Quotations: Taubes on "The Establishment"

The way I see it is that the establishment has an immune system to protect itself from challenges. Every science needs that kind of immune system to protect itself from quacks and easy-to-swallow but erroneous ideas that might infect the good science in the field. My question is whether I can infect enough people, enough serious scientists, that I can pose a threat to this immune system, that I could compromise the immune system of the establishment and make them take this idea seriously. Because some times these immune systems work against challenges that are legitimate. I honestly don't know if I can. It's going to be an interesting year. I hope I don't become one of those bitter old men who, when I fail to do so, who can't let it go.
~ Gary Taubes, January 2008

Has he infected any serious scientist yet?


Diana said…
I ain't no scientist and I am happy to report that I am over the Taubes infection.
g2sb said…
Did you ever think that it might be prudent to tone down the Taubes criticism, you know, just a decibel or two?

Could High Insulin Make You Fat? Mouse Study Says Yes

The Study:
Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production

The paper has a long list of authors. Perhaps a few would qualify as serious even by Evelyn standards?
Puddleg said…
He needn't worry. Scientists in search of funding will support the status quo once it changes. They'll reinterpret their old research in support of the carbohydrate hypothesis (not that hard). It didn't take good science to usher in the low-fat folly, it won't take good science to get rid of it.
Puddleg said…
P.S. what is the "activity factor" that protects against metabolic inflexibility? Isn't it lactic acid?
A hypothesis; glucose will tend to take over from fat as a substrate given half a chance. Occasionally elevated levels of alternative substrates - either lactate (exercise) or ketones (intermittent fasting or carbohydrate restriction) - lessen the dominance of glucose, allow the use of fatty acids, and protect against metabolic syndrome.
Alternatively, lactate or ketones are signals to the CNS and genome that more fatty acid oxidation is needed to spare glucose.
Tsimblist said…
The New Model graphic in the study shows that a High Fat Diet causes the Hyperinsulinemia.
CarbSane said…
I see the problem with metabolic flexibility of the mitochondria as being determined at the "delivery" point. The use of fatty acids is intended to be primarily backup -- e.g. they get used when you need them -- and glucose is used when it's readily available. Problem is, when fat cells release too MANY fatty acids, the cells have to take them, this backs up glucose metabolism and you have nutrient overload all the way around.
CarbSane said…
Hmmm ... I posted a quotation and that's criticism? If anything I have toned down my criticism, but the guy just won't go away with his scientist-bashing and "alternate hypothesis" that is neither supported by observation so as to be formulated, nor the science out there he ignores, nor even the bulk of the cherry-picked science he misinterprets/misrepresents.

I'll effort the full text on the Cell paper, but as Tsimblist points out, even the "new model" shows high fat diet as proximal cause which I believe Gary would dispute.

CarbSane said…
It's been a decade and we're now to a point where Gary has gotten some $$ to fund his own research. Will scientists change their tune for $$ funneled through NuSI? Time will tell.

g2sb said…
Jeez, Evelyn, it is a *mouse* model, and they weren't testing for causes of hyperinsulinemia in mice, but rather for its effects.

This is just one study, it may not be reproducible, the paper's interpretation of the data may be in error, and the results might not be relevant to humans.

But it is serious consideration by "serious sceintists" of the idea that hyperinsulinemia might be a causal factor in obesity.

And yes, in context of your postings about Taubes, the presentation of the quote with a sarcastic question as follow-up counts as criticism.
Puddleg said…
the metabolic inflexibility through inactivity (bed rest) paper listed a shift towards glucose as a substrate. The problem may be that glucose is too available, even when fasting, because in this state hepatic glycogen may be looted ahead of fatty acids, and its depletion leads to more hunger, even though the FAs are available.
It's glycogenolysis, not gluconeogenesis, driving elevated BG.
Puddleg said…
Not for the NuSi funds which are relatively small and once-off, but for the funds available from all over to support any status quo.
Imagine this; the Republicans get it together (hard I know) and win the next election by a landslide. Governor Christie is president. Only he is slim and fit by then with the help of Taubes and Attia (and so is Rush Limbaugh). He makes nutrition reform a priority.
like McGovern in reverse.
That's an example of what it will take to change things, and science will be the handmaiden of politics once again. Good research will be done - has always been done - along with the bad, but it will be interpreted in the light of the new understanding instead of the old.
g2sb said…
I notice that Stephan Guyenet is mooting this tweet as frame:


"This one will be misinterpreted" ... Such as by the paper's lead author?

Puddleg said…
Hey, apparently carbs can kill cows:

"In May last year, the Taranaki Daily News reported the deaths of 35 cows from nitrate poisoning on a Tikorangi dairy farm.

The cows died after eating new pasture on a cloudy day. Similar cases were reported in South Taranaki.

Three months ago Taranaki Veterinary Centre vet Stacey Bateman, of Manaia, warned a seminar that cows were at risk of the illness in spring if carbohydrates were introduced too quickly into their diet.

Nitrate poisoning occurred when nitrates in forage was converted to nitrite, which starved animals of oxygen, causing them to collapse and possibly die. Those who recovered were likely to abort if pregnant.

On cloudy days photosynthesis may not occur, so plants do not convert nitrogen in the soil into protein."

So what did the cows eat before - were they in nutritional ketosis?

Maybe the vet's been reading "Why We Get Fat".
Anonymous said…
'Tone down' the Taubes criticism? Oh, no... please don't. I mean it - someone's got to do it.
blogblog said…

nitrite poisoning:


Nutritional ketosis is common in dairy cows. They only get about 2% of their energy from carbohydrates when eating natural pasture. Cattle normally get about 80% of their energy from volatile fatty acids produced via rumen fermentation.
CarbSane said…
Do you have access to the full text of that paper? It's hard to make a claim that the paper's lead author might be the one misinterpreting the study if all you have to work off of is the abstract. If you have it, feel free to email me carbsane at gmail dot com. Thanks!
Jane said…
Taubes says this in his 2002 NYT article: 'Which comes first -- the obesity, the elevated insulin, known as hyperinsulinemia, or the insulin resistance -- is a chicken-and-egg problem that hasn't been resolved. One endocrinologist described this to me as ''the Nobel-prize winning question.'''

Actually it has been resolved, at least in the minds of people who work on magnesium. What comes first, they would say, is magnesium deficiency which then causes the rest. A high-fat diet can in theory cause Mg deficiency, by discouraging the kind of gut bacteria which help its absorption.

Taubes does mention refined carbs and micronutrient deficiencies, but it seems none of the scientists he talks to knows anything about them, or if they do, they're not saying.
Anonymous said…
'That's an example of what it will take to change things, and science will be the handmaiden of politics once again.'

Reading this, I can't help but think of Bill Clinton. Now, what exactly is it that his newly-slim physique tells us, again?
CarbSane said…
Ha! Not likely to occur any time soon. Someone has to speak out about these charlatans. And since like a nutritional remake of Groundhog Day Taubes is back (with Attia) on TV (Stossel, blog post coming soon), folks need to be reminded over and over again and as many times as needed and then some.
g2sb said…
To be clear, I am making no such claim, nor am I asserting that Stephan is making such a claim. However, I do think that the framing and the assertion in Stephan's tweet are not especially useful at this point.

Co-author (and lead?) James Johnson tweets in reply:


I don't have the full text yet, but some interesting info can be gleaned from the figures and their captions:

CarbSane said…
Citations please! This is how I first "tangled" with Kruse, because he made a blanket statement that Mg deficiency precedes everything and I asked for a cite. He dragged the discussion over to PaleoHacks where some others provided some, but none of them demonstrated this pretty bold assertion you are making.

The overwhelming body of evidence vis a vis the crappy American diet is that -- whatever you want to call it -- we consume too much food, pack on the pounds, exceed our body's ability to contain it appropriately (in fat tissue), overload our other cells with nutrients and our poor pancreas is stimulated to secrete more and more insulin to try to keep the fat where it was/is supposed to be stored.

Every single time isocaloric studies have been done in controlled settings, the lean and the obese maintain fat/weight. Every single time calories are restricted, the lean and the obese lose fat/weight. Every single time you overfeed, the lean and the obese gain fat/weight. Some lean tissue is added/reduced along the way as well.

I await the first NuSI study.
rodeo said…
"Those differences traced to a "reprogramming" of the animals' fat tissue to burn and waste more energy in the form of heat. In other words, the mice had white fat that looked and acted more like the coveted, calorie-burning brown fat most familiar for keeping babies warm."

That will not happen in humans.
CarbSane said…
Exactly rodeo. Perhaps I'll put on my holiday wish list, dusting off a manifesto of sorts on the pros and cons of rodent animal models. While we have many things in common, being little critters, a vastly greater percentage of their metabolic rate (expenditure) is devoted toward maintaining body temperature than in humans. They also have a far greater amount of brown fat than do humans and UCP-1 therefore plays a much more critical role in metabolic rate.
g2sb said…

Among the many ways that you have enlightened me is in teaching that the energy expended by an inefficient metabolic process like gluconeogenesis is not necessarily wasted - as long as the ambient temperature is lower than body temperature.

I've come agree with you in thinking that conventional dietary views about energy homeostasis are central, and that the key to long term weight loss is in achieving satiety at a level of energy intake that the body is burning. Thus, in order to explain my own successful experience in weight loss using a prescription that was inspired in part by the writings of Taubes, I have become interested in the emerging ideas from Ian Spreadbury and others that gut-sourced endotoxemia is a likely prime suspect in the typical initiation of leptin resistance.

However, there do seem to be some good hints supporting the existence of diet-inducible metabolic regimes in which people and mice do generate and dissipate more heat than might otherwise be required for base temperature control.

In likely support, I will of course cite Ebbeling et al:

and Hatori et al:

and now, possibly, Mehran et al:

Such effects my not be very large for humans, but even 50 kcal per day could accumulate into roughly 5 pounds of body weight per year, and Ebbeling et al measured even larger effects in their admittedly controversial, short, and fairly small study.
rodeo said…
I'm sure you've seen this but Stephan discusses mice and insulin here:


Interestingly in mice with higher insulin levels (not high enough to induce hypoglycemia though) protects against weight gain on a high-fat diet.
g2sb said…

"That will not happen in humans."

It might be prudent to qualify such bald assertions:


I have a related comment in the Jane-Evelyn thread below.
Unknown said…
It tells us that he looks weak, fragile and unnatural. Clearly doing all the wrong things and defiling our nature and mother Earth in managing to get away in the act. Lol!
rodeo said…
Your link has nothing to do with my "bald assertion". I'm not questioning wheather humans to some degree have brown or beige fat. That would be silly to do.

The point is that the amount is too small to make any difference.
g2sb said…
The link, of course, speaks to biological similarities between humans and mice that might be relevant in metabolic regimes that promote thermogenesis.

Out of curiosity, are you asserting that diet-induced thermogenesis has no relevance in human obesity, or are you asserting that insulin signaling has no relevance to diet-induced human thermogenesis? Or both?

As fodder, note that population densities of human BAT cells seem to correlate inversely with obesity.
CarbSane said…
@George, I do not see that happening. Let's face it, the USDA guidelines were for relatively minor changes which we on average did not heed anyway. Sure there are a ton of LF products out there, but aside from the dairy aisle, even during the heighth of the Snackwell, low fat is not what's selling unless you want to be ridiculous and include Coke and Skittles. While I've occasionally seen some items that could pass for candy if not technically so being promoted on the basis of being low fat, I've never seen Coke promoted to people who want to lose weight -- that's the realm of Diet Coke.

BTW, Rush Limbaugh is another example of the failure of LC diets as magical cure-all. He yo yos every couple three years and has done some sort of LC diet each time in recent ones. And speaking of Republicans and LC, Huckabee isn't fairing well in the weight department lately.
CarbSane said…
I've got the full text of that first study and will take a closer look over the weekend.

I'll have to browse my Mendeley (hopefully I put it in there), but whenever I hear about diet-induced thermogenesis I keep coming back to Jequeir's factors used by Feinman & Fine and everyone else promoting MAD. Fat is the LEAST thermogenic.

Per your other comment (thanks!, glad some of what I write here is informative) the study I'm thinking of TEF was far greater on HC but it seemed to balance out otherwise leading to there being little advantage over the full day and such.

Puddleg said…
Yet these animals switched to natural pasture, and the vet blamed their demise on carbs?
Must have been reading Taubes - it doesn't make sense otherwise.
Puddleg said…
Surely it is the loss of the ability to regulate magnesium, possibly due to IR, that is to blame for the modern "deficiency'. It doesn't seem that much more deficient in the food supply (people didn't used to eat fruit and veges much anyway) and the amounts in water have always been paltry.
Puddleg said…
I don't actually know the diet history of the Republicans, i'm just fantasising. When the mood of the people shifts - and it is shifting - the interpretations of the science will change - not the data, but the assumptions reflected in the abstracts - because the people are ultimately the funders, and the science has always supported either interpretation to some extent.
Thesis, antithesis, synthesis - we are on the cusp of the antithesis.
About time too, but the sooner we get to the synthesis, the better.

P.S. USDA guidelines may not recommend the SAD, but they have gone a long way towards excusing it in the past.
CarbSane said…
The reason I know about Rush and Huckabee is b/c of Jimmy's blog and/or forum ;-)

I do not see science on any sort of cusp. Scientists are not funding obsessed drone idiots. There are a few bad apples, but most are truly interested in finding answers. Where nutrition science is bad we mostly have non-scientists posing as scientists to blame. If one thinks obesity researchers are evil, at least give the diabetes researchers a break. They are amazing in my opinion.

As to your PS, I think they go a long way towards folks excusing their SAD by saying they tried to follow the USDA guidelines. I'm thinking I'm coming across shrill, but I'm in a bit of a giddy sarcastic mood tonight so please excuse.
CarbSane said…
@George: Regarding the bedrest paper, I must say it has given me even more food for thought that it is carbs that the sedentary should consume with less restraint and fat only as increased activity levels require. Not necessarily in the obese/IR state, but even there a truly low fat diet with good compliance has not been tested just as most LC diets tested don't restrict nearly enough to see the difference either.

That's a pretty radical POV, and I'm not saying it's necessarily correct, but I'm hoping to flesh out some thinking out loud type thoughts when time frees up.
Anonymous said…
I believe Clinton went on his diet not to look slim but to reverse heart disease.


It doesn't seem to me that he is doing 'all the wrong things.' He does look older - he is older. He does look fragile - because he looks much, much thinner (more than 24 lbs thinner, IMO). This regimen was to reverse heart disease. Was it successful? Dunno.
blogblog said…
The cows died due to a LACK of carbs.

Nitrite posoning is due to excess ammonia production in the rumen. Carbohydrate and fibreintake counteracts ammonia production.
rodeo said…
g2sb: I think that when one focuses on small details like TEF due to beige fat one misses out on the greater picture. Which is that it has been proven again and again that there is no metabolic advantage in manipulating fat and carbs. And the proven advantage in increasing protein is diminished compared to the role of protein in satiety and in keeping muscle mass when dieting (which, I think, is one reason why the Ebbeling study is flawed).

Also when you focus on one single process in the body you tend to forget that other factors are influenced as well. I think there is much more support for low carb decreasing body heat due to lower thyroid stimulating hormone than for low carb increasing body heat due to beige fat.

Taken as a whole it these processes evens out and the most productive way of moving forward is to think of a calorie as a calorie.

I agree with you that irisin and other hormones secreted by muscle mass is intriguing though, but the research is just in its infancy. I think the hype is similar to the leptin hype and we have to wait and see what happens.
CarbSane said…
It seems we're back to the metabolic advantage argument? It all gets so confusing because there are essentially two factions of LC theory -- The TWICHOOBs and the MADders. These are on the same side but promoting different ideas. There are factions within each group, for example among the MADders you have TEFfers and the Uncoupled. In metabolic ward studies they have not been able to produce any of these magical phenomenon and thus the possible explanations become more "sciencey" and less testable by the individual. They sound feasible but do we even see it?

Unknown said…
Just to be clear, I was being grossly facetious in that comment and making an indirect reference to another thread where I provoked defensiveness in a visitor of this site when I asserted that plant-based diets--even veganism--may be in closer proximity to a conventionally healthy diet. Instead of provoking that, "Hmm, perhaps a plant-based diet can work for people," thinking, I provoked more of a, "They're freaks out to change our establishment," response. So. . . yeah.
Jane said…
Evelyn, I don't know anyone more muddled than Kruse but he isn't the only one talking about Mg. Here's what Stephan says.

'Magnesium is an essential mineral that's slowly disappearing from the modern diet... Magnesium status is associated with insulin sensitivity... Magnesium supplements largely prevent diabetes in a rat model... In insulin resistant volunteers with low blood magnesium, magnesium supplementation for four months reduced estimated insulin resistance by 43 percent and decreased fasting insulin by 32 percent. ..' http://wholehealthsource.blogspot.co.uk/2010/02/magnesium-and-insulin-sensitivity.html
CarbSane said…
My argument is with the PRECURSOR role. It's been a while since I looked at the studies, but I do recall looking at a litany of studies posted up at PH and none bore that out. Let's look at this more simply. If there' one supplement that is almost universally used it's Mg. Usually if you have a deficiency, fix it, problem solved. Does not seem to occur. So the explanation of that might be that the situation has degenerated past the point of reversal. And yet we have the crash diet, GBP, and early insulin therapy that all have rather impressive track records for reversing your "classic" T2/IR. So this is where I'm coming from on this.

Your last "blurb" -- in IR volunteers with low blood magnesium supps improved IR and fasting insulin. I'm going to bet if I look at the study they had to select from a larger population of IR to assemble the volunteers with low Mg.
Anonymous said…
Hi Everyone,

I’m the serious scientist ☺ who wrote the recent paper in Cell Metabolism some of you are discussing. I’m not a blogger (yet?), or a science writer, or someone’s struggling post-doc. I don’t favor any kind of freaky all-of-this or all-of-that-diet. I’m new to social media and I had never seen a nutrition or dieting blog before 48 hours ago. Wow, there is a whole universe of opinions out there (here)! Seriously, it is fantastic that so many people are thinking about metabolism etc.

Anyway, as a sort of experiment and learning process for myself, I decided I would follow my latest paper as it found its way into the ‘public sphere’. Many scientists are uncomfortable out in public, but I think it is important. So I decided, as a responsible scientist in this new online age, that I would not hide in my ivory tower and I would help people understand the experiments if they were interested (rather than let other people speak on my behalf or just make stuff up). So, you can ask me on Twitter @JimJohnsonSci and I’ll do my best to answer your questions. I figure that if I can teach metabolism and physiology to a class of >700 3rd year students, the whole internet should not be too hard, eh… (this may or may not be the dumbest thing I have done in a while).

I have found a few places, like this, where people are ‘discussing’ the paper but seem not to have a copy of it. Send me an e-mail and I’ll send you the paper. If you have any questions about the data, or our interpretation, you are welcome to ask me (instead of asking someone else who might not have read it or might have a particular agenda). I’m a basic scientist and I have no vested interest in any of the possible actions of insulin, or any of the other hormones or processes I study. I just want to find out how stuff works. In the current paper, we did a pretty straight forward experiment and got a pretty clear result.

I also can tell you what the paper does not address, and that includes different types of diets. We used a standard 58% high fat diet that is known to make mice (at least male mice) hyperinsulinemic. We have not yet tested other meal types, such as a high sugar diet. The paper was the culmination of 7 years and hundreds of thousands of dollars of work, so just doubling the number of experiments by adding another diet groups was not in the cards. I see no reason not to expect that any diet that chronically increases basal insulin, would show the insulin-dependent weight gain.

The press has some interest speculation about meal types, meal sizes and meal timing. There are some good data around these things, but our study does not directly address any of them.

Also, for the ‘mice-are-not-people’ crowd. Yes, I know. However, virtually all the studies on people can only come out with correlations, at best. Insulin and obesity have been correlated since the first radioimmunoassay was done decades ago. If you want to establish a causal role for a gene on a specific physiological function, you have to remove it and find out whether the physiology changes.

Also, with regards to brown fat and white fat browning in people, there is a lot of new stuff (much more not even published yet that I've seen at recent meetings). Probably highly relevant to people.

gernb4 said…
Thanks so much Jim for your willingness to engage in this discussion. I suspect you will gain much in the exchange as well. I wish all scientists could be as giving of their time and expertise.
Jane said…
Very good points. All I can say is that the crash diet, GBP and early insulin therapy are all expected to improve magnesium status, and that supplements of a single nutrient can cause worse imbalances than they cure.
Jane said…
Have you seen what Stephan Guyenet has written about your paper? He isn't very polite, but it's understandable considering the enormous amount of flack he's had to take for years from people convinced insulin causes obesity. Do please read it, and perhaps add to the comments?

'..Observational studies in humans overall have found that elevated insulin levels do not predict future fat gain (8), offering further evidence against the idea that hyperinsulinemia is required for obesity. ...the majority of studies that found an association actually reported that higher insulin predicts less fat gain over time (8). ..'

PS I'm a scientist too, and if my experience is anything to go by you will find the blogosphere very interesting and stimulating. Evelyn's blog is one of the best.
Jane said…
It's spelt flak, not flack, isn't it. I can't count either.
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