Good Science Bad Science ~ Good Schtick Bad Schtick
Note: This version slightly differs (only at the end beginning with italics) from my original post so I "bumped" the publish date and noted where I made a few changes.
So Jimmy Moore recently posted an interview with Gary Taube$: Podcast HERE
I have much more to say about this interview, Taubes' most recent lecture and his upcoming book, but that will have to wait for another day.
So Jimmy Moore recently posted an interview with Gary Taube$: Podcast HERE
I have much more to say about this interview, Taubes' most recent lecture and his upcoming book, but that will have to wait for another day.
What I am bothered by is Taubes continued trashing of the scientific community while basically admitting the same for himself (though not realizing it).
I would agree with Taubes that one of the problems with scientific research in general these days is the funding process/stream. Been there, done that. If you're a nobody with big ideas, good luck. If you're a big name trying to get another MS or PhD thesis on some minor topic, it shouldn't be a problem. There's ALWAYS a lag between funding, research and publication -- several years is more the norm than the exception here.
But Taubes' premise is that scientists develop a "schtick" -- the PhD thesis or whatever puts them on the map -- that keeps them from ever correcting themselves or pursuing the research they obviously really want to do if only they were independently wealthy. All the old science is golden because it was done by rich folks who funded their own work and didn't need to answer to anyone. These were folks of high character and principle and beholden to no one. I have one name for you on that note Gary: Michael Bloomberg.
But Taubes goes on to lament that he really would like to get back to writing on other science (e.g. that which he has the background and qualifications to write about), but he has kids to put through college. He rambles on and on about mistakes in GCBC as pertains to the whole G3P issue (again, I have a post in the hopper on this but have a bit more work on that before I'll publish it). Mea culpa? Hardly, IMCO. For starters, he further laments not having a public forum on which to correct himself. NONSENSE. But he failed in 2007 in a far more critical manner than the scientists he lambastes do in publishing their research. He was wrong, but won't acknowledge that this point is the absolute KEY to all of his theories on how fat miraculously accumulates irrespectively of calories. He also keeps calling for metabolic ward studies to test his theories, when these WERE done long ago.
No doubt the worst of his transgressions, to me, is that he claims that in 2007 (or in the intervening years of writing the NYT & the book) the science of GlyNG was still rather vague and he presented only the current knowledge in GCBC. Try again Gary. The two papers I referenced in this post were to 2002 and 2003 REVIEW papers -- IOW papers that summarized older research, most or all of which predated even the NYT article.
The paragraph below has been edited slightly from the original after re-listening to the interview.
The paragraph below has been edited slightly from the original after re-listening to the interview.
Open query to Gary Taubes: Care to name names? Who was this "biggest expert in the country" whom you consulted in prepping your book in 2007, the "smartest guy" around at the time, who vetted 3-4 versions of this section in your book to make sure it was accurate? I doubt it was Hanson's group (AND YET ANY CURSORY LOOK INTO THE REFERENCES FROM THE 2003 PAPER WOULD HAVE LED YOU TO CONTACT THEM!!!). And what 2008 paper did he inform you of to let you know all the textbooks (hint: scientific research should perhaps begin with texts, but never end with them) were wrong? Who is the English guy who confirmed you were wrong? Newsholme? And who, pray tell, are these anonymous two biophysicists who informed you that you were wrong on G3P, but supposedly said *it doesn't matter* because "insulin so fundamentally drives fat accumulation"? Any reason why you painstakingly identify the authors of various statements in your book and lectures, but won't name names now???? (I know ;-) )
Yep. Taube$ has his $cience and his $chtick. Proven wrong on a key component of this theory, he's chosen to simply leave it out and hope insulin is enough to snow people.
If carbs drives insulin drives fat accumulation, then protein drives insulin drives fat accumulation.
(Or, consuming fat and/or carbs and/or even protein in chronic excess of energy needs does.)
Yep. Taube$ has his $cience and his $chtick. Proven wrong on a key component of this theory, he's chosen to simply leave it out and hope insulin is enough to snow people.
If carbs drives insulin drives fat accumulation, then protein drives insulin drives fat accumulation.
(Or, consuming fat and/or carbs and/or even protein in chronic excess of energy needs does.)
Comments
G3P is not the key to fat accumulation irrespective of calories. The key is fat deposition exceeding fat mobilization. The idea that dietary carbohydrates raise insulin levels, and chronically elevated insulin levels lead to fat accumulation and fat deposition exceeding fat mobilization can still hold true. G3P or GNG does not refute the hypothesis that we don't get fat because we overeat, rather we get fat because the carbs make us fat.
Also, what metabolic ward studies are you referring to? I was recently reading the Foster et al. (2010) study that cited three metabolic ward studies that were invoked to show that nutrient composition didn't affect weight, but they had serious limitations, and none of them were "overfeeding" studies, which is what Taubes is proposing.
The idea that dietary carbohydrates raise insulin levels, and chronically elevated insulin levels lead to fat accumulation and fat deposition exceeding fat mobilization can still hold true.
****************
That idea doesn't hold true either. See my latest article series on insulin:
http://weightology.net/weightologyweekly/?cat=63
I read through 'part 1' of the series (Insulin...and undeserved bad reputation), and it was an interesting read. I'll hold any final conclusions until I read the entire series, but part 1 seemed to be mostly about what happens to a healthy individual after eating a meal.
I read a little while back Jacques Le Magnen's book 'Hunger,' in which he writes about an insulin secretion occurring in anticipation, or within a few seconds of eating a meal. This is before the glucose enters the bloodstream so it might explain why there is an insulin response to foods containing both "low-carbohydrate" (75g) and "high-carbohydrate" (125g), but it should be noted that the differences in insulin response were not statistically significant, and these are both high-carbohydrate meals, and with all of the carbohydrate coming from glucose syrup, the loose equivalent of consuming 60 oz. and 100 oz. of coca-cola, respectively, in 10 minutes, the fact that one group was also consuming a bunch of protein along with it becomes almost irrelevant in terms of insulin response.
Also, and I apologize since I haven't finished your series and perhaps you explain it, but the issue with the overweight and obese, according to Taubes, would be abnormally chronic elevated levels of insulin aiding weight gain, who may be represented in your graph of the lean vs. the obese with excessive insulin secretion due possibly to insulin resistance.
I'm wondering what your take is on how people become insulin resistant and whether insulin resistance/hyperinsulinemia is a factor in weight gain (cause, effect, no association)?
I will check out the links.
I may be totally wrong, and I don't speak for Taubes, but I think the "biggest expert" he was referring to is Richard Hanson. I think the paper he was referring to was "Reassessing triglyceride synthesis in adipose tissue" (pdf) (Nye et al., 2008 - includes Hanson as an author) - and there was a similar thesis that you should find if you do a google search for "Nye et al., 2008 glyceroneogenesis" which includes a reference of a computational model by Kim et al. (2008).
I think if you contact Taubes he would probably answer these questions for you.
Hope this helps.
I think the paper he was referring to was "Reassessing triglyceride synthesis in adipose tissue" (Nye et al., 2008).
There is also a thesis you can find online entitled "ASSESSING THE ROLE OF GLYCERONEOGENESIS IN TRIGLYCERIDE METABOLISM," by Nye - and in the paper, there is a reference to a computational model of adipose tissue metabolism, entitled "A computational model of adipose tissue metabolism: Evidence for intracellular compartmentation and differential activation of lipases" by Kim et al.
I'm not sure what you're implying about knowing why Taubes didn't mention the names of the authors, but I think if you contact Taubes he will provide you with the answers you're looking for.
And I think you may be right about the Nye thesis. Good find!! I'm embarrassed to say I think I've seen it. I guess I didn't put two & two together... :`O
Taubes is a name dropper extraordinaire. Why not drop those names now??? I don't think he wants people to delve further, let alone us lowly bloggers that he sneered at in that interview.
Another major reference in GCBC as regards this issue does not jive with what he says in the book either.
"AFAIK, it has never been shown experimentally that glyceroneogenesis is up-regulated in humans when eating a low carb diet, especially to a degree that could cause significant fat accumulation. Practically all the research in humans has focused on the role of glyceroneogenesis in fatty acid/triglyceride recycling during fasting. A speculative connection can be made between fasting & low carb dieting because of the hormonal similarities between the two, but nothing can be stated firmly."
I would say that it would be highly unlikely that GlyNG is NOT upregulated under LC feeding conditions. If every other fasting mechanism kicks in with carb deprivation, I see no reason this related pathway wouldn't be.
There's a fat overfeeding study that is widely cited as proving some portions of the so-called metabolic advantage theory. As I recall the subjects consumed up to like 600g fat/day in the context of ~150g carbs/day. Although the participants didn't gain weight by a strict calorie calculation (they got sweaty at the high levels of fat intake indicating that at some point of severe overconsumption futile cycling may play a role in wasting excessively excessive caloric intake), they did gain considerable weight. The 150g carb is in line with basic brain glucose requirements, and I don't think it's unreasonable to assume that most of the dietary carb was directed towards this purpose and wasn't the major source of the much needed G3P to esterify all that fat consumed. We know fat cells can't make it from the glycerol itself, so that pretty much leaves GlyNG.
Sorta seems to me that the body makes glucose when it needs it if it doesn't get it externally. Seems equally logical that the body makes the G3P it needs to deal with both dietary fat ingestion and the essential triglyceride/fatty acid cycle. Got a lot of fatty acids around, make the G3P to store them. What say you?
"G3P is not the key to fat accumulation irrespective of calories. The key is fat deposition exceeding fat mobilization. The idea that dietary carbohydrates raise insulin levels, and chronically elevated insulin levels lead to fat accumulation and fat deposition exceeding fat mobilization can still hold true. G3P or GNG does not refute the hypothesis that we don't get fat because we overeat, rather we get fat because the carbs make us fat."
Re-read Chapter 22 in GCBC: The Carbohydrate Hypothesis II: Insulin
G3P WAS integral in the original hypothesis, and all we have to fall back on now is Taubes' assertions that two unnamed biophysicists now think it doesn't matter because the insulin part is so strong.
Taubes likes to confuse transient insulin spikes due to insulin-stimulating dietary intake with chronic high basal insulin. Basal insulin correlates with one's degree of adiposity and the evidence points the arrow of causality from obesity --> hyperinsulinemia rather than the other way around. Chronic hyperinsulinemia is related to insulin resistance, that can be induced by poor diet, but it is not the result of eating a lot of carbs absent other complicating factors. If you read further in my blog and linked sources, I think you'll find it hard to conclude that insulin RESISTANCE is caused by carbs per se.
But, just as we see any number of counter-examples to the theory of positive caloric balance, there are any number of counter-examples to Taubes' carbs cause obesity theory. Basically, until the 20th century, few got fat, regardless of what they ate, high carb diet or not.
The Chinese eat 70% carbs, and unless they do it S.A.D. style (i.e., eat wheat and vegetable oils), they don't get fat apparently (http://rawfoodsos.com/2010/09/02/the-china-study-wheat-and-heart-disease-oh-my/).
Wheat is inflammatory for most people, just as vegetable oils (which are fats, duh). Fructose may be worse than either, but the Chinese are not swigging Cokes and eating grapes all day to exceed the body's threshold. Truly, the most toxic foods are carbs (in the Food, Inc. world), which gives an edge to low-carb diets.
The manufactured food staples and fruits bred for high sugar/fructose tend to be treated by the body as an infection and/or cause chronic infections. Often obesity results (but it might "just" be cancer or any autoimmune disease). Missing that entire point is the major flaw in Taubes' message. And, if he is wrong in the large, he must be technically wrong in the small.
I'm intrigued by your comments about Gary Taubes and your belief that he is merely motivated by dollars and not the science. Would you like to come on my podcast show to talk about this? I think it would be quite illuminating to my listeners to hear an alternative viewpoint. E-mail me at livinlowcarbman@charter.net and we'll work out the details. :)
And Jimmy if you're reading this, have you ever tried to get Stargazey from the Low Carb 4 U blog? She had a series of posts a while back on blood sugar issues and low carb in the 50+ age group that would be interesting to discuss.
The more I delve into this topic the more I am convinced that Taubes knew substantial portions of GCBC were wrong (as he now admits) prior to the publication of the book. This is at the root of my opinion that his judgement is clouded by financial interests. That opinion is not up for debate.
I guess firstly I would have to take issue with the notion that carbs are truly the most toxic foods from "Food, Inc." Umm.... list such foods. I can see the likely culprits containing carbs, but a fair dose of fats and other chemicals to boot.
"just as we see any number of counter-examples to the theory of positive caloric balance, there are any number of counter-examples to Taubes' carbs cause obesity theory.
I've yet to see a counter-example to the theory of positive caloric balance, while there are millions of counter-examples to Taubes' theories.
Part of the problem is that Taubes sets up a strawman as regards caloric balance. Nobody ever said that the two sides of the equation were independent. They are dependent. But compensatory changes in one in response to the other are not without limits.
If we lock an obese person away and feed them 1000 cal/day of a high carb diet for a year, they WILL lose fat.
It sounds like you and I agree on Taubes but you still credit him for exposing the evil food industry? I'm having a hard time reconciling the first part of your comment with the rest of it.
I'm inclined to believe that for the most part, the food suppliers give us what we want. Surely subsidies and such have influenced the mix (and I wish the government would get the hell out of all of this), but if our society didn't gobble the crap up, the suppliers would stop making it.
Re: "list such foods". My most toxic (to fat metabolism anyhow) are grains (especially wheat), legumes (especially soy), fructose (especially HFCS), and vegetable oils. The many other darlings of Food, Inc (for flavoring or shelf-life) may be more toxic in some sense (e.g., more carcinogenic), but eliminating carbs knocks out three of the "big four" above, and often promotes weight loss.
Re: "positive caloric balance". If obesity is caused by gluttony and sloth, we would expect that calories are very correlated with obesity/BMI, but the correlation is weak. There are surely better examples, but from this excellent China Study analysis (http://rawfoodsos.com/2010/09/02/the-china-study-wheat-and-heart-disease-oh-my/), "So once again, we’ve got a paradox: The wheat eaters are consuming lower or average levels of calories, doing more physical labor, and yet… they’re fatter."
Largely, I'm convinced Paul Jaminet (http://perfecthealthdiet.com/?p=606) has obesity perfectly nailed as caused by "food toxins, malnutrition, and infections". The minutiae of fat storage do not matter, in some sense, particularly if that leads to the simplistic conclusion that carbs ==> insulin ==> obesity. Rather, it is manufactured foods (and/or other crap) ==> disease/dysregluation ==> (often) obesity.
The obese might eat more, but the obese also likely have impaired guts (due to toxins or infections) or poor diets (e.g., the wheat centric, USDA recommended diet). So, to absorb enough nutrients, many are driven to the overeat. This is not gluttony (a human frailty), but basic survival instinct. Overeating may be positively correlated to obesity, but overeating is not driving obesity.
Re: "if our society didn't gobble the crap up, the suppliers would stop making it." That is truly blaming the victims of massive disinformation campaigns. A majority of people changed their diets to be more in line with "eating healthy". The corporatocracy says eat whole grains until they come out of your ears, drink only skim milk, avoid saturated fat, and go to the gym more. Compliance is ever increasing (with ever more negative results). And some non-compliance is largely due to wishy-washy, conflicting advice; the diabetes promoting America Diabetes Association preaches "your body doesn’t care if the extra food comes from cookies or beef" (http://www.diabetes.org/food-and-fitness/food/what-can-i-eat/sweeteners-and-desserts.html). Say anything to peddle insulin, I guess.
Even if you start doubting your education/doctor/nutritionist/government when eating "healthy" causes your heart disease, just hope you don't stumble onto http://www.vegsource.com/ or some other even more moronic nutrition dogma. The Internet is a dangerous place.
As http://freetheanimal.com/2010/10/the-us-surgeon-general-regina-benjamin-is-a-caricature-of-fat-america.html says,
"it's so difficult and unlikely for people to get sound health, fat loss and exercise advice."
The same thing happens with psychopharmacology research, as described (in fascinating detail) by Robert Whitaker in his recent book, Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America.
Thanks for your input Alex & welcome :)
I'd suggest the modern woman's toxic bagel and fruit, low-fat, low calorie diet causes obesity along the lines of
http://thehealthyskeptic.org/the-autoimmune-inflammatory-model-of-diabesity.
Adult women would presumably include those who have gone through menopause with it's concurrent reduction in TDEE if nothing is done to counter that. (I have a post or two in the hopper on this topic). This population would also contain the highest proportion of perennial dieters (yo yo) and this is known to suppress metabolic rate. I don't see this to be a paradox at all or inconsistent with calorie balance. I'll check out that autoimmune-inflammatory post soon. I've been on a bit of an inflammation research kick of late so this is timely. Thanks!
Re: "list such foods"....loss.
You make a good point here! I tend to believe that many of the "miracle" stories I hear on LC forums associated with eliminating carbs are due to having eliminated something toxic to the person. And many of those who insist they must eat VL or ZC because one bite of something causes them to gain several pounds are likely having an allergic reaction to that toxin. No doubt wheat is a toxin for many people. Also, I'm convinced that antibiotic abuse and/or the prevalence of NSAID's has contributed to the increase in gluten intolerance.
Re: "positive caloric balance". they’re fatter."
This does not violate calorie balance. If wheat is "fattening" it could have a metabolic suppressive quality (e.g. lower thyroid?). Or, it could result in the development of more lean body mass in those agricultural societies. Higher BMI does not necessarily equal fatter.
Largely, I'm convinced Paul Jaminet ... obesity.
I'm looking forward to receiving a copy of Paul's book to read and review. This will be interesting. There are certainly scenarios whereby obesity is the byproduct of underlying disease, but the progression of Type 2 diabetes seems to indicate otherwise in many cases. Those NEFA's I'm so obsessed with :) ...
The obese might eat more,.... driving obesity.
Speaking of wheat, when's the last time you ate plain bread? I tend to think that much of the data and ills we assign to wheat might be what else we're consuming with it, especially where obesity is concerned. I've had a few friends diagnosed with celiac, and they all experienced weight LOSS prior to diagnosis and adopting a gluten free diet.
Re: "if our society didn't gobble the crap up... results)
Here's where I have to strongly differ with you. When I was a kid in the 60's and 70's we had sodas and Twinkies and Sugar Frosted Flakes (before they took Sugar off the box), etc. If you look at the obese, they didn't get that way eating USDA guidelines/recommendations, however misguided they may be (and I agree they ARE woefully so!). For all the low fat nonsense, we aren't eating much less (men) and even eating more (women) in absolute amounts. OK, so maybe some folks will now eat whole grains because of those stupid commercials, but they'll eat them instead of refined grains, not instead of butter! OTOH, there are fast food restaurants still rolling out new gluttonous sized meals. Why did we start drinking those big gulps? Are "all you can eat" buffets an evil invention of the government? When did two cheese burgers become the double cheeseburger? Why did McD's decide to offer these huge portions of french fries? ALL of this is consumer driven. And none of this is anywhere near *compliance* with dietary recommendations.
And some non-compliance ...I guess.
Surely there are some who will throw their hands up at all the conflicting advice and just eat what they want. Why don't they choose steak and eggs then?
Even if you start doubting ... exercise advice."
I agree! I'm not sure all of the low carb advocates are the best ambassadors either, however. Does one need to be able to successfully implement good advice to be qualified to dole it out? (Leaving out what we would define as "good"). Last time I was visiting someone in the hospital I couldn't help but notice the prevalence of weight issues amongst health professionals. There are many people eating and preaching low carb diets who don't shed excess weight and whose faces remain as chubby as Ms. Benjamin's. Even the Eades supposedly accumulated a pair of paunches prompting 6WC.
Hypothesis (A) is somewhat countered by increased exercise and interest in health issues (even if listening to bad advice). (B) is bolstered by the fact the number of gut issues, including celiac disease has exploded since the 1970s (http://www.medicinenet.com/script/main/art.asp?articlekey=120165).
I would hope you would at least agree autism (usually an impaired gut disease) is not caused by gluttony and sloth (http://www.autismsecrets.com/autism-symptoms/overcoming-food-obsessions), unless that of the mother. You'll notice the "cure" is often a gluten-free-casein-free diet. Curiously, grains and dairy are the workhorses of a "healthy" USDA diet. Autism is actually more prevalent among the well educated (and presumably more health conscious and less slothful).
Barry Groves' (http://barrygroves.blogspot.com/) book "Trick and Treat: how 'healthy eating' is making us ill" covers hypothesis (B) well. The vitamin D council, http://www.vitamindcouncil.org/health/autism/, suggest dermatologists partly caused the autism explosion (with paid sunscreen endorsements, in effect). Groves makes similar points on sunscreen.
So, greed, rather than gluttony and sloth, is the cause of obesity. Technology/psychology/marketing/automation have multiplied the powers of the greedy.
Remember those paintings of Henry VIII? Quite fat. His diet was probably mostly meat, cheese, beer, wine. Only the beer contains significant carbs. Bread (coarse-ground wholegrain back then) would have been scorned as food for the poor, oats as food for horses, and veggies as food for donkeys and sheep. The rich have always eaten an Atkins style diet, and it didn't stop them from getting fat nor from suffering from gout and other diseases of excess. Even Hippocrates recognized that most chronic disease was the result of overindulgence at the table, and I doubt he was talking about overindulgence in coarse-ground wholegrain bread.
> fat. His diet was probably mostly meat, cheese,
> beer, wine. Only the beer contains significant
> carbs
http://www.suite101.com/content/henry-viii-s-feast-at-windsor-in-1528-part-1-a175940
Only the rich could afford a lot of sugar. There was a reason the European empires sought out all the ways to get sugar they could ... it was a high margin, high profit commodity. The rich paid handsomely for it.
Marie Antoinette didn't say "let them eat cake" because she wasn't having any ... she (and her court) was, in fact, having all the cakes, and most of the sugar
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