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Brillyant comments on Critiquing Gary Taubes, Part 2: Atkins Redux - Less Wrong
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Comments (186)
Unless I'm wrong, there is a large chunk of the population who believe diets have some magical element that differentiates them from other diets. Atkins, from my limited understanding, involves a magical element, coming up with a sciency-sounding explanation for it.
Any insufficiently understood biological process will be indistinguishable from magic.
So people undergoing insulin treatment (for example) get fatter because they start overeating and stop exercising enough?
I think Chris is probably taking Taubes a bit literally (and I agree with the revenue-cost analogy), but I like http://wholehealthsource.blogspot.com/2011/08/carbohydrate-hypothesis-of-obesity.html , which he linked to in Part 1. There's quite a lot in it about insulin (too much for me to summarize here), but I've copied a couple of particularly relevant paragraphs below. Obviously if you can see any issues with them then I would be interested in hearing them.
"The idea of fat gain in insulin-treated diabetics (argument #3) is not as airtight as it might at first seem. On average, diabetics do gain fat when they initiate insulin therapy using short-acting insulins. This is partially because insulin keeps them from peeing out glucose (glycosuria) to the tune of a couple hundred calories a day. It's also because there isn't enough insulin around to restrain the release of fat from fat cells (lipolysis), which is one of insulin's jobs, as described above. When you correct this insulin deficiency (absolute or relative), obviously a diabetic person will typically gain weight. In addition, short-acting insulins are hard to control, and often create episodes where glucose drops too low (hypoglycemia), which is a potent trigger for food intake and fat gain.
"So what happens when you administer insulin to less severe diabetics that don't have much glycosuria, and you use a type of insulin that is more stable in the bloodstream and so causes fewer hypoglycemic episodes? This was recently addressed by the massive ORIGIN trial (17d). Investigators randomized 12,537 diabetic or pre-diabetic people to insulin therapy or treatment as usual, and followed them for 6 years. The insulin group received insulin glargine, a form of long-acting "basal" insulin that elevates baseline insulin throughout the day and night. In this study, insulin treatment brought fasting glucose from 125 to 93 mg/dL on average, so it was clearly a high enough dosage to have meaningful biological effects. After 6 years of divergent insulin levels, the difference in body weight was only 4.6 lbs (2.1 kg), which is at least partially explained by the fact that the insulin group had more hypoglycemic episodes, and took less metformin (a diabetes drug that causes fat loss). A previous study found that three different kinds of long-acting insulin actually caused a slight weight loss over three months (17e). This is rather difficult to reconcile with the idea that elevated fasting insulin is as fattening as claimed."
Edit: Fixed link.
So I don't take the weight gains from a high-carb diet to be directly analogous to a diabetic injecting insulin. Mainly, I'm talking about artificial insulin injection here just as a simply rebuttal to the notion that weight gain/loss is entirely about eating too much/ not exercising enough. People naturally tend to underestimate how much biochemistry influences decisions, mood and personality. It's a product of lingering Cartesian mythology.
That said, most of what I've seen on insulin and leptin resistance emphasizes peak insulin level in the minutes to hours after eating rather than a moderate difference in baseline insulin. What is going on is probably more complicated than a straight-shot from carbohydrates to insulin to fat. We probably need a more committed, more knowledgeable or less busy defender of Taubes here.
Then it's a good example, and I'm with you that your weight is determined by more than whether you have the willpower to say "today I'm going to exercise and not eat too much". (Though most researchers probably agree with Taubes on this: http://wholehealthsource.blogspot.com/2013/01/comment-in-nature.html .)
I think Stephan on Whole Health Source does a good job of refuting Taubes' claims on the particular importance of insulin resulting from carbohydrate consumption (I can't remember specific posts, but I think there are several others in addition to the one Chris linked to), but it might be that I would think otherwise if I were a bit more knowledgeable. He had some sort of falling out with Taubes at some point, and, like Taubes, he has a theory about what causes obesity (http://wholehealthsource.blogspot.com/2011/11/brief-response-to-taubess-food-rewad.html) and is presumably disproportionately likely to interpret evidence in ways that support his theory.
For example, it's not clear to me whether you are for or against this position in form of a question. Should it be?
I don't think weight gain from insulin treatment has anything to do with the diet and exercise decisions people make. Obviously, as a matter of fact they take in more calories than they burn.
I think you're correct, but I'm not sure how this translates to low carb dieting. You can make any healthy person eat too much if you give them insulin. Give them enough, and they will die if they don't.
Some diabetics obviously take too much insulin, and this will make them eat more. Taking too much insulin is a decision. Do you find this agreeable?
A common problem with diabetics is many of them eat unnecessarily large evening snacks out of fear of nocturnal hypoglycemia even if they take just the correct amount of insulin. This leads them to get hyperglycemia in the morning, which leads to upping the dose and the cycle continues.
Gary Taubes argues that someone who eats more carbs is going to produce more insulin.
Froom Good Calories, Bad Calories:
I think the hypothesis is plausible, and if it were true the amount of carbohydrates people tolerate before their insulin secretion went crazy probably would vary greatly. I'm not sure if it applies to fructose, since its cell uptake doesn't seem to be regulated by insulin. I'm pretty much ready to accept this idea as one of the major causes of obesity, but not necessarily the most important.
Does he say anything about insulin resistance in relation to this idea?
Far as as I understand he see a lot of insulin resistance as the result of elevated levels of blood insulin. I think he makes that argument in more detail and I'm probably not the right person to recount all the details.
I personally don't think that there's something like a ultimate cause of common obesity and that there are probably a lot of different factors at work.
From what I've read about diabetes, the need for insulin varies somewhat unpredictably. It's hard to be sure one has taken just the correct amount.
That's true especially in the beginning, but people become incredibly good at predicting how their needs vary through experience. Getting sick is an important exception, that's when things go wacky.
Do you think whether we use the word "just" or "roughly" was important to my main point?
I'm ignorant as to why that happens, and I'll assume it is true.
Why does it happen?
And what percentage of the general population do circumstances like this (or other such examples) apply to?
Well that's what insulin does. It's the hormone that mediates growth in adipose cells. If a person has broken insulin regulation (aka diabetes) and then you start injecting them with the stuff there is a good chance they'll get fat (the effect of insulin is a little more complicated than that, such that people react differently-- obesity has a significant genetic component).
There are a lot of known hormonal and metabolic disorders that can cause obesity. They don't make up a very significant fraction of people who are obese in the modern, western world-- but it in some societies it's probably the only way some people ever get /got fat.
Examples?
Basically all hunter-gatherer societies, as far as I know.
Ah, that's reasonable, but could be just because food is more difficult to get, and exercise isn't optional.
The issue's a bit more complicated than that. Skeletal evidence shows us that overall nutrition is usually worse after the agricultural transition, with average heights (a decent proxy for nutrition) usually dropping by several inches after a region switches to an agrarian lifestyle.
This doesn't necessarily mean that agrarians are making fewer calories per unit effort, though. They may be limited in protein or micronutrients but not in calories, with stunting thanks to deficiency issues; actually that's rather plausible. Alternately agrarian methods might by limited by expenditure of effort during some limited season (plowing, say, or harvest -- I don't know exactly how bronze-age agriculture worked), which could give you higher peak effort but lower average effort. Or the aristocratic classes that usually come with an agrarian transition might be confiscating all the good stuff for their own use.
(Agrarians are making more calories per unit land no matter how you slice it, but that's more historically than nutritionally significant.)
The question was whether there were any non-hormonally obese people, not what the average person looked like. I'm pretty sure agriculture made it much easier for high status people to overeat. In fact, obesity was probably a status symbol.
What's weird is that agriculture-- or at least the modern food system apparently also makes it much easier for low-status people to get fat, even when their children are starving -- pdf.
The example is hunter-gatherers, not agriculturists. The point of discussing farmers is to address your suggestion that food is hard for hunter-gatherers to get. By many measures, it appears easier for hunter-gatherers than for farmers. In particular, hunter-gatherers appear to eat more and work less.
That's a harder question to answer, partly because fat doesn't preserve well in the archaeological record.
A quick trawl through Google Scholar isn't picking much up for the archaeological side of the question, although I've found a surprisingly large number of cites discussing the proportions of the apparently-obese "Venus" figurines sometimes found in Upper Paleolithic sites. This paper on the other hand seems to suggest that the answer is "no" for at least one group of modern foragers, at least to a first approximation (the sample size is rather small) and modulo the usual caveats re: modern foraging cultures.
I would agree this is true. From my recall and simple research, something like ~17% of individual metabolism is dependent on factors that are suspected to be genetic, and this, as a result of simple arithmetic, can lead to obesity fairly easily. (e.g. we eat and exercise identically and end up at very, very different weights).
I still don't understand what the mechanism by which -- apart from simple caloric arithmetic -- Atkins works? Are you saying it is a result of its effect on insulin in the body?
Since, like you, I don't suspect (though we may be wrong) insulin-caused obesity is a significant % of the western world, it still is my view that the Atkins diet is primarily nothing more than an "eat less" diet disguised as pseudoscience.
The genetic component could also affect hunger and eating behavior.
It seems to me reasonable (and likely) that it does. Of course we have individual differences in appetite and metabolism.
The crux is what Atkins, or any diet, does besides improve caloric arithmetic. I'd say it does primarily nothing in the majority of people. I'd love to hear a suitable counterproposal.
If they get hypoglycemia because of too much insulin then yes, this would make them eat more. If you're hypoglycemic you won't like to exercise either. If insulin can store energy from thin air, I would like to understand the mechanism.
Again, huh? All of your replies in this thread sound like they're replying to a position I haven't taken.
Perhaps you should make it clearer what your position is then. The ifs were there because I wasn't sure I understood you, so I was replying to a hypothetical.