancreas and the liver. The higher blood concentrations of both insulin and glucose provide extra impetus to assimilate sugars and manufacture fats. Thus the abdominal fat cells are more efficient in storing food than the peripheral fat cells. They will also tend over time to increase in size and multiply, in order to distribute the task load among their neighbors and reduce the burden carried by each individual cell. The additional fat cells will further deplete the available calcium and vitamin D in the blood, leading to an even poorer ability on the part of the muscle cells to take up glucose.

Alongside the growth of fat cells, other cell types also need to become more abundant, to support the increased burden of a larger body size, combined with reduced energy supply. As already mentioned, the heart becomes enlarged. Muscles must increase in size both to be able to haul around the extra weight and because of their innate inefficiencies in fuel utilization [14]. Bones must grow bigger and stronger to support the excess weight. Blood supplies have to be extended to supply nutrients to all of these proliferating cells. All of this means that the body's overall nutritional needs continue to grow, which puts futher burdens on the fat cells, thus completing the vicious cycle. Over time the person with a severe deficiency in calcium, vitamin D, and fats grows steadily larger, eventually reaching a condition of morbid obesity.

8. The Metabolic Syndrome

A person with impaired glucose uptake as a consequence of calcium and vitamin D deficiencies ends up in a situation where both glucose and triglyceride levels in the blood are abnormally high. The heart and muscles are very poor at utilizing glucose, and hence they will depend to a large degree on fats (triglycerides) to supply their nutritional needs. The fat cells must release excess amounts of triglycerides during fasting conditions, such as at night, because they will not be able to release triglycerides once they are reassigned to the task of taking up excess glucose. After a meal, when glucose levels are high, the triglycerides will be steadily drawn down by the heart and muscles, while the fat cells absorb the glucose and begin the process of converting it into more fat.

Under conditions of aerobic exercise, the muscles and heart are reprogrammed to consume additional glucose, which causes glucose levels to plummet. This sets off alarm bells in the pancreas, which induces the liver to release more sugar, and in the hypothalamus, which stimulates the appetite for foods with a high glycemic index. The signalling mechanisms in the pancreas and the hypothalamus are likely also defective due to the calcium and insulin deficiencies [6][29] (Details) , and so they maintain a set point for glucose in the blood that is abnormally high. But the high glucose levels are in fact required, in order to compensate for the inefficient transport of glucose across the membrane of the muscle cells. The excess available glucose in the blood is taken up by the fat cells, the fat cells enlargen and multiply and the person becomes obese. Furthermore, the heart, a muscle, enlarges and becomes encased in fatty tissues, and its arteries become laden with fatty deposits, i.e., arteriosclerosis.

I believe the low HDL and high LDL can also be explained as follows. HDL is the carrier for cholesterol that is to be returned to the liver, where it can be disposed of via the gall bladder. It is dispensed by the gall bladder into the gut along with bile, and performs the very useful function of helping digest fats. Anyone who is consuming a low-fat diet requires less cholesterol for digesting the reduced dietary fat, and HDL levels fall. LDL is likely high because it is the carrier that transports cholesterol to the tissues. One of those tissues is the fatty deposits in the artery walls of the heart, that were placed there, according to my interpretation, to supply extra fuel to the heart. But these fatty deposits are also vulnerable to invasion by bacteria and viruses, entering through the lungs. High levels of cholesterol would need to be made available in the blood stream to help keep these invasive microbes under control.

Thus plausible outcomes of the calcium, vitamin D, and dietary fat deficiency are obesity, high blood sugar, arteriosclerosis, high levels of triglycerides, elevated LDL and low HDL, six key aspects of the metabolic syndrome (Details) .

9. Metabolic Syndrome: The Solution

Most of the foods that contain vitamin D naturally have been taken off the menu of the American diet due to the belief that fats are harmful to your health. Since vitamin D is manufactured by animals, a strict vegetarian won't get any vitamin D from their food intake. Foods that are high in vitamin D are also very high in fat and cholesterol as well, and have therefore been for the most part "black-listed." These include pork lard, bacon, egg yolk, liver, caviar, butter, and raw milk. Americans have recently been responding to the claim that fats are healthy as long as they are omega-3 fats, which has fortunately brought fatty fish, such as sardines, salmon, and mackerel, back on the menu. A fantastic source of vitamin D is cod liver oil, which used to be routinely given as a natural vitamin supplement to children, and still is in many parts of Europe. But Americans seem to have unfortunately abandoned this practice. Several foods in the American diet have been fortified artificially with vitamin D, but many of these, such as cereals, orange juice, and non-fat milk, contain little or no fat, so it is mysterious to me how the fat-soluble vitamin D can possibly be properly distributed in the product or properly absorbed.

The lack of adequate dietary fat contributes to the metabolic syndrome in at least four ways: (1) vitamin D is only available in fatty food sources because it is a fat-soluble vitamin, (2) calcium uptake is more efficient when the calcium is consumed with dietary fats, (3) calcium uptake depends critically on the presence of vitamin D, which is deficient due to (1) above, and (4) the burden of fat cells to manufacture fatty acids from sugar is alleviated by the dietary availability of fats from ingested food sources.

By far the best way to acquire adequate vitamin D is through sun exposure. Possibly one of the most important components of a healthy lifestyle is to spend ample time outside in the sunlight. However, today's lifestyle in America often leaves little time for outdoor activities. Furthermore, Americans have been trained to fear rather than bask in the sun, mainly due to the aggressive ad campaigns of the sunscreen industry arguing that the sun causes cancer. Of course, one needs to avoid sunburn, but, building up exposure slowly by developing a tan in the spring affords natural protection from burning in the summer. This strategy is, in my view, far preferable to liberally applying sunscreen. Sunscreen at an SPF level of 8 or greater effectively wipes out any opportunity to manufacture vitamin D in the skin. The protection acquired from all cancers due to the vitamin D that is manufactured in the skin upon sun exposure more than compensates for any increased risk to skin cancer caused by sun exposure.

Another healthy choice is to eliminate 'empty carbs' as much as possible. This includes such foods as cookies, donuts, candies, and soft drinks. Switch from white to whole wheat bread, and from white rice to brown rice. When eating potato, be sure to put lots of butter and/or sour cream on it. Potato ingested with fat has a much lower glycemic index than potato ingested without fat. This practice will help prevent blood sugar levels from spiking, which is healthy in terms of combating diabetes and heart disease. However, fixing the metabolic syndrome caused by high blood sugar is only possible if, along with limiting consumption of empty carbs, you also repair your deficiencies in calcium and vitamin D.

I would also argue that one should make sure to ingest adequate amounts of dietary fat, especially dairy fat [33]. Whole milk is particularly outstanding because it contains substantial amounts of calcium and vitamin D, and it contains the necessary fat to assure that these two elements will be well utilized rather than just passing through the digestive system unabsorbed. Animal fats such as bacon are good sources of vitamin D, while also supplying fatty acids to help with energy needs. Fatty fish such as salmon and sardines are particularly good because they contain both omega-3 fats and vitamin D. One should assiduously avoid the trans fats found in processed foods such as cookies, crackers, and margarine. Butter and eggs are also healthy choices. Egg yolk is particularly good because it contains both fats and vitamin D. Nuts, particularly walnuts, almonds, and macademia nuts, are excellent sources of omega 3 fats.

Finally, it is essential to get enough calcium. Ingest the calcium with dietary fats. If you're fond of milk and cheese, then you can probably supply all of your calcium needs through dairy products, as long as you choose ones that contain fat (i.e., avoid non-fat dairy products). If you don't like milk or are allergic to lactose, then bean curd is an excellent choice for calcium. Bean curd can be prepared in lots of ways, from raw soybeans to soy milk to Chinese tofu dishes. However, it's not standard fare in the American diet, so it might be preferable to go with the third option for calcium, which is to eat lots of leafy green vegetables such as spinach, broccoli, kale, and mustard greens. Again, these need to be eaten with fats to be properly absorbed, which means frying them in oil or liberally adding butter.

It has been amply demonstrated in research studies that most vitamins and minerals taken in pill form are far less effective than the forms found naturally in foods. In many cases, you may be just wasting money on something that passes through the digestive system unabsorbed, and also creates abnormal situations of anomalously high levels of concentrated nutrients in the gut, which seems intuitively to be a bad idea. However, sometimes due to lifestyle constraints, it may be impossible to get enough sun exposure, and a vitamin D suppplement would likely be beneficial in such situations.

10. Metabolic Syndrome: Summary

For several decades now, Americans have come to believe that the following two practices are foundational in a healthy lifestyle: (1) eat a low-fat diet, and (2) stay away from the sun. I believe that, to solve the obesity epidemic, we need to abandon these two practices. Additionally, if people consume adequate amounts of calcium, then all three nutritional deficiencies that have led to obesity will be overcome: vitamin D, calcium, and dietary fat.

The result of these three deficiencies is defective glucose uptake in both muscle and fat cells. The obese person becomes trapped in an endless metabolic cycle of trying to supply the energy needed for a steadily increasing demand. The fat cells are at the center of the storm, because they are burdened with the arduous assignment of converting the excess consumed sugars and carbohydrates into fat. The fat cells must do this because the muscle cells are impaired with a malfunctioning ability to metabolise sugars. Even if the metabolic problem were not fixed, if the obese person simply ate more fat, and therefore consumed fewer carbs, the fat cells' burden would be greatly alleviated. In addition, getting plenty of vitamin D and calcium, either through diet or sun exposure, would alleviate the core problem of impaired glucose transport across the cell wall. Now that the heart and muscles can utilize sugars directly, the excessive burden on the fat cells to expand and proliferate is relieved, and the body fat will inevitably melt away.

11. What's Next?

Not all people who have deficiencies in vitamin D, calcium, and dietary fats become obese. Whether the person accumulates excess body fat to compensate probably depends on genetic make-up. However, those who stay thin suffer consequences that are at least equal in severity, and perhaps exceed, the health issues associated with obesity.

Dr. Fred Baughman, a pediatric neurologist, has recently published a book, How Psychiatry Makes 'Patients' Out of Normal Children , [1] in which he proposes that Attention Deficit Hyperactivity Disorder (ADHD) is a fake disease, invented for the sole purpose of pushing drugs like Ritalin that are claimed to combat it. He cites the case of a 14 year old child, Matthew Smith of Royal Oak, Michigan, who fell off his skate board and died suddenly. Matthew had been on Ritalin since first grade, due to a diagnosis of ADHD. Upon autopsy, his heart was found to be diffusely enlarged, scarred, and riddled with fat. The medical examiner blamed Ritalin for the heart damage, and certainly Ritalin may have aggravated the problem. It may be the case that Ritalin works by making the brain more efficient at utilizing fats, but this would be at the expense of the heart. The heart would then be compelled to further enhance its own private store, to satisfy its nutritional needs. However, I believe that the fatty and enlarged heart and the ADHD are both a consequence of an underlying defect in glucose metabolism.

In my next blog post, I will discuss how defective glucose uptake in children may explain a number of problems assoicated with an inadequate supply of fat to the brain, such as ADHD, Asperger's syndrome, depression, and sleep disorders. The brain is an extremely fatty organ. All of its nerve fibers are coated with a fatty myelin sheath that insulates them to keep their signals intact. The brain does not use fat for fuel. This would be extremley unwise, becauseit would be unable to avoid feeding off of itself. However, with inadequate fat supply, it is unable to build healthy nerve fibers, and this has dire consequences to mental health. The consequences are especially disturbing for children, whose immature brains are constantly integrating new knowledge, concepts, and experience, to make sense of the world they live in and their role in it.

References for Metabolc Syndrome Essay

[1] F. Baughman, Jr., MD, How Psychiatry Makes 'Patients' Out of Normal Children , Trafford Publishing, 2009.

[2] A. M. Borissova, T. Tankova, G. Kirilov, L. Dakovska, and R. Kovacheva, "The effect of vitamin D3 on insulin secretion and peripheral insulin sensitivity in type 2 diabetic patients," Int J Clin Pract, Vol. 57, pp. 258 -- 261, 2003.

[3] B.J. Boucher, N. Mannan, K. Noonan, C.N. Hales, and S.J. Evans, "Glucose Intolerance and Impairment of Insulin Secretion in Relation to Vitamin D Deficiency in East London Asians,"Diabetologia Vol. 38, 1239-- 1245, 1995.

[4] J.I. Botella-Carretero, F. Alvarez-Blasco, J.J. Villafruela, J.A. Balsa, C. Vazquez, and H.F. Escobar-Morreale, "Vitamin D deficiency is associated with the metabolic syndrome in morbid obesity," Clin Nutr., Vol. 26 No. 5, pp. 573-80, Oct, 2007.

[5] M. Blum, B. Dawson-Hughes, G. Dolnikowski, E. Seyoum, and S. Harris, "Vitamin D3 in Fat Tissue," Endocrine Journal, Vol. 33, No. 1, March, 2008.

[6] J.B.C. Carvalheira, E.B. Ribeiro, E.P. Araujo, R.B. Guimaraes, M.M. Telles, M. Torsoni, J.A.R. Gontijo, L.A. Velloso, M.J.A. Saad, "Selective Impairment of Insulin Signalling in the Hypothalamus of Obese Zucker Rats," Diabetologia, Vol. 46, No. 12, pp. 1629-40, 2003.

[7] C. Castillo, C. Bogardus, R. Bergman, P. Thuillez, S. Lillioja, "Interstitial insulin concentrations determine glucose uptake rates but not insulin resistance in lean and obese men, J Clin Invest Vol. 93, pp. 10-16, 1994.

[8] R. Coppari, M. Ichinose, C.E. Lee, A.E. Pullen, C.D. Kenny, R.A. McGovern, V. Tang, S.M. Liu, T. Ludwig, S.C. Chua Jr, B.B. Lowell, and J.K. Elmquist. "The hypothalamic arcuate nucleus: a key site for mediating leptin's effects on glucose homeostasis and locomotor activity," Cell Metab. Vol. 1 No. 1, pp. 63-72, Jan, 2005.

[9] J. Ding, S. Kritchevsky, T.B. Harris, G.L. Burke, R.C. Detrano, M. Szklo, and J.J. Carr, "The Association of Pericardial Fat with Calcified Coronary Plaque," Obesity, Vol. 16, No. 8, pp. 1914--1919, 2008.


[11] A. Glavaski-Joksimovica, E.W. Rowea, K.Jeftinijaa, C.G. Scanesa, L.L. Andersona,and S. Jeftinijaa, "Effects of Leptin on Intracellular Calcium Concentrations in Isolated Porcine Somatotropes," Neuroendocrinology Vol. 80, pp. 73-82, 2004.

[12] L.M. Gartner, MD and F.R. Greer, MD, "Prevention of Rickets and Vitamin D Deficiency: New Guidelines for Vitamin D Intake," Pediatrics Vol. 111, No. 4, pp. 908-910, April 2003,

[13] W.T. Garvey, L. Maianu, J. Zhu, G. Brechtel-Hook, P. Wallace, and A.D. Baron, "Evidence for defect in the trafficking and translocation of GLUT4 transporters in skeletal muscle as cause of human insulin resistance," The Journal of Clinical Investigation, Vol. 101, pp. 2377-2386, 1998.

[14] K. HNdllsten, H. Yki-JNdrvinen, P. Peltoniemi, V. Oikonen, T. Takala, J. Kemppainen, H. Laine, J. Bergman, G.B. BolliN', J. Knuuti and P. Nuutila, "Insulin- and Exercise-Stimulated Skeletal Muscle Blood Flow and Glucose Uptake in Obese Men," Obesity Research Vol. 11, pp. 257-265, 2003.

[15] D G Hardie, "AMPK: a Key Regulator of Energy Balance in the Single Cell and the Whole Organism," International Journal of Obesity Vol. 32, pp. 7-12, 2008.

[16] S. Khosla, MD; L.J. Melton III, MD; M.B. Dekutoski, MD; S.J. Achenbach, MS; A.L. Oberg, PhD; B.L. Riggs, MD, "Incidence of Childhood Distal Forearm Fractures Over 30 Years: A Population-Based Study," JAMA. Vol. 290, pp. 1479-1485, 2003.

[17] B. Kola, "Role of AMP-Activated Protein Kinase in the Control of Appetite," Journal of Neuroendocrinology, Vol. 20, No. 7, pp. 942--951, July, 2008.

[18] B. Kola, A. B. Grossman, and M. Korbonits, "The Role of AMP-Activated Protein Kinase in Obesity," Obesity and Metabolism, Korbonits M., Editor, Vol. 36, Front Horm Res. Basel, Karger, pp. 198--211, 2008.

[19] I. Kojima and M. Nagasawa, "TRPV2: A Calcium-Permeable Cation Channel Regulated by Insulin-Like Growth Factors," Chapter 7 in TRP Ion Channel Function in Sensory Transduction and Cellular Signaling Cascades,, Taylor & Francis Group, LLC, 2009.

[20] J. Kumar, P. Muntner, F.J. Kaskel, S.M. Hailpern, and M.L. Melamed, "Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001-2004," Pediatrics, Vol. 124, pp. 362-370, 2009.

[21] Y. Li, P. Wang, J. Xu, F. Gorelick, H. Yamazaki, N. Andrews, and G. Desir, "Regulation of Insulin Secretion and GLUT4 Tracking by the Calcium Sensor Synaptotagmin VII," Biochem Biophys Res Commun, Vol. 362, No. 3, pp. 658--664, October 26, 2007.

[22] W. Lim, MD; S. Hong, PhD; R. Nelesen, PhD; J.E. Dimsdale, MD, "The Association of Obesity, Cytokine Levels, and Depressive Symptoms With Diverse Measures of Fatigue in Healthy Subjects," Arch Intern Med. Vol. 165, pp. 910-915, 2005.

[23] S. Liu, Y. Song, E. Ford, J. E. Manson, J. E. Buring, and P. M. Ridker, "Dietary Calcium, Vitamin D, and the Prevalence of Metabolic Syndrome in Middle-Aged and Older U.S. Women,"

[24] A. Martia, F.J. Novob, E. Martinez-Ansoa, M. Zaratieguib, M. Aguadoa and J.A. Martineza, "Leptin Gene Transfer into Muscle Increases Lipolysis and Oxygen Consumption in White Fat Tissue inob/obMice" Biochemical and Biophysical Research Communications, Vol. 246, No. 3, 29 pp. 859-862, May 1998.


[26] Y. Minokoshi, Y.B. Kim, O.D. Peroni, L.G. Fryer, C. Muller, D. Carling, and B.B. Kahn, "Leptin stimulates fatty-acid oxidation by activating AMP-activated protein kinase," Nature. Vol. 17, pp. 339-43, Jan. 2002.

[27] P.D. Mountjoy and G.A. Rutter, "Glucose Sensing by Hypothalamic Neurones and Pancreatic Islet Cells: AMPle Evidence for Common Mechanisms?," Experimental Physiology, December, 2006.

[28] A.W. Norman, J.B. Frankel, A.M. Heldt, and G.M. Grodsky, "Vitamin D Deficiency Inhibits Pancreatic Secretion of Insulin," Science, Vol 209, Issue 4458, 823-825, 1980.

[29] S Obici, BB Zhang, G Karkanias, and L Rossetti, "Hypothalamic insulin signaling is required for inhibition of glucose production." Nat Med Vol. 8, pp. 1376-82, 2002.

[30] E.O. Ojuka, T.E. Jones, L.A. Nolte, M. Chen, B.R. Wamhoff, M. Sturek, and J.O. Holloszy, "Regulation of GLUT4 biogenesis in muscle: evidence for involvement of AMPK and Ca2+," Am J Physiol Endocrinol Metab Vol. 282, NO. 5, May 2002.

[31] A.L. Olson and J. E. Pessin, "Structure, function, and regulation of Mammalian facilitative glucose transporter gene family," Annual Reviews Nutrition, Vol. 16, pp. 235-256, 1996.

[32] S. Park, T.L. Scheffler, A.M. Gunawan, H. Shi, C. Zeng, K.M. Hannon, A.L. Grant, and D.E. Gerrard, "Chronic elevated calcium blocks AMPK-induced GLUT-4 expression in skeletal muscle," Am J Physiol Cell Physiol Vol. 296,pp. C106-C115, 2009.

[33] M. A. Pereira, D. R. Jacobs, Jr, L. Van Horn, M. L. Slattery, A. I. Kartashov, and D. S. Ludwig, "Dairy consumption, obesity, and the insulin resistance syndrome in young adults: the CARDIA Study." JAMA Vol. 287, pp. 2081 -- 2089, 2002.


[35] J.P. Reis, D. von Muhlen,E.R. Miller, 3rd, E.D. Michos, and L.J. Appel, "Vitamin D Status and Cardiometabolic Risk Factors in the United States Adolescent Population," Pediatrics, August 3, 2009.

[36] K. Stefikova, V. Spustova, K. Sebekova, and R. Dzurik, "Magnesium deficiency impairs rat soleus muscle glucose utilization and insulin sensitivity." Biomed Experts, 1992.

[37] W.W. Winder, "Energy-sensing and signaling by AMP-activated protein kinase in skeletal muscle," J Appl Physiol.Vol. 91, No. 3, pp. 1017-1028, Sep., 2001.

[38] R.L. Wolf, J.A. Cauley, C.E. Baker, R.E. Ferrell, "Factors Associated with Calcium Absorption Efficiency in Pre-and Perimenopausal Women," American Journal of Clinical Nutrition,, Vol. 72, pp. 466--471, August, 2000.

[39] M. B. Zemel, and S.L. Miller, "Dietary Calcium and Dairy Modulation of Adiposity and Obesity Risk," Nutr Rev. Vol. 62, No. 4, pp. 125--131, April, 2004.

[40] M. B. Zemel, H. Shi, B. Greer, D. Dirienzo and P. C. Zemel, "Regulation of adiposity by dietary calcium," The FASEB Journal, Vol. 14, pp. 1132-1138, 2000.

[41] J.M. Zigman and J.K. Elmquist, "Minireview: From Anorexia to Obesity -- The Yin and Yang of Body Weight Control" Endocrinology, Vol. 144, No. 9, pp. 3749-3756, 2003.

Creative Commons License
The Obesity epidemic: is the Metabolic Syndrome a Nutritional Deficiency Disease? by Stephanie Seneff is licensed under a Creative Commons Attribution 3.0 United States License.