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Gary Taubes on Obesity and Bad Science
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http://www.dieselbookstore.com/event/oakland-gary-taubes-and-frederick-crews-discuss-why-we-get-fatGary Taubes recently wrote an essay about the causes of modern obesity. In it, he correctly points out that modern medical science is woefully ignorant of the true causes of obesity. I haven’t yet read Taubes’s book, and I’m not particularly convinced of his carbohydrate hypothesis (which I’ll address shortly), but I wanted to comment on some excellent words on the practice of science as it’s often used in the human sciences (including both medicine and social science):

Another problem endemic to obesity and nutrition research since the second world war has been the assumption that poorly controlled experiments and observational studies are sufficient basis on which to form beliefs and promulgate public health guidelines. This is rationalised by the fact that it’s exceedingly difficult (and inordinately expensive) to do better science when dealing with humans and long term chronic diseases. This may be true, but it doesn’t negate the fact the evidence generated from this research is inherently incapable of establishing reliable knowledge.

The shortcomings of observational studies are obvious and should not be controversial. These studies, regardless of their size or number, only indicate associations—providing hypothesis generating data—not causal relations. These hypotheses then have to be rigorously tested. This is the core of the scientific process. Without rigorous experimental tests, we know nothing meaningful about the cause of the disease states we’re studying or about the therapies that might work to ameliorate them. All
we have are speculations.

As for the experimental trials, these too have been flawed. Most conspicuous is the failure to control variables, particularly in free-living trials. Researchers counsel participants to eat diets of different macronutrient composition—a low fat, a low carbohydrate, and a Mediterranean diet, for instance—and then send them off about their lives to do so.

Rather than acknowledge that these trials are incapable of answering the question of what causes obesity (assumed to be obvious, in any case), this research is still treated as relevant, at least, to the question of what diet works best to resolve it—and that in turn as relevant to the causality question.

What can we do about this? It seems we have two choices. We can continue to examine and debate the past, or we can look forward and start anew.

We believe that ultimately three conditions are necessary to make progress in the struggle against obesity and its related chronic diseases—type 2 diabetes, most notably. First is the acceptance of the existence of an alternative hypothesis of obesity, or even multiple alternative hypotheses, with the understanding that these, too, adhere to the laws of physics and must be tested rigorously.

Second is a refusal to accept substandard science as sufficient to establish reliable knowledge, let alone for public health guidelines. When the results of studies are published, the authors must be brutally honest about the possible shortcomings and all reasonable alternative explanations for what they observed. “If science is to progress,” as the Nobel prize winning physicist Richard Feynman said half a century ago, “what we need is the ability to experiment, honesty in reporting results—the results must be reported without somebody saying what they would like the results to have been—and finally—an important thing—the intelligence to interpret the results. An important point about this intelligence is that it should not be sure ahead of time what must be.”

Finally, if the best we’ve done so far isn’t good enough—if uncontrolled experiments and observational studies are unreliable, which should be undeniable—then we have to find the willingness and the resources to do better.

I almost couldn’t say it better myself. 😉

In general, medical wisdom in general, particular when it comes to diet, exercise, obesity, and health related to such is based on generally bad science. This has been a general theme of my posts on the matter, and indeed, one of the overall themes of my blog, at least with respect to human differences. These are points I’ve made when discussing this topic, and Taubes pretty much speaks to my thoughts on the matter.

Of course, the very standard that Taubes wishes to hold hypotheses on the causes of obesity to apply to his own hypothesis, namely, that it is excessive carbohydrate consumption per se that is leading surging obesity rates. I’m not sure that that is the case, and this hypothesis needs to be examined with research conducted to the same standard Taubes holds the prevailing wisdom.

And, with all that said, Taubes seems to glance over a very powerful point he raised in his essay:

In these trials, carbohydrate restricted diets almost invariably show significantly better short term weight loss, despite allowing participants to eat as much as they want and being compared with calorie restricted diets that also reduce the quantity of carbohydrates consumed and improve the quality. In these trials, the ad libitum carbohydrate restricted diets have also improved heart disease and diabetes risk factors better than the diets to which they’ve been compared. But after a year or two, the results converge towards non-significance, while attempts to quantify what participants actually eat consistently conclude that there is little long term compliance with any of the diets.

Let’s say that Taubes is correct, and it is excessive carbohydrate consumption that is leading the obesity rate. What do you do about it? Simply suggesting that people go on low-carb diets isn’t going to work because most people cannot adhere to such a diet.

But, theoretically, if we did definitely identify carbohydrates as the problem, massive government intervention in the food market might be able to address this. Through taxes and subsidies, perhaps we could make “fattening” foods considerably expensive, discouraging their consumption. I’m not going to comment of the feasibility of such a plan, but Taubes is certainly correct that we need more and better research into this whole topic.

(Republished from JayMan's Blog by permission of author or representative)
 
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  1. Anonymous • Disclaimer says:

    “Simply suggesting that people go on low-carb diets isn’t going to work because most people cannot adhere to such a diet.”

    Will not. Fixed that.

  2. Anthony says:

    Part of the point of Atkins-like diets is that it’s easier to stick to them than it is to low-fat diets, because fat sends your brain satiety signals faster than do carbs.

    • Replies: @JayMan
  3. JayMan says: • Website
    @Anthony

    It may be easier to stick to than a low-fat diet, but not easy for most people who try it, as with any diet…

  4. The US gov’t already subsidizes carb production, largely through corn subsidies, which translate into high fructose corn syrup, one of the main refined sugars consumed in the US. Simply removing those subsidies would decrease the amount of sugar being produced.

    I drastically reduced the amount of refined carbs I eat about 3 years ago, and have stayed that way. I am not on a ‘diet’ (I am not looking to lose weight), but have just adopted better long-term eating habits. I don’t avoid *all* carbs (that would be very hard,) but I do not consume any juice, breakfast cereals, oatmeal, or sweets of any kind, and limit my bread and pasta.

    Interestingly, my first two pregnancies, when I was eating a relatively ‘normal’ American diet, I gained 50 lbs each pregnancy (then lost it again before the next.) My most recent pregnancy, during which I had stopped drinking milk and cut most of my carbs (replaced with microwavable veggies, nuts, meat, butter, and fish,) I only gained 35 lbs.

    Hardly scientific data, but we start somewhere.

  5. Staffan says: • Website

    Not as an example of great science, but I’ve made the observation that people who are more into ideas than actual experiences tend to stay lean. They don’t seem any more disciplined than the rest but simply less interested. Possibly due to high dopamine levels. Maybe we should put all the fatties on ADHD meds : )

  6. JayMan says: • Website
    @Staffan

    Is this with IQ considered?

  7. Staffan says: • Website

    It’s more than just IQ, again just in my experience. I’ve met several of this type who have been pretty average. Female journalists of this type seem very common for some reason. They are often very impulsive but it’s usually idea-oriented.

    • Replies: @JayMan
    , @JayMan
  8. JayMan says: • Website
    @Staffan

    Maybe the truth correlate is how “driven” the person is? Thinner people are more energetic and probably this manifests in many other ways. Interesting nonetheless.

  9. @Staffan

    I have seen studies that fat people degenerate more quickly, mentally speaking, than thin people. There are a lot of obvious correlates, but I find it very strange that, for example, African Americans are more likely to develop Alzheimer’s than African Africans. Since we hear so much about the quest for genetic bases to these diseases, I’d expect a closer match. (I see three possibilities: 1. bad data, 2. black folks aren’t adapted to something in the environment here, eg, low sun levels, 3. something in the environment here which they are disproportionately exposed to, eg, stress.)

    ADHD meds suppress appetite, so they might do something for folks who just over-eat.

    • Replies: @JayMan
  10. maciano says:

    jayman, you should read gcbc. it is an exceptional good book on food science.

    even if he omits hbd, which he does, it is still a very good review of existing literature.

  11. JayMan says: • Website
    @EvolutionistX

    I have seen studies that fat people degenerate more quickly, mentally speaking, than thin people.

    Is that controlled for IQ? Lower IQ people tend to be fatter. This is why I suspect that genetic load is in good part responsible for the health issues that are common with obese people.

    but I find it very strange that, for example, African Americans are more likely to develop Alzheimer’s than African Africans.

    Maybe because Africans in Africa don’t live as long as African Americans?

    ADHD meds suppress appetite, so they might do something for folks who just over-eat.

    Maybe. I doubt there’s been clinical trials for obvious reasons…

  12. “but I find it very strange that, for example, African Americans are more likely to develop Alzheimer’s than African Africans.”

    “Maybe because Africans in Africa don’t live as long as African Americans?”

    Higher prevalence of Alzheimer’s disease in African American populations relative to African populations may be due to longer life expectancy in America versus Africa, and maybe environmental, lifestyle, and dietary factors also contribute (inflammation etc.?). However, it is well known that African American populations are partly admixed with Europeans. Previous studies have shown an association with Alzheimer’s disease and the HLA region. The paper below finds a link between Alzheimer’s and the HLA B7 allele in linkage with HLA Cw*0702 :-

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764414/

    If presence of the HLA Cw*0702 – B7 haplotype in human populations does confer susceptibility to Alzheimer’s, it is worth looking at the frequencies of this in different human populations worldwide:-

    http://www.allelefrequencies.net/hla6003a.asp?hla_locus1=A_not&hla_locus2=B*07%3A02&hla_locus3=C*07%3A02&hla_locus4=DRB1_not&hla_locus5=DPA1_not&hla_locus6=DPB1_not&hla_locus7=DQA1_not&hla_locus8=DQB1_not&hla_population=&hla_country=&hla_dataset=&hla_region=&hla_ethnic=&hla_study=&hla_order=order_3&hla_sample_size_pattern=equal&hla_sample_size=&hla_sample_year_pattern=equal&hla_sample_year=&hla_loci=

    Note the high frequency of this haplotype in North-West European derived populations [eg Northern Ireland 17.00%; USA Caucasians 11.10%]. Now contrast African American frequency [6.90%] with frequency in a native West African population [Mali Bandiagara 4.30%]. If African Americans are intermediate in frequency of HLA Cw*0702 – B7 between native West Africans and USA Caucasians, the data appears to support North West European ancestry being a component in higher rates of Alzheimer’s, alongside the other factors mentioned.

    • Replies: @JayMan
    , @EvolutionistX
  13. @chrisdavies09

    African Americans develop Alzheimer’s at a higher rate than whites (despite shorter life expectancies,) so a genetic factor which they possess less of than whites does not seem like a good theory. (http://www.ncbi.nlm.nih.gov/books/NBK25535/)

    Thankfully the people doing these studies are not complete idiots, so very often they are not measuring ‘What is the most common cause of death in this population overall?’ but ‘Among members who are FOO years old, how prevalent is disease X?’ For example, one study I read compared the progression of atherosclerosis in the hearts of accident victims in their 30s-50s in the US and, I believe, Uganda. (The Ugandans had far, far less heart disease than their equally-aged American counterparts.) Or they will look at a population of people who have made it to 80 (even in the third world, there are some very old people,) and try to measure the rates of Alzheimer’s, heart disease, etc.

    The best book I can recommend on this subject is Food and Western Disease: an Evolutionary Perspective, by Lindberg. (http://www.amazon.com/Food-Western-Disease-Evolutionary-Perspective/dp/1405197714/ref=la_B002P8YG9G_1_1?ie=UTF8&qid=1366572545&sr=1-1)

  14. (To cut to the chase, I think our bodies have evolved to handle/process certain foods, get a certain amount of exercise of specific sorts, receive certain amounts of sunlight, etc., store certain amounts of fat, etc., and when you radically change that over a very short time period, the body has trouble.

    The Paleo Diet supporters often go a bit overboard in their claims (hunter-gatherers did eat grain, for example, when they could find it growing in their environment–how else could they have gotten the idea to plant it?) but the idea that we should pay attention to what we’re adapted to eat is not a bad one. (And basically none of us is adapted to highly *refined* carbs, because refining technology is very recent and its widespread use even more recent. Most grain has been eaten straight or as slightly fermented porridge for most of agricultural history, because grinding flour and making bread is a lot of work.)

    When we get a result which doesn’t square with genetics (Africans in Africa having much lower obesity rates than Africans in America, for example,) then environment is a likely culprit. )

    • Replies: @chrisdavies09
  15. As for intelligence and obesity, there’s an obvious chicken and egg problem: stupid people, for many reasons, end up fatter, and fatter people have conditions (eg, diabetes, atherosclerosis,) which kill brain cells.

    “Researchers in another study compared MRI-assessed manifestations of cerebral degeneration in 89 non-demented subjects with type-2 diabetes to 438 age-matched healthy controls over a three-year period. Individuals with diabetes displayed increased progression of brain atrophy, and performed less well on tests of cognitive performance and learning. The investigators concluded that “our data show that elderly patients with [type-2 diabetes] without dementia have accelerated progression of brain atrophy with significant consequences in cognition compared to subjects without [type-2 diabetes]. Our findings add further evidence to the hypothesis that diabetes exerts deleterious effects on neuronal integrity.” ”

    “Mid-life obesity was strongly linked to later-life dementia in over 1,000 participants in a longitudinal study carried out over a 36 year period. Subjects with the greatest waist diameters at baseline were nearly three-fold more likely to develop dementia over the following three decades. The investigators in this study concluded that “central obesity in midlife increases risk of dementia independent of diabetes and cardiovascular comorbidities.””

    “Adipose tissue secretes molecules that directly influence multiple functions within the brain.114 There is a clearly established reciprocal relationship between adiposity (amount of body fat) and overall brain volume and cognitive function. In other words, as bodyweight increases, brain volume drops and cognitive function worsens.”

    http://www.lef.org/protocols/neurological/age_related_cognitive_decline_01.htm

    Chickens, eggs.

    • Replies: @JayMan
  16. @EvolutionistX

    I must admit that my theory is flawed, I didn’t know that Alzheimer’s rates are higher in african americans than in US caucasians.

  17. JayMan says: • Website
    @EvolutionistX

    As for intelligence and obesity, there’s an obvious chicken and egg problem: stupid people, for many reasons, end up fatter, and fatter people have conditions (eg, diabetes, atherosclerosis,) which kill brain cells.

    Not so much as you might think. Most of those things are late-onset, where obviously low IQ is evident early, so we can be fairly confident the causality doesn’t run obesity -> cognitive impairment.

    Indeed, I wouldn’t be surprised of much of health problems associated with obesity (perhaps, except type II diabetes) stem from the lower average IQ of obese people. I’m pretty certain obesity studies don’t control for IQ.

  18. HBD guy says:

    You know, Cochran/Harpinding’s book raises this point briefly about carb consumption, agricultural and HBD. If you look at certain disease rates, like obesity, heart-disease and alcoholism, those who have practiced agriculture the longest tend to have gene variants that help in the digestion of the altered diet. People who had never eaten a grain or sipped alcohol in their entire evolutionary history suffer horribly from adopting a western diet. Australian Aboriginals are a prime example.

    • Replies: @JayMan
  19. I have a Vietnamese friend who, amazingly, does best when eating a traditionally Vietnamese diet. Lactose intolerance + celiac disease is really annoying when living in Western society, but what can you do?

    Jay, I agree that stupidity sets in earlier than diabetes, but my original comment was about brain degeneration, which does appear to happen faster in fat people, and is very likely exacerbated by conditions like type II diabetes, which skyrockets in incidence as countries “develop”, especially in populations which did not historically eat things like refined wheat. (Also, obesity sets in pretty darn early, if “Epidemic of overweight 6 month olds” means anything. Babies born to fat people are over-fed in the womb, making the chicken and egg problem pretty pernicious.)

    Farmers fatten cattle on corn, but only at the ends of their lives–too much too early will make the cow grow fat instead of big, hit puberty early, and generally mess up their lifecycle. Cows aren’t people, but it’s difficult to devise effective, ethical human experiments on food and growth with the same scientific rigor as animal husbandry. Humans may explain away their obesity as ‘lack of willpower’, but a farmer facing lost profits has an incentive to be honest.

    Of course, I don’t know if anyone has tried feeding the cows refined fats 🙂

    I’m not saying there isn’t a genetic component. Of course there is. But people are much fatter now than a hundred years ago, and environmental changes (including food) to which we aren’t adapted (and some folks are less adapted than others,) are likely culprits.

    Mind and body exist together, one and the same, and the idea that the one influences the other is only sensible; inducing faster growth in an organism likely triggers faster brain maturation simply because growth and maturation have always been physiologically linked, thus leading to the “prematurely aged” brains of fatter people. Intelligent species always develop more slowly and have extended childhoods for brain growth. Short-circuiting this through feedlot-style fattening of children is probably a bad idea.

    • Replies: @JayMan
  20. JayMan says: • Website
    @EvolutionistX

    Jay, I agree that stupidity sets in earlier than diabetes, but my original comment was about brain degeneration, which does appear to happen faster in fat people, and is very likely exacerbated by conditions like type II diabetes,

    Perhaps. I’ll be more convinced when I see more evidence that isn’t merely correlational.

    (Also, obesity sets in pretty darn early, if “Epidemic of overweight 6 month olds” means anything. Babies born to fat people are over-fed in the womb, making the chicken and egg problem pretty pernicious.)

    Behavioral genetic studies settle this one: the transmission from parent to child is genetic, not through prenatal effects.

    Short-circuiting this through feedlot-style fattening of children is probably a bad idea.

    Probably.

    I’ve have yet to look at that Manly & Mayeux paper you’ve cited. I’ll check it out and get back to you on it.

  21. JayMan says: • Website
    @HBD guy

    Yes, I strongly suspect that there is a considerable element of that at work here. However, it’s not quite so simple. I took a look at health statistics in the Middle East, the people who have had the longest to adapt to agriculture. As modernization commences, Western-style illnesses, including obesity, are setting in there. The mystery continues…

  22. JayMan says: • Website
    @Staffan

    Interesting. More study is needed!

  23. Anonymous • Disclaimer says:
    @Staffan

    [quote]ADHD meds suppress appetite, so they might do something for folks who just over-eat.[/quote]

    For a time. Like other effects, that tends to diminish over time without an increase in dose.

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