The emphasis in the previous installment was on the role of insulin as the transport vehicle for glucose in the bloodstream. Insulin has an equally important role in fat accumulation (synthesis and storage) which relates to obesity. Insulin must be in the bloodstream whenever there are elevated levels of glucose present. Insulin transports the glucose to the cells for energy, and at the same time acts to block the breakdown and entry of energy from stored fat into the bloodstream. The reason is this: The body prefers to burn glucose as a quick and readily available source of energy. So, if glucose energy is available, that is, if we can eat it (any/all sugars and starches), or the body can find it (glycogen) in storage, or synthesize it (by gluconeogenesis) in the liver, the body will do that. If there is energy available from any one of these sources, then there is no need for energy from fat. So, the fat stays locked up in storage, awaiting famine, as in Paleolithic times.
The fat in storage in our bodies, as well as the fat we eat, is in the form of triglyceride molecules. A triglyceride molecule is comprised of three fatty acid molecules linked to one glycerol molecule. The triglyceride molecule is too big to get into the blood stream intact. Lipolysis is the breakdown of fat molecules. When the protein lipase in the adipose tissue is activated by any of numerous hormones, the triglyceride molecule breaks down into its component parts and the fatty acids are released into the blood and are then available for cellular uptake. Ketone bodies, produced as a byproduct, and the glycerol molecule, are used for energy too. This process occurs at night during an overnight fast and is called ketosis.
So, to summarize and repeat: We can’t be a fat burner and a sugar burner at the same time. Our body prefers to burn sugar (glucose) and will do so as long as 1) we eat things that will break down into glucose (all sugars and all carbohydrate foods), or 2) we have glucose stored (as glycogen) in the liver and the muscles, or 3) the liver can make glucose from excess amino acids (stored in the liver) from eating too much protein. Since insulin must be present in the bloodstream to transport glucose to the cells for energy, so long as there is an elevated level of insulin in the bloodstream, the unneeded food energy from any of the excess fat or carbohydrates consumed (that cannot otherwise be stored in the liver and muscles) will be accumulated as body fat (by de novo lipogenesis), instead of broken down and burned for energy. That is why we get fat. We’re living on refined sugars and starches, and saving our fat (and accumulating more) for “hard times.”
This is particularly easy for us to do today - get fat – by eating a so-called “balanced” diet that is heavily skewed towards carbohydrates (see installment #2 at http://danbrown-thenutritiondebate.blogspot.com). And we’ve done this to avoid dietary fats, and particularly saturated fats and dietary cholesterol that we’ve been told erroneously are bad for us. The low fat diet was supposed to protect us from “killer diseases” like heart disease, stroke and cancer; today there is little evidence that it provides protection and mounting evidence that limiting fats in the diet may do more harm than good. Obesity is the precursor (but not necessarily a requisite) condition for Metabolic Syndrome and other Diseases of Civilization, including many cancers.
A couple of years ago a New York Times page -one story reported on a new treatment modality being recommended for patients presenting with hypertension, hypercholesterolemia, and Type 2 diabetes or prediabetes with obesity. The impetus for the new modality was the failure of clinicians to treat obesity effectively, and this was due, they said, to patient noncompliance! (not the wrong “prescription” of “diet and lifestyle changes,” meaning a restricted-calorie, balanced diet and more exercise.) The new paradigm they recommended was a “workaround” using just pharmacological solutions. High blood pressure and high cholesterol both respond to medications. And many more new medications are now available for Type 2 diabetes.
Unfortunately, this solution often results in the pre-diabetic developing full-blown Type 2 diabetes (25% within 3-5years) and the diabetic patient getting progressively worse until they become insulin dependent (multiple daily injections!) and eventually develop one of the complications or co-morbidities, from which they will most likely -- almost assuredly, die.
Gary Taubes’s new book, “How We Get Fat: And What to Do About It” (Knopf, 2010), offers a different approach. I can’t wait to see how well this more “accessible” book is received, both by the medical community and the lay public.
© Dan Brown 2/13/11
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