How we become over-fat


There is evidence to show that over-fatness and obesity is a problem involving both sugar and fat metabolism, resulting in fat deposition and an inability to mobilize fat from the fat tissue.

In the two previous tips here and here I have been trying to suggest that there is a fair bit of evidence showing that low calorie, low fat diets don’t work, and that historically speaking, we have eaten meat and saturated fat for millennia, whereas grains are relatively new to our diet. Once farming began, some traditional cultures did eat grains, but they were soaked first (probably to soften them up and make them easier to chew), reducing the amount of sugar in them and increasing their digestibility. Only in the last 150-200 years or so have our diets included growing amounts of processed sugar and such huge and growing quantities of baked goods, pasta, and other foods that contain unfermented flour. To me, just knowing that information alone is enough to make me suspect that perhaps it is the sugar, flour products and alcohol that are the cause of the rise of modern diseases of civilization (obesity, type 2 diabetes, heart disease, osteoporosis, cancer, etc.), as opposed to saturated fat and cholesterol, as we have been told by medical/nutritional pundits.

According to Gary Taubes in his book Good Calories Bad Calories, much of the research on the metabolism of obesity occurred prior to World War 2 in Germany, and for the most part, has not been considered much since. In the 1920s, biochemists such as Rudolf Schoenheimer realized that our fat tissue is very metabolically active, and not simply a place to store fat like a safety deposit box, that only gets looked at once in a blue moon. Instead Hilda Bruch suggested that fat metabolism works more like a coin purse, where free fatty acids are continually being deposited into our adipose (fat) tissue and turned into triglycerides for storage, and also are continually being broken back down into fatty acids, and sent into the bloodstream to be burned as fuel depending on the requirements of the moment. Fat provides the ready coin for the momentary energy needs of the body.

Triglycerides are a combination of 3 fatty acids held together with glycerol, and they come from the fat in the diet and they are made in the liver and fat tissue from the carbohydrate in the diet. Triglycerides are the form in which fats are stored, and free fatty acids are the form in which fats are burned as fuel. So, people become over-fat when their body is very good at storing triglycerides, and not good at breaking down the triglycerides into free fatty acids to be sent into the bloodstream to be burned. It is not so much about the quantity of food being consumed, but rather about whether the environment in the body is forcing deposition or mobilization of the triglycerides in the fat tissue. Ernst Wertheimer said in 1948 in a review of the science of fat metabolism at that time, that “The ‘classic theory’ that fat is deposited in the adipose tissue only when given in excess of the caloric requirement has been finally disproved”.

In 1956, it became possible to measure free fatty acids in the bloodstream, and it was discovered that after a meal, blood sugar levels tend to be high, and fatty acid levels are low, but fatty acid levels rise in the hours after the meal. If sugar or insulin is injected into the bloodstream, fatty acid levels plummet. This is the key. When sugar is available for fuel, fats get stored as triglycerides. When no sugar is available, fats get mobilized into free fatty acids to be used as fuel. Robert Gordon of the NIH published this information in 1956. Why have we forgotten it today??? The more carbohydrate consumed, the more triglycerides get made and stored. The more glucose/insulin in the bloodstream, the more "stuck" the fat is in the fat cells. When blood glucose/insulin is low, free fatty acids can escape from the fat cells into the bloodstream to be burned. Therefore, how many free fatty acids can be burned depends entirely on the amount of glucose and insulin in the bloodstream.

Furthermore, in order for triglycerides to be manufactured, the molecule glycerol phosphate is required, and that molecule is supplied only by carbohydrates. So, if there is little or no carbohydrates in the diet, little or no glycerol phosphate is available to make triglycerides and store fat, so little or no fat deposition can occur.

So a diet high in starchy carbohydrates (baked goods, pasta, other flour products, sugar, fruit and alcohol) leads to fat accumulation in two ways. First, it sharply increases blood sugar which increases insulin, our storage hormone, which in turn controls the production of glycerol phosphate and therefore the conversion of sugar into triglycerides and the storage of fat in the fat cells, causing fat deposition. Secondly, when blood sugar and blood insulin levels are high, fat is stuck in the fat cells and cannot be mobilized, resulting in an inability to use fat as a fuel. A combination of fat deposition and an inability to mobilize our fat for fuel leads to fat accumulation, over-fatness and obesity. Some of us can tolerate more carbohydrate in our diet than others without suffering negative consequences (biochemical individuality), and those that can't tend to develop problems like over-fatness, type 2 diabetes, heart disease etc.

Next week we'll explore why the medical / scientific community has not endorsed low starchy-carb diets as being a healthy way to eat, do a cost / benefit analysis, and see what conclusions we come to.

I HIGHLY recommend the recent book by Gary Taubes, Good Calories, Bad Calories if you are interested in the topics of diets, obesity, heart disease and diabetes. Or watch this webcast of a lecture given by Gary Taubes at Berkeley last November on this topic.

Related tips
Obesity, Type 2 Diabetes and Heart Disease – what does history tell us?
Obesity – a behavioural or a metabolic problem?
Insulin, our storage hormone
Sugar, the disease generator
Another “healthy heart guide” that got it wrong
Saturated fat, the misunderstood nutrient
Cortisol, our stress hormone

Taubes, Gary Good Calories, Bad Calories, Challenging the Conventional Wisdom on Diet, Weight Control, and Disease Alfred A. Knopf, New York, 2007.

Chek, Paul; You Are What You Eat CD Series Chek Institute, San Diego, CA, 2002.

McGarry, JD. What if Minkowski had been ageusic? An alternative angle on diabetes. Science. Oct 30;258(5083):766-70, 1992.

Greenwood MR et al. Normal and abnormal growth and maintenance of adipose tissue In Hirsch and Van Itallie, eds. 1985, 20-25.

Greenwood MR et al. Adipose tissue metabolism and genetic obesity In Bjorntorp, Cairella, and Howard, eds., 1981, 75-79.

Bruch, H. Eating disorders, obesity, anorexia nervosa, and the person within New York, Basic Books, 1973.

Gordon E. The metabolic importance of obesity In Symposium on Foods: Carbohydrates and their roles ed. HW
Schutz. Westport, Conn.: Avi Publishing, 322-46, 1969.

Reynold A. and Cahill G, eds. Handbook of Physiology. Section 5. Adipose Tissue. Washington DC; American Physiological Society, 1965.

Randle P.J. et al. The Glucose Fatty Acid Cycle: It’s role in Insulin Sensitivity and the Metabolic Disturbances of Diabetes Mellitus Lancet Apr. 13; 281(7285):787-89, 1963.

Schoenheimer, R. The Dynamic State of Body Constituents Cambridge, Mass. Harvard University Press, 1961.

Yalow RS and Bernson SA. Immunoassay of endogenous plasma insulin in man J Clin Investigation July; 39:1157-75, 1960.

Krebs, H. The cause of the specific dynamic action of food-stuffs Arzneimittelforschung May; 10:369-73, 1960.

Wertheimer, E and Shafrir R. Influence of Hormones on Adipose Tissue as a Center of Fat Metabolism Recent Progress in Hormone Research 16:467-95., 1960.

Yudkin J. The causes and cure of obesity Lancet Dec. 19; 274(7112):1135-38, 1959.

Yudkin J. Diet and Coronary Thrombosis: Hypothesis and Fact Lancet July 27; 270(6987):155-62, 1957.

Bruch, H. The importance of overweight New York, WW Norton, 1957.

Dole VP A relation between unesterified fatty acids in plasma and the metabolism of glucose J. Clin Investigation Feb. 35(2):150-4, 1956.

Gordon R et al. Unesterified fatty acid in Human Blood Plasma J Clin Investigation Feb.; 35(2);206-212, 1956.

Laurell S. Plasma free fatty acids in diabetic acidosis and starvation Scandinavian J of Clin and Lab Investigation 8(1):81-82, 1956.

Wertheimer, E and Shapiro R. The Physiology of Adipose Tissue Physiology Reviews Oct.; 22:451-64, 1948.

Bruch, H. Dietary Treatment of Obesity in Childhood J Am Dietetic Ass 20:361-364, 1944.

Copyright 2008 Vreni Gurd

Comments are closed.