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“To kill an error is as good a service as, and sometimes even better than, the establishing of a new truth or fact”
~ Charles Darwin (it's evolutionary baybeee!)

Friday, September 30, 2011

Mitochondria and High Fat Diets

Lots of buzz over mitochondria of late.  So I thought I'd share this find:

High-fat diets cause insulin resistance despite an increase in muscle mitochondria
It has been hypothesized that insulin resistance is mediated by a deficiency of mitochondria in skeletal muscle. In keeping with this hypothesis, high-fat diets that cause insulin resistance have been reported to result in a decrease in muscle mitochondria.    In contrast, we found that feeding rats high-fat diets that cause muscle insulin resistance results in a concomitant gradual increase in muscle mitochondria.
This study used male Wistar rats, a "normal" strain not prone to diabetes, etc.  They were fed ad libitum
  1. Standard chow diet (PicoLab Rodent Diet 20, 5053):  23.5% P/ 11.9% F/ 64.5%C.  (I'll use SC)
  2. High-fat flax seed/olive oil diet:  20% P (casein) / 50% F(2:1 flax:olive oil) / 30% C (2:1:0.5 corn starch:sucrose:bran.  (I'll use HFFO)
  3. High-fat lard/corn oil diet:   23% P (casein) / 50% F (1.8:1 lard:corn) / 27% C (sucrose).  (I'll use HFLC)
The study lasted 4-5 weeks, and although this timeframe was not long enough for a significantly greater increase in body weight for HF's vs. controls:
"... the omental, epididymal, and retroperitoneal fat depots were significantly greater in the high-fat diet-fed groups than in the chow-fed group (7.7 vs. 12.2g). The high-fat diet-fed rats had higher serum FFA levels than the chow-fed animals (756 vs. 249 μM)."
All of the increased fat depots are visceral fat, and I note the NEFA levels tripled for the high fat diets.
In our previous study of the effect of raising FFA on mitochondrial biogenesis in skeletal muscle, we fed rats a high-fat diet and gave them daily injections of heparin to raise serum FFA to high levels ... to mimic the effects of exercise on FFA levels. One purpose of the present study was to determine whether the more modest increase in FFA that results from feeding a high-fat diet also induces an increase in muscle mitochondria.   
They observed an increase in mitochondrial proteins in the muscles of HFFO rats vs. SC at 5 weeks accompanied by a significant increase in palmitic acid oxidation in skeletal muscle (17.8 for HF vs. 10.2 for SC units: nmol/min/g) that is evidence for increased functional mitochondria.  They also observed an increase in mitochondrial DNA.  Feeding HFLC -- e.g. altering the fatty acid content of the diet to 32% lard -- also produced the increases in muscle mitochondria.

Further, the HFFO diet also induced IR (of muscles, as evidenced by reduced muscle glucose transport).  Thus,

Because the high-fat diet-induced increases in mitochondria and in the capacity to oxidize fat occurred during the period in which insulin resistance developed, the muscle insulin resistance is clearly not due to mitochondrial deficiency.
And from the Discussion:

The major findings of the first phase of this study are that feeding rats high-fat diets results in an increase in mitochondria and in the capacity of muscle to oxidize fat concomitant with development of muscle insulin resistance. It has been hypothesized that skeletal muscle insulin resistance is mediated by a mitochondrial deficiency that limits fat oxidation and results in accumulation of intramyocellular lipids. This concept is based on the finding that muscles of insulin-resistant individuals generally contain  30% less mitochondria than those of insulin-sensitive control subjects. This phenomenon has also been referred to as mitochondrial dysfunction, although a detailed evaluation has provided evidence that the remaining mitochondria function normally. The present findings seem incompatible with the concept that muscle insulin resistance is mediated by mitochondrial deficiency. ...
... It is surprising that the mitochondrial deficiency causes insulin resistance concept has been so widely accepted, because it seems untenable in the context of what is known regarding the capacity of skeletal muscle for oxidative metabolism.  The mechanism by which a 30% decrease in muscle mitochondria has been proposed to cause muscle insulin resistance is an impairment in the ability to oxidize fat, resulting in accumulation of intramyocellular lipids. Actually, the rate of substrate oxidation in resting muscle is not determined/limited by mitochondrial oxidative capacity but by the rate of ATP breakdown/ADP formation, which is regulated by the cells’ need for energy.  The energy/substrate requirement of resting muscle cells is determined by ‘‘housekeeping’’ functions ... and is very low relative to the maximal capacity of muscle for substrate oxidation.   Increasing the supply of FFA or glucose to resting muscle can change the relative proportions of these substrates that are oxidized but does not result in an increase in substrate oxidation above that required to supply the energy needed for ATP repletion, regardless of its content of mitochondria.
This seems consistent with what leptin does in obesity which is to stimulate fatty acid oxidation.  Further, obesity is accompanied by an increased delivery of fatty acids to cells, contrary to the "starving cells myth".  The IR measured by reduced glucose uptake in obese and/or diabetic seems wholly consistent with the fact that the cells are forced to burning more fatty acids thus needing/burning less glucose, reducing clearance rate from plasma.  Perhaps the build-up of metabolites from the increased "turnover" w/o an accompanying increase in energy needs results in a bit of inefficiency where fats are not oxidized as cleanly and fully.  The association of IR with ceramides and/or diacylglycerols in cells would be consistent with this theory.

My thoughts on this whole mitochondrial dysfunction -- whatever that may actually be -- is more the result of diet and/or a condition such as diabetes or obesity, rather than the cause.

29 comments:

Kindke said...

Whoa, one of the few times I find myself agreeing with you CarbSane! I too think that mitochondrial dysfunction is an effect, not a cause.

I was convinced of this, in part, by this study..

Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposity.

Quarrel said...

"
The IR measured by reduced glucose uptake in obese and/or diabetic seems wholly consistent with the fact that the cells are forced to burning more fatty acids thus needing/burning less glucose, reducing clearance rate from plasma.
"

Does this imply a pro-LC advantage for people with IR?

Certainly these days I think this is where most of the LC blogosphere rallies around an LC advantage- that it is hugely beneficial in people who have mitochondrial damage.

Of course if the LC is isocaloric, then I'm not sure that even given what you've said that they gain any advantage..


--Q

john said...

Why isn't the data shown for bodyweight, etc? They say the fat depot weight of the high fat rats is more but then reverse the respective numbers when given within parentheses?...then, when they give the FFA levels, the numbers are re-reversed? Are these papers scrutinized at all? ...Remember the diazoxide paper from a few weeks back that apparently couldn't find authors that could add correctly? I have no idea what to make of this garbage because I don't know what they're trying to say or if they're making mistakes. Here's a wild thought too: instead of giving the HFLC rats a new diet that's 27% sucrose, they simply dilute the standard chow by adding lard*? Yesterday I ate coconut milk curry, shrimp, eggs, potato, and cream: is this paper supposed to scare me from repeating that?

*I guess in that case you could also add more micros to make both diets equal in terms of micros per calorie.

I don't want to be the new anti-Carbsane troll, but c'mon--you cannot so often criticize others' evidence and not see the flaws in this. Of course a 27% sucrose, 32% lard, 18% corn oil diet will lead to more skeletal muscle insulin resistance than a diet of 13% fat. This paper simply provides evidence against the idea that more skeletal muscle mitochondria is better regardless of diet (and that's not even necessarily true considering my above mention of their weird/suspicious way of giving the data). Anyway, I'm not certain of this, but I think obese humans have fewer skeletal muscle mitochondria than lean, and mitochondrial density is inversely associated with insulin resistance. So again, you may be generalizing too much from this study.

Kurt G. Harris MD said...

@John

I don't read here that Evelyn is trying to tell you what to eat.

She is merely discussing evidence that supports the idea that the mitochondrial dysfunction is an EFFECT of energy imbalance and not an an upstream cause of obesity or carbohydrate sensitivity or whatever...

john said...

Kurt, I don't know where this 180-degree sycophantic behavior towards Evelyn came from, but she isn't supporting what you [both] say. Where is the "EFFECT"? The high fat rats get fat* and IR, but there is no mitochondrial dysfunction as they define it.

This is why I said what I did about Carbsane on WHS: this post is not even entirely coherent, and yet she constantly pokes fun at others. Show me the Massas' mitochondrial dysfunction if it a result of "energy imbalance" itself, and I would gain interest in this idea.

*Apparently--I'm skeptical of this because of the oddity I mentioned in my original comment. I normally would pass it off as simply strange, but I've seen an error in two papers (diazoxide and another posted in someone's WHS comment) in the last month.

Kurt G. Harris MD said...

@John


As if you are not kissing asses of your own with your lame behavior trying to rescue the carbohydrate hypothesis .

I agree with whomever I choose to when I think they are right rather than clinging to stupid dogma, so piss off for your name-calling.

So let me re-phrase that then.

You have a comprehension problem.

You asked if you should change the way you eat, and I pointed out that she did not say a damned thing, nor any did quotes from the paper, about the advisability of your particular diet.

Maybe you can quote the part where she spoke about your coconut milk and shrimp intake because I missed it.

You said:

"Where is the "EFFECT"? The high fat rats get fat* and IR, but there is no mitochondrial dysfunction as they define it.

That is precisely the point! It cannot be a CAUSE of pre-diabetes and IR if it has not occurred (yet). If it is observed later it may therefore be an effect, but it can't be a cause in this model.

"The present findings seem incompatible with the concept that muscle insulin resistance is mediated by mitochondrial deficiency. ..."

That is the message of the paper's discussion. Where is the part about avoiding fat consumption in Evelyn's discussion?

Are you confused because they manipulated FFA levels high to mimic the state of cellular overnutrition? That was the point, to see if forcing the prediabetic state, to the point of insulin resistance, was CAUSED by diminished mitochondrial function due to decreased mitochondrial number. It was not.

Get it?

Read it again as I am not going to parse it for you.

Evelyn aka CarbSane said...

@john: You find an insignificant typo in a table in a paper and this raises serious problems for you about all researchers? C'mon man! The typo doesn't even cast doubt on the study it was in, let alone all research. Here you're dismissing a study because the exact body weights weren't reported. Does that make a difference? The body weight differences were not significant, so no.

You seem to have missed the point of this study which was not what produced IR but that it was not accompanied by mitochondrial dysfunction. Therefore in the chicken-egg debate, this study demonstrated that IR is not likely caused by mitochondrial dysfunction, and wasn't in this specific study.

You say some ridiculous things like: " instead of giving the HFLC rats a new diet that's 27% sucrose, they simply dilute the standard chow by adding lard*?" Umm because (a) that would dilute out protein and (b) rats tend not to eat high fat diets that are sucrose free. Nonetheless, the sugar may have induced IR but not at the expense of the mitochondria, that's the point.

Regarding WHS conversations: As you can see, I run a rather active blog here. Yet I still do like to read others' and will comment when there's something important enough to me. I felt this BS about body fat coming from sugars and not dietary fat was important enough. But when comments get long I'm not going to go woo on Stephan's blog -- not to mention how limiting formatting is on comments. Which is why I just turned one intended comment into a blog post when it started to grow in length. I bowed out of our exchange over there as "not productive" because in one comment you contradicted yourself. First you said this wasn't about what random whack job commenters say (when I was addressing their comments on same blog post) it's about what the well known experts say, and then you say you don't care what one well known expert says, it's about anecdotes from commenters.

I can spot a dead horse in comments much sooner these days. I choose to bow out when it starts smelling.

john said...

Kurt and Evelyn,

Okay, sorry, I shouldn't have name-called, but give me a break Kurt, you've spent a long time going out of your way to insult Evelyn. Anyway, when have I ever said anything positive about the carbohydrate hypothesis, Taubes, Eades, etc?...I've never been a part of that, and that kind of accusation is what causes me to throw in name-calling: you put words in my mouth, then laugh at me because of them, despite not existing. I've said a few times over the last few years what I think about carbs vs fat, and that if I had to guess, carb restriction is preferable over fat. The only thing I've been criticizing lately is evidence against the insulin hypothesis, and I don't care which side ends up being correct; I follow people's writings and agree/disagree according to argument.

john said...

I still contend the study here doesn't provide evidence that energy imbalance per se causes mitochondrial dysfunction. It does provide evidence that it's not [always] mitochondrial dysfunction that causes obesity and/or IR though. Otherwise, like I said, we should see the mdysfunction in the Massas' (we may, but I'd want to see). Providing evidence against one idea doesn't make the other idea more right, and you both know that.

Kurt, I don't know why you're stuck on my quote about my diet--whatever, it wasn't important. Carbsane generally has an anti-low carb sentiment, though I'm not sure she actually has a problem with low carb per se.

john said...

Evelyn, I don't have a problem with all researchers, but it did jump out at me. My first thought was that they incorrectly said the high fat rats had more fat, not that they just reversed the respective fat depot weights. To make it stranger though, they re-reversed the numbers in the very next set of parentheses, following no pattern of respective, opposite-of-respective, or higher-number-first...so yea, when the data then isn't available, I get suspicious/skeptical.

I see you posted again--I'll read it later. Sorry for 3 comments in a row.

Evelyn aka CarbSane said...

Hi john: Two things ...
1. You might want to consider a more recognizable ID. Jack Kruse has posted as lower case j john various places, there's an uppercase J John that commented here and elsewhere and no-doubt many others. So it gets difficult to follow. I try to know who I'm talking to here, but even that is time consuming and I've mixed folks up.

2. Regarding: I still contend the study here doesn't provide evidence that energy imbalance per se causes mitochondrial dysfunction. Who said it did? This study had nothing to do with that! It showed no mitochondrial dysfunction related to IR or the increased fat accumulation. I don't get your poing.

No problem for several comments ;)
I don't think the weight/fat accumulation was a factor here. They were rather more meticulous in detailing the various things they measured for IR and mitochondrial function. So I don't see reason to be suspicious.

Kurt G. Harris MD said...

@John

'Okay, sorry, I shouldn't have name-called, but give me a break Kurt, you've spent a long time going out of your way to insult Evelyn."

Yes, I hope you found our mutual antipathy entertaining. But we have set that aside now in the interest of discussing science.

"Anyway, when have I ever said anything positive about the carbohydrate hypothesis, Taubes, Eades, etc?...I've never been a part of that, and that kind of accusation is what causes me to throw in name-calling: you put words in my mouth, then laugh at me because of them, despite not existing."

On WHS you responded to my post answering a query from Rick with the following:

"

"What?!?! You're basically implying that hormones/proteins/etc regulate only appetite, not metabolic rate and/or macronutrient fate. So a forcefeed experiment of coconut oil vs cake [added to normal diet] would show no difference? "


So you address me for the first time with a lead-in with a passive aggressive mock incredulity (?!?!) that implies I said something outrageous or stupid, then you PUT WORDS INTO MY MOUTH that I did not say.

And nowhere in your unbidden response to me do you say what YOU actually think.

And your only nutrition blog listed in your profile is Hyperlipid, written by Peter, who describes himself as "hopelessly biased" towards the CIH.

And then I notice that in addition to implying that I might be stupid/crazy in my response to Rick, you are nitpicking with/ insulting Evelyn.

And you seem annoyed that Evelyn and I are no longer flinging insults at each other.

So you can see how I might think you are in the CIH camp, right?

If you insist on being critical at the same time that you are cryptic about your own beliefs, you can't blame us for trying to figure it out for ourselves.

I look forward to you telling us what YOUR ideas are.

john said...

Carbsane,

I've thought about adding my last name, but I have a picture too, so I don't know. You and Kurt suggested mdys is an effect of obesity/energy imbalance.

Well it would be important data if they weren't getting fat, because then it wouldn't counter the mitochondria idea. I'll wait it out and see.

john said...

Kurt,

Geez, relax man...I said that shocked quote in response to your point about foods and excess calories. If by excess calories you mean above normal intake, then I disagree because there are plenty of studies of diet alterations that change metabolic rate; if you meant excess calories as calories stored as fat, then I guess there's no problem, but then the quote was obvious and redundant. I have a slight problem with looking at the American 400 calorie increase or whatever and basing an obesity theory solely from that (as in, "Why are we eating more?") because calorie intake itself doesn't necessarily lead to increased weight. Also, the extra caloric intake in the past 100 years doesn't necessarily have to be mostly from fat people eating more; it's possible that tall people, for example, are more responsible.

I don't have a problem with anyone, and I don't enjoy reading others' insults either. It bothers me when anti-low carbers make condescending remarks about an unrelated carb/insulin point towards anyone who defends any part of the carb/insulin hypothesis.

I have Hyperlipid and a couple math/physics blogs as public; I use to have a long list, but I chose only a few because I guess they probably best represent what I follow--in case anyone cared to look. I appreciate Peter's tone because he doesn't make storming declarations. That's also why I like Stephan.

I don't really have any innovative nutrition ideas. I think Lucas Tarfur makes good arguments for carb restriction, and I think there is good evidence for intermittent fasting. I don't know if many of the fly/worm life extension interventions can be generalized to humans, but I like to read about that too.

john said...

...Oh, and yes, I tend to agree with Peter and the insulin hypothesis. But, I also think food reward is interesting--"palatability" too. I know I can eat many more eggs for example with hot sauce than without, and the rat study with Ensure is good support too. As for the condescending and sarcastic nature of your comment toward my ideas, do you think you are some dietary revolutionary?...because I'm pretty sure your ideas have relied heavily on Stephan and Peter as well.

Evelyn aka CarbSane said...

Hi john: I'm not sure how it works on other blogs/software, but on Blogger you can change your ID and/or add or delete a pic and it doesn't change retroactively. So that folks see a pic makes one have to go look at the profile and such. My old posts before I "came out" still bear just CarbSane name and a cartoon bunny-eared avatar. Before that I was "Me" ... so this is how it can get confusing. No problems here now that I realize who you are, but just an FYI on that front.

From your comments to Kurt it seems you're entrenched in the either/or competition between what I call TWICHOO and food reward. I'm of the let each stand on their own merits, and the former is untenable except in cases of true metabolic defect (e.g. hypothalamic obesity, insulinoma and such). The latter makes sense as A dominant factor -- many seem to equate dominant with sole factor or the ultimate majority factor. I've said before, and I'll say it again, one dominant factor can coexist with another one or even several. For example any number of players can be dominant factors for the success of their teams in the NCAA, NFL, MLB, NBA, whatever.

john said...

Evelyn,

I don't think there is just one factor either. I acknowledge that people will eat more calories of certain foods. Whether that's "reward" or palatability, I don't know--probably both? But, I also know that certain diets allow one to eat more calories and allow for overeating without fat gain. I know you usually argue against that idea, but it seems pretty clear when we're talking about ketogenic diets or "fat free" diets. What happens when you move from 1% carb to 5% to 10% to 20%? (or same with fat)...it's not as clear.

cwaiand said...

hey john;
can you provide me with some proof(as in scientific)of these diets that allow overeating and eating more calories?i assume you mean eating beyond caloric requirement?or do you mean eating to maintanence requirement while eating a diiferent type of diet?

cj

Frank said...

Hi John

Reducing carbs has not been shown to affect BMR, at least in obese women (only study that I can remember quickly for now).

If reducing carbs or fat would have an effect on metabolism, carbs would have a slight advantage as

a) they have a higher TEF
b) converting carbs to fat is more ''energy-expensive'' from a metabolic standpoint.

What diet should make it possible for someone to overeat (ie, consome more than he expend) and, in the long term, not put on weight? There could be a compensatorial mechanism short/middle in some individual (those ''fast'' metabolism) with an increase in BMR to compensate for the overeating, but they are clearly not the majority of the population.

Other than that, I don't see by which mechanism (and yes, I've read Feinman rethoric about the 2nd law of thermo) - but it does not happen when it is tested in controlled setting, on a hypocaloric diet where you play around with fat and carbs.

What I have been told very often now is that there might not be a difference when it comes to weight loss, but there is one when it comes to fat gain, hence we would need an overfeeding study with a ketogenic diet as baseline, and then we would see the magic. But what's the point with that? People want the best way to lose weight, not the best way to overeat without gaining weight. Calorie restriction is clearly showing us that overeating, whatever macro it is, is a bad thing in regard to longevity.

So, we know that

1) Carbs have a higher TEF
2) They are less likely and less efficiently (read, more energy-costing) to be store as fat than dietary fat
3) under iso-hypocaloric and isoproteic diet, playing around with carbs and fat brings the same weight loss.

So the only thing we don't have a study out for and that people keep fighting for is that overeating fat on a keto diet would not result in fat gain. Should I be thrilled about that?

john said...

cwaiand and Frank,

For diets that require more calories to maintain weight, check ketogenic diet puts mice in "unique metabolic state" or diets looking at EFA deficiency or one of the many experimenting with coconut oil. For an example of added fat [to a mixed diet] causing less weight gain, check Jaminet's recent thyroid series. You both seem to be forgetting that I'm saying context matters. It is 100% true that in specific contexts, certain foods/nutrients lead to less weight/fat gain. I never made an overarching absolute statement about one macronutrient or one macronutrient ratio--it's not always fat; it's not always carbs.

I don't eat rock-bottom carbs and don't go around preaching others to do so. If you want my guess then yes, I would bet that on heavy keto, fat forcefeeds would lead to less weight gain than fat or carbs added to mixed. Whether it's UCPs, D2R agonism, or whatever, I'm not sure--a lot changes on extreme diets.

cwaiand said...

john;
my guess is your guess would be wrong.i guess all your guessing is not helpig ayone learn anything,i guess.

cj

Evelyn aka CarbSane said...

Oh quitcherguessing cj! LOL

@John, I understand your point about context, but here's the rub: You don't have to guess, most of the studies have been done. The diets used in Grey & Kipnis (search on that here) were essentially ZC vs. ZF -- can't get much more extreme than that.

I'll be posting today where a high fat diet in rats lowered energy expenditure. Even Feinman relies on replacing carb with equal amounts fat and protein -- because the average TEF will exceed that of carbs -- but this is not what is advocated in LC circles. By their own logic, a 1:1 swap of carbs for fat would favor the carbs. Oh ... you'll be interested in this one, there's a fundamental math error in the Feinman and Fine paper.

john said...

cwaiand, well the world is safe because I don't have a blog with a list of all my guesses.

Carb,

The G & K study with which I'm familiar used 0 & 0 only for hypocaloric. From the abstracts I've seen, very low calories diets usually cause more weight loss with carbs/sucrose...? Anyway, food choices seem to be just as important as macros, so...

Look guys, I have no reason to push any specific idea--I'm just a commenter around here trying to learn what I can for personal use; obesity talk is pretty unuseful to me actually. I wrote my original comment as a skeptic of mdys being a result of energy imbalance itself, as well as in part due to Kurt's comment on WHS, which I now feel was overly aggressive (both of ours). I have nothing against him and almost always agree.

Overall, neither the argument for nor against the insulin hypothesis is airtight, but I lean toward it, with Strontium pup making some good recent points. Let's not rehash the discussion here, for we are all already aware of the research.

Tonus said...

I think it's good having people who disagree or at least challenge some of the info here; it helps prevent it from becoming an echo chamber, which is what I think is harming many of the LC sites.

I just don't like the swarm of people whose challenges amount to "I disagree, what are you gonna do about it?" Reading the comment section in Stephan's latest blog post gave me a headache. Something like 2/3 of the comments were from people who either misunderstood or simply disregarded Stephan's definition of Food Reward in order to present their anecdotal, N=1 story and demand that Stephan address it, lest it completely derail his hypothesis.

(And a few of the other comments were from people wondering aloud if it's worth it to test his hypothesis at all. Errr... did any of them read the first paragraph? Do any of them understand how science and understanding of the world around us progress? You often learn more from the stuff you wind up disproving. It's mind-boggling, really.)

Evelyn aka CarbSane said...

On the one hand I'm happy about what happened at AHS because it has really moved discussions forward. On the other hand, I'm frustrated by the choosing sides nonsense as if the concepts of reward and insulin/fat trapping are somehow competing hypotheses in all of this. Taubes seems to have won that whole "framing the debate" issue to large extent, at least with the masses. But I think more are coming around.

Kurt G. Harris MD said...

@John

"As for the condescending and sarcastic nature of your comment toward my ideas, do you think you are some dietary revolutionary?"

You came on like a Mack truck the first time you addressed me with your faux-shock cryptic comments. Now I see you are staying true to form.

I acknowledge all my sources and have never done otherwise.

As far as being a revolutionary, I would venture that I've helped a lot more people achieve health with my blog than you have done so far in your internet career limited to being an unoriginal internet harpie - sorry, "skeptic"...

Tonus said:

"I just don't like the swarm of people whose challenges amount to "I disagree, what are you gonna do about it?"

This I agree with.

Kurt G. Harris MD said...

@Evelyn

"I'm frustrated by the choosing sides nonsense as if the concepts of reward and insulin/fat trapping are somehow competing hypotheses in all of this. Taubes seems to have won that whole "framing the debate" issue to large extent, at least with the masses."

I agree and this basically happened by accident. Taubes famously objected to Stephan's FRH talk, and this released SG from any conjunctions he may have had about dealing with the CIH. So the temporal linkage of Taubes challenge to FRH with Stephan's deconstruction of the CIH reinforced Taubes' claim that they were alternative hypotheses. But they are not.

Kurt G. Harris MD said...

compunctions, not conjunctions....

Evelyn aka CarbSane said...

Oh ... I don't think it was by accident. It was by design by Taubes. This is part of his modus operandi and something Stephan tried to nip in the bud with his (now deleted) "framing the debate" post. Folks need to realize that scientists like Stephan, especially those starting out in their careers, have far less leeway to express themselves in this sort of debate. Meanwhile, if it sells books and/or brings notoriety/publicity to his employers, anything Taubes does is fine by them.

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