Tuesday, April 13, 2010
Good Calories Bad Calories Is Not Necessarily Infallible
When Good Calories Bad Calories (abbreviated here as GCBC) was published in 2007, the low-carb community was ecstatic. Dr. Robert Atkins and the Doctors Eades had discussed the scientific basis for the low-carb lifestyle, but their writings were usually presented in the context of clinical observations. With GCBC, Gary Taubes gave low-carbers 460 pages of tightly reasoned discussion and another 113 pages listing many specific citations from the scientific literature.
For a layperson, the book was not easy to read, but with effort it was comprehensible. At last low-carbers had access to information that cast doubt on the hypothesis that excessive consumption of fat raises cholesterol levels, which in turn causes heart disease and early death. Taubes presented plausible evidence for an alternative hypothesis--that excessive carbohydrate consumption, not fat consumption, is the cause of diabetes, heart disease, hypertension and even cancer.
Since the publication of GCBC, two interesting things have happened. (A) GCBC has moved into the position of holy writ in the eyes of many low-carbers and (B) several low-carb blogs and forums have arisen to discuss the scientific and practical aspects of low-carbing.
A rereading of GCBC in 2010 shows that many of its ideas have been supported by the subsequent publication of prospective dietary studies, including Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet, published in the New England Journal of Medicine. However, recent discussions in the blogosphere show that some statements in GCBC may need to be reconsidered.
Specifically, on page 394 of the hardbound edition of GCBC, Taubes states, "By the mid-1960s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated levels of circulating insulin and a 'greatly exaggerated' insulin response to carbohydrates in the diet..."
Let's address these statements in order.
1. Although consumption of carbohydrates does prompt insulin secretion, it is a well-known physiological fact that consumption of proteins also prompts insulin secretion. The amount of insulin released in response to protein is about a third of that released in response to carbohydrate on a gram-for-gram basis, but the increase is still measurable. Dr. Mike Eades has an illustration of this on page 37 of the paperback edition of Protein Power. Scientific articles measuring the insulin release in response to protein can be found here and here. Insulin response to various foods in terms of 120 minute area under the curve can be found in Table 4 here.
2. Insulin release does promote the storage of fat in adipocytes, but it is not the only signaling protein that produces fat storage. Acylation Stimulating Protein (ASP) is secreted by fat cells and allows fat to be removed from chylomicrons and stored in fat cells. Acylation Stimulating Protein permits the body to store fat in the absence of insulin. The process is discussed here by Dave Dixon and here by Petro Dobromylskyj (Hyperlipid).
3. While it is difficult to accumulate excess fat in the absence of dietary carbohydrates, it is not impossible. On various discussion boards, a few zero-carbers have related anecdotal evidence that they gained weight while eating large amounts of protein and fat. From a theoretical perspecive, on pages 388-392 of GCBC Taubes goes into great detail about the necessity of glycerol phosphate for the storage of fat in adipose tissue. (Glycerol phosphate is the precursor to the molecule used as the backbone of a triglyceride, the storage form of fat.) On page 392 Taubes says, "Dietary glucose is the primary source of glycerol phosphate. The more carbohydrates consumed, the more glycerol phosphate available, and so the more fat can accumulate. For this reason alone, it may be impossible to store excess body fat without at least some carbohydrates in the diet and without the ongoing metabolism of these dietary carbohydrates to produce glucose and the necessary glycerol phosphate." This sounds logical. However, biochemists know that glycerol phosphate can readily be produced from protein via glyceroneogenesis. The absence of dietary carbohydrate in no way prevents the synthesis of triglycerides from a high-protein or even a high-fat diet.
(4) It is true that high insulin is often associated with type 2 diabetes, but it is important to remember that type 2 diabetics do not always have an excess of circulating insulin. Instead they have insulin resistance. If their body tries to control high blood glucose levels with excess insulin production by the pancreas, this can result in beta cell burnout and a patient who actually has less endogenous insulin production than a person without diabetes.
As described here the scientific method is an ongoing process. Good Calories Bad Calories is an excellent book and provides many good arguments for the low-carb lifestyle. But the scientific method requires that we keep testing and evaluating our hypotheses, and it is important to realize that not everything we read in GCBC will necessarily stand the test of time.