Sorry, but I had to go there. I visited Vietnam in my mid-20's and remember a group of young guys in their early 20's in some sort of Navy or something cruising up to the beach I was hanging out on one day. The boys jumped off the boat and started running around tackling each other in their Speedos and other weird things that only someone who has traveled to Vietnam could grasp the true strangeness of. Anyway, even though I was 5'9", 175 pounds soaking wet, several of the boys ran up to me, asked me how old I was, and started pinching the 1-inch of extra fat around my abdomen and laughing. They of course played with my arm hair too, which seems almost like a pasttime of Vietnamese citizens in the presence of an apelike foreigner like myself.
Anyway, the point of the story is that, even though I was lean by American standards, and didn't consider myself fat at all, I was still fat enough for these boys to look at it like it was some kind of novelty - like they had never seen a guy my age with a body fat percentage above 10%. And I must say, during that trip I did not see a single male with a waist that appeared larger than mine, which was somewhere between 33 and 34 inches at the time. This was typical of every rice-based culture I have ever had the opportunity to see (I have visited 7 Asian countries), with the exception of Japan - where at least you did see an occasional overweight person.
With that, we will resume our starch vs. sugar conversation and breakdown or Ray Peat's article Glycemia, Starch, and Sugar in Context.
"More important than the physiological vacuity of a simple glycemic measurement was the ideology within which the whole issue developed, namely, the idea that diabetes (conceived as chronic hyperglycemia) is caused by eating too much sugar, i.e., chronic hyperglycemia the illness is caused by the recurrent hyperglycemia of sugar gluttony. The experiments of Bernardo Houssay (1947 Nobel laureate) in the 1940s, in which sugar and coconut oil protected against diabetes, followed by Randle's demonstration of the antagonism between fats and glucose assimilation, and the growing recognition that polyunsaturated fatty acids cause insulin resistance and damage the pancreas, have made it clear that the dietetic obsession with sugar in relation to diabetes has been a dangerous diversion that has retarded the understanding of degenerative metabolic diseases."
Peat is getting onto something with this passage. Perhaps the 2nd largest pseudoscientific sasquatch of them all (behind the belief that eating saturated fat and cholesterol is the cause of heart disease), is that eating carbohydrate somehow causes insulin resistance, metabolic syndrome, and type 2 diabetes after the insulin mechanism “wears out” from repeated carbohydrate ingestion – sugar in particular. It doesn’t. In fact, fat competes and interferes with glucose’s journey out of the bloodstream and into cells, which is why the hormone cortisol, which dumps fatty acids into the blood, is such a powerful root cause of insulin resistance as Peat goes on to discuss.
"Starch and glucose efficiently stimulate insulin secretion, and that accelerates the disposition of glucose, activating its conversion to glycogen and fat, as well as its oxidation. Fructose inhibits the stimulation of insulin by glucose, so this means that eating ordinary sugar, sucrose (a disaccharide, consisting of glucose and fructose), in place of starch, will reduce the tendency to store fat. Eating “complex carbohydrates,” rather than sugars, is a reasonable way to promote obesity. Eating starch, by increasing insulin and lowering the blood sugar, stimulates the appetite, causing a person to eat more, so the effect on fat production becomes much larger than when equal amounts of sugar and starch are eaten. The obesity itself then becomes an additional physiological factor; the fat cells create something analogous to an inflammatory state. There isn't anything wrong with a high carbohydrate diet, and even a high starch diet isn't necessarily incompatible with good health, but when better foods are available they should be used instead of starches. For example, fruits have many advantages over grains, besides the difference between sugar and starch. Bread and pasta consumption are strongly associated with the occurrence of diabetes, fruit consumption has a strong inverse association."
I have no idea what planet Peat was on when he wrote this paragraph. It makes absolutely no sense and is totally incongruent with reality. The meal that produces the most postprandial insulin is a high-starch, low-fat meal. Interestingly, a high-starch, low-fat diet, during overfeeding, has been shown to be the least fattening – corresponding with the higher insulin levels. http://www.ajcn.org/content/62/1/19.full.pdf+html At the same calorie levels, the subjects with the lowest insulin levels (because they were eating more calories as fat and thus not spiking insulin as high) stored more fat, had less of an increase in thermogenesis (heat production), and less of an increase in lean body mass.
A rise in insulin causing more fat storage? This just doesn’t make sense. It should cause more muscle storage and less fat storage, as insulin, if anything, is the primary anabolic muscle storage hormone. Insulin does not cause carbohydrates to be converted to fat, and the little bit of carbohydrate that may be converted to fat is a very inefficient process compared to storing fat that you ingest as fat that is already pre-packaged and ready to find its home in adipose tissue.
Increasing insulin makes a person eat more? This really pisses me off. That’s like saying that stapling someone’s stomach makes them eat more, as both stapling your stomach and insulin are known to have an anti-hunger effect. Sure, inject insulin into someone without carbohydrate being ingested along with it, and they will get super hungry from blood glucose dropping to dangerous levels – appetite is stimulated because it’s a better option for the body than dying. But the normal rise and fall of insulin and blood sugar levels to baseline (not below baseline as is commonly seen in hypoglycemia after sugar ingestion) in response to eating is not something that should be construed as appetite-promoting.
Of course, this is only a glimpse of the frustration I have with this myopic view of one isolated and rather insignificant variable. It ignores the more complex science of satiety, which doesn’t have much to do with how much insulin you produce after eating a meal, and a lot more to do with the palatability of the food, water content, fiber content, chewing time, particle size, and countless other factors that affect the dopaminergic system and beyond – including even lighting, social setting, food texture, salt content, packaging, and so on. One biggie that Peat doesn’t account for is the appetite stimulation caused by sweetness, which fructose has the most of in the carbohydrate realm. Starch is not sweet. What, are we gonna call shit fattening if we find out it triggers a greater rise in insulin upon ingestion vs. an isocaloric amount of apple pie a la mode?
One really needs to look at the whole picture. A person who is susceptible to fat gain (which I propose is, in many cases, a person who eats out of addiction to satisfy reward centers in the brain vs. eating strictly to satisfy physiological appetite) can easily get fat eating to appetite of a diet containing lots of burgers, pizza, pork ribs, soda, beer, ice cream, chicken wings, French fries, chocolate, peanut butter, apple juice, milkshakes, bread, pasta, and potato chips because this diet as a whole promotes greater calorie consumption without much of a corresponding rise in metabolic rate or drop in appetite. Even I, with an average rectal temperature during the day of around 100 degrees F can gain fat rapidly eating a diet like that, because my calorie consumption goes to the stratosphere and I even feel MORE hungry than I do eating 2,000 fewer calories of less stimulating foods (I even start to get major hunger pangs in the late evening when I do that consistently for a week or longer).
"Although pure fructose and sucrose produce less glycemia than glucose and starch do, the different effects of fruits and grains on health can't be reduced to their effects on blood sugar."
Ah, finally talking some sense here!
"After decades of “education” to promote eating starchy foods, obesity is a bigger problem than ever, and more people are dying of diabetes than previously. The age-specific incidence of most cancers is increasing, too, and there is evidence that starch, such as pasta, contributes to breast cancer, and possibly other types of cancer."
Oh yeah, there's a lot of scientific integrity in that paragraph. You know we all followed the dietician’s advice to the letter. Oh wait, the biggest changes in the diet in recent times are an increase in sugar, poultry, and vegetable oil intake – which displaced the mostly wheat, corn, and potato-based diet of the United States prior to that. But even that is probably less significant than the fact that we started eating more food at restaurants and less at home, we saw the introduction of powerful flavor enhancers like MSG, aspartame, “natural flavors,” “artificial flavors,” and the increased sweetness of high fructose corn syrup – not to mention the general increase in the sophistication of the food scientists who have had several more “decades” to perfect their craft at making “products” more interesting than old-fashioned food.
"The epidemiology would appear to suggest that complex carbohydrates cause diabetes, heart disease, and cancer. If the glycemic index is viewed in terms of the theory that hyperglycemia, by way of “glucotoxicity,” causes the destruction of proteins by glycation, which is seen in diabetes and old age, that might seem simple and obvious."
True, unless you turn the epidemiological data right-side-up and see that the eaters of starch-based diets all over the world – particularly Asians and Africans, have far lower rates of diabetes, heart disease, and most cancers – especially those living in the greatest isolation from food “products.”
"But there are many reasons to question that theory."
I wouldn’t consider it a valid theory at all anymore, especially when people eating starch-based diets have far lower levels of fasting and postprandial glucose levels – showing clearly that such a diet, when looked at as a whole, lowers “glucotoxicity” and glycation. Meanwhile, real practicing doctors like Terry Shintani and John McDougall are lowering glucose levels, including overcoming type 2 diabetes, with starch-based diets (note, I’m sure a fruit-based diet could perform just as well).
Anyway, that’s enough for the sugar vs. starch masturdebate. There are advantages and disadvantages to all forms of carbohydrates. What is probably the most useful to you as an individual looking to improve your health is finding which type of carbohydrate triggers the greatest heat production – keeping fingers and toes warm in between meals and body temperature elevated, and seems to yield the greatest amount of health benefits. But even this is usually a mixed bag. Displacing tons of starch with fruit and juice, for me, has had many health positives – everything from increases in vasodilation, energy levels, exercise recovery, heat production, breathing, and, shockingly, a complete elimination of tooth pain. But it has also given me more pimples on my back and gums that bleed more easily. Even in my mouth it has had both a positive and a negative effect! Ha! A blend of plenty of starch and sugars seems to be the best fit for me personally, and is the most palatable, socially functional, and economical.
So play with this for yourself, just don’t play WITH yourself. Actually, see which type of carbohydrate or combination of carbohydrates makes you want to play with yourself the most, and stick with it!
Stay tuned for the next Peat post, as we get into Peat’s more interesting views about sugar and carbon dioxide, the superiority of glucose oxidation, and the role polyunsaturated fat plays in insulin resistance.
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