The Obesity Epidemic: is the Metabolic Syndrome a Nutritional Deficiency Disease?

by Stephanie Seneff
September 29, 2009

Note: I have long believed that inadequate dietary fat is responsible for many different health issues in the United States today. It is reassuring to know that I am not alone in this belief -- I am now aware of at least four books written by doctors and scientists that make a strong case in favor of fats, alongside a harsh critique of 'empty carbs.' The African Masai and Alaskan Eskimos have demonstrated that it is possible to avoid heart disease even with a very high fat diet. I now believe, in fact, that a low-fat diet promotes heart disease, as I have argued in the essay accessible from the links below.

1. Introduction

Here the case is presented for the idea that the obesity epidemic in America, and the closely related metabolic syndrome, may be a consequence of three principle nutritional deficiencies: vitamin D, calcium, and dietary fats. The claim is made that defective calcium metabolism leads to impairment in glucose uptake in the muscles and heart, which compels them to utilize mainly fats as an energy source. However, fats are in short supply, due to the low-fat diet. The only recourse is to build up a steady supply of fats and store them on the body, both as adipose tissue and as arterial fat deposits.

2. Why are these Deficiencies Prevalent in America?

This section points out that a majority of Americans are currently deficient in both vitamin D and calcium. This is not surprising, given our fear of sun exposure and avoidance of foods containing vitamin D due to their high fat content. It also discusses the intricate interdependencies among these three nutrients.

3. The Basic Problem: Impaired Glucose Uptake

This section introduces the biological mechanisms by which the body manages homeostatis, and describes why calcium deficiency leads to an inability of muscles to effectively take up glucose (sugar) for their energy needs, through an impaired ability to transport both insulin and glucose across cell walls.

4. Fat Cells to the Rescue This section describes the important role that fat cells take on in trying to compensate for the problem of impaired glucose uptake. The solution they devise is to program the muscles to prefer fats over sugars, and then to insinuate themselves into the loop, by taking on the arduous task of converting incoming sugar into fats. However, they must maintain a significant buffer because they are unable to release fats while they are taking sugar in.

5. How does the Heart Cope?

In the absence of sufficient calcium, the heart also suffers from an impaired ability to utilize glucose for fuel. It was an epiphany when I gained the insight that fat deposits in the arteries of the heart might be nothing more than an auxiliary food supply stashed away to assure that the heart is never without energy supplies. These deposits can, over time, grow out into the surrounding cavity to become "pericardial fat." They are also susceptible to infection by bacteria and viruses, and I suspect that this, more than anything else, is what leads to heart attacks.

6. Hormones and Enzymes that Control Appetite

Here I talk about the various hormones that control the appetite, and describe how they are malfunctioning in the obese person. Leptin, which signals satiety, is set high, whereas adiponectin, which signals hunger, is set low. Yet the obese person clearly overeats, despite these indicators that should prevent them from eating. I argue that the misfiring signaling agent that leads to overeating is AMPK, which is hypersensitized to indicate dangerously low sugar levels even when levels are not actually low, due to the slow permeability of glucose across the cell wall of the neurons controlling appetite.

7. The Body Grows Larger

This section discusses how aerobic exercise allows the muscles to take up glucose even in the absence of calcium, and hence leads to a dramatic decrease in the blood glucose levels. Because the poor transport problem exists in the neural cells detecting low glucose, they are misled to believe that glucose is low, and they trigger a craving for foods with a high glycemic index. As the body grows larger, the energy demands also increase, and the fat cells must proliferate to maintain adequate supplies of fats, especially after high carb meals when their fat stores become temporarily unavailable.

8. The Metabolic Syndrome

This section explains how impaired glucose uptake can lead to many of the factors associated with the metabolic syndrome. For example, the fat cells release abundant triglycerides into the blood in the morning before the first meal, as these must last throughout the day while the high-glucose meals are being consumed. High blood sugar levels (diabetes) are a direct consequence of insulin impairment. Fatty deposits in the heart's arteries build up to supply fuel to the heart. Plausible reasons are also given for high LDL and low HDL levels associated with metabolic syndrome.

9. The Solution

This section gives specific recommendations for lifestyle changes that will, over time, correct the problem. Foods that are rich in calcium include milk products, soy beans, and dark green vegetables. Spending more time outdoors on sunny days is the best way to get vitamin D. Changing the diet to include more fats will help significantly in both absorbing calcium and vitamin D and in supplying an alternative fuel source from food intake rather than depending constantly on the fat cells.

10. Summary

This section briefly summarizes the points made in the essay.

11. What's Next?

In my next blog post, I expect to address issues related to certain childhood brain disorders that are, in my view, directly tied to inadequate dietary fats. I introduce a short story here about a teenager who died suddenly. He had lived with ADHD for most of his life, and, upon autopsy, his heart was found to be riddled with fat. I hope to be able to explain why ADHD and fatty heart might be related to each other, and to low-fat diet.

Supportive Scientific Evidence

These sections form a long appendix that includes descriptions of referenced journal articles and shows how the arguments given in the essay on metabolic syndrome are supported by facts provided in the articles.

1. Obesity and Fatigue 2. Vitamin D Deficiency and Metabolic Syndrome 3. Calcium, Fats, and Fiber 4. Calcium Deficiency and Obesity 5. Vitamin D and Obesity 6. Vitamin D and Insulin 7. Vitamin D Deficiency Epidemic in America 8. Calcium and Glucose Metabolism 9. Muscle Glucose Utilization and Obesity 10. AMPK and Hypothalamus and Appetite 11. Calcium and Insulin Stimulation in Hypothalamus 12. Leptin Resistance in the Hypothalamus 13. Pituitary, Leptin, and Calcium

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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.

Bosnian translation created by Amina Dugalić.

Bulgarian translation created by Zlatan Dimitrov.

Chinese translation created by Austin Cole.

Estonian translation created by Martin Aus.

Georgian translation created by Ana Mirilashvili.

Kazakh translation created by Alana Kerimova.

Norwegian translation created by Zoltan Solak.

Polish translation created by Grzegorz Adamski.

Portuguese translation courtesy of Artur Weber

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Russian translation courtesy of Rustam Paskaev.

Ukrainian translation courtesy of Sandi Wolfe.