Wednesday, February 27, 2019

Retrospective #11: Why We Get Fat

If memory serves me correctly, Gary Taubes’s book, “Why We Get Fat: and What to Do About It” was published after Christmas 2010. This column was written in anticipation of its publication and is re-written here as part of a daily Retrospective series begun 10 days ago. In an earlier tome, “Good Calories – Bad Calories” (2007), Taubes proffered his “Alternative Hypothesis” (scroll down Retrospective #5) to the Conventional Wisdom about “why we get fat.” His Book, “Why We Get Fat,” was written to be “more accessible,” and to be read by the lay public.
The previous Retrospective #10 was on the role of insulin as the transport vehicle for glucose in the bloodstream. As Taubes describes in #5, and we recap in #10, insulin levels in the blood rise whenever there are elevated levels of glucose present. Insulin transports the glucose to the cells for energy uptake, but at the same time blocks the breakdown and entry of energy from stored fat into the bloodstream. This is insulin’s role in “fuel partitioning.”
The fat stored in our bodies are triglycerides. A triglyceride molecule is big, comprised of three fatty acid molecules linked to one glycerol molecule. When the enzyme lipase in fat tissue is activated by insulin (and other) hormones, triglyceride molecules break down into their component parts. The fatty acids are released into the blood and are then available for cellular uptake. Ketone bodies, produced as a byproduct of the breakdown (lipolysis), and the glycerol, are used for energy too. This process can occur at night during an overnight fast and is called ketosis.
That being said, our bodies burn “sugar” (glucose) when it is available. And that’s the problem. That is “why we get fat.” Glucose is always available! In the Standard American Diet (SAD), our “balanced” diet is heavily weighted towards carbohydrates, all of which become glucose in the blood stream. Your body can’t be a fat burner and a sugar burner at the same time, and glucose is the preferred fuel when and BECAUSE it is available.
This is a conservation strategy by design.  The body will run on glucose for so long as 1) we eat things that will break down into glucose – that includes all carbohydrates and all sugars (which are carbs) – or 2) we have glucose stored (as glycogen) in the liver and the muscles. And if it runs out of eaten or stored glucose, the body can also make small amounts of glucose from “glucogenic” amino acids (from protein) or from glycerol from fats (lipolysis).
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) must be accumulated as body fat (by de novo lipogenesis). We’re living on sugars and processed carbs, and saving and accumulating more fat for “hard times.”
For almost half a century we’ve done this to avoid dietary fats, and particularly saturated fats and dietary cholesterol. We’ve been told that they are bad for us. The low-fat diet was supposed to protect us from “killer diseases” like heart disease, stroke and cancer. Ironically, today there is little evidence that it provides protection and mounting evidence that limiting saturated fats in the diet may do more harm than good. Obesity is the precursor for Metabolic Syndrome and many other Diseases of Western Civilization: CVD, AZ and many cancers.
In the late 1990s I recall reading a New York Times front-page, column-1 story reporting on a new treatment modality being recommended for patients presenting with hypertension, hypercholesterolemia, and Type 2 Diabetes or Pre-diabetes 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 low-fat, balanced “diet and exercise” prescription (“eat less and move more”). The new paradigm they recommended was a workaround: using just pharmacological solutions: High blood pressure and high cholesterol both respond to medications!
Unfortunately, this solution often results in the Pre-diabetic developing Type 2 diabetes (25% within 3-5 years), then the T2 getting progressively worse until they become insulin dependent (multiple daily injections!) and eventually develop one of the complications or co-morbidities (CVD), from which they will, most assuredly, die. 

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