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.
Belief changes
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.


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Your comment "grassland elephants had extensive atherosclerosis but woodland elephants -- living on leaves more so than grasses -- did not" reminded me of a study contrasting diet and behavior of howler monkeys to spider monkeys.
"the colons of howlers were considerably wider and longer than those of spider monkeys. Food had to travel much farther and remained much longer in howler guts, and the monkeys had room for much more bulk. As a result, bacteria had a chance to ferment masses of fibrous leaves in the monkeys’ colons, producing energy-rich fatty acids. Milton eventually found that howlers receive more than 30 percent of their daily energy from such fatty acids."
http://discovermagazine.com/1995/may/gutthinking503/?searchterm=howler%20monkeyTherefore, thanks to their gut bacteria, howler monkeys were actually surviving on a much higher fat (and subsequently lower carbohydrate) diet than the spider monkeys. Would the howlers also have lower insulin levels and significantly less atherosclerosis than their fruit eating cousins? And is it absorption of fatty acids via bacterial conversion of fiber in their guts that also helps give the leaf eating elephants their cardiovascular advantage? i'm sure some biologists somewhere are trying to answer these questions. Thank you Gary, for provoking more thoughts.