Editor's note: Gary Taubes, the famous writer of Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control and Disease, answers the third and final round of your questions here. Check out the original posts here, Gary's first set of answers, and his second set of answers.
In some follow-up reading, I ran into the concept of the insulin index, which purports to index the insulin response of foods. This index appears to indicate that certain protein rich foods (like beef and fish) may actually have more impact on insulin that certain carbohydrate foods. This is counter-intuitive based on the science that Gary writes about. I would be interested to know whether Gary has any comments about this index.
It's always been known that protein stimulates an insulin response, because some of the amino acids in the protein are converted to glucose. The assumption has always been that this effect is small compared to that of carbohydrates, and that it is muted because it takes considerably longer to digest protein from meat, for instance, than it does glucose from high glycemic index carbohydrates. Moreover, protein also stimulates secretion from the pancreas of a hormone called glucagon, which is not the case with carbohydrates. Glucagon works opposite insulin on the fat tissue itself and so would be expected to mute or counteract entirely any fat accumulation stimulated by the insulin.
Another factor to keep in mind is that the paper cited most often as evidence for the insulin secretion in response to meat and fish -- a 1997 paper in the American Journal of Clinical Nutrition titled "An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods" -- used extremely lean steaks and whitefish for the measurement. The fish was roughly 90 percent calories protein and 10 percent fat and the meat was 70-30. The more interesting question, and the one more relevant to the arguments in the book, is what happens when the meat and fish are more in the neighborhood of 70 percent or even 80 percent fat by calories. That hasn't been addressed. In short, the assumption that our insulin is primarily regulated by the carbohydrates in the diet is a reasonable one and will tell us most of what we need to know when it comes to fat accumulation and chronic disease.
I read somewhere that despite their high-protein, low-carb diet, Eskimos living their traditional lifestyles don't go into ketosis. Do you know if anyone has ever studied this among the Masai, another population with a traditionally low-carb lifestyle?I have never seen such a study. I did see the study you mentioned on Eskimos not being in ketosis. It wouldn't surprise me if the body adjusts to the long term absence of carbohydrates by reducing ketone synthesis, but it raises the question of what fuels the brain and the nervous system if that's the case. Certainly most research in this area is very short term, a few days to weeks. And it's hard to do such studies today of populations like the Masai because of the ready availability of carbohydrates, even to such isolated nomadic populations.
You said that the Masai living a traditional lifestyle, despite their low cholesterol levels and lack of coronary heart dsease, have extensive atherosclerosis. Is this atherosclerosis more or less extensive than that found among populations living a traditional lifestyle with a high-carb diet?What I cited was a study from George Mann nearly 40 years ago reporting that the Masai did indeed have extensive atherosclerosis. Again I know of no further studies to replicate Mann's findings, so we have to assume that he got it right. I don't know of similar studies in other populations, but I did see studies of various wild animals, in which atherosclerosis was fairly common, but mostly among herbivores. I saw one study, for instance, noting that grassland elephants had extensive atherosclerosis but woodland elephants -- living on leaves more so than grasses -- did not. So, again, good questions, and I don't know of sufficient evidence to answer them.
In one of your interviews you said that after the exhaustive research for this book, you only believed about 40% (I may be misremembering the number) of what you wrote in your article What If It's All Been a Big Fat Lie? Can you indicate what you said in that article that you no longer believe? Some people might not get through this new book and would read the shorter article instead.
Perhaps a better way to have put it was that much of what I now believe, I did not believe or have any inkling of when I wrote What If It's All Been a Big Fat Lie? At the time, I assumed that calories consumed was the critical variable in weight loss. It never crossed my mind that it wasn't. Hence the discussion in that article about how insulin or insulin resistance might effect hunger. So I no longer believe the underlying assumption of the article and that's how I came up with that 40 percent number.
Anything that implied that calories consumed was relevant -- for instance, David Ludwig's belief that the effect of carbohydrates is these blood sugar swings which induce eating or Michael Schwartz's ideas about insulin resistance in the brain -- I now believe was wrong or off the point. I think that the fundamental factor is insulin's effect on fat accumulation, which is an entirely different thing. I also assumed, as most of us did, that exercise played a role in weight maintenance if not weight loss, and I had no idea that carbohydrates could play a role in chronic diseases -- certainly not Alzheimer's or cancer.