Stick a Toothpick in It? Taubes' 4-pronged Carb/Insulin "Fork" Loses its Tines
This post updated slightly 6/22/2012. Original publication date 1/23/11
In the comments at Jimmy's blog on my interview podcast, several comments either directly or by inference say I failed to make my case against Taubes. Well, I think I did pretty much get to what I consider the four prongs of Taubes carb/insulin hypothesis, but I've decided to try and summarize this in a blog post. Another common comment is that I'm somehow nit-picking at minutia, basically if folks lose weight on low carb, it doesn't matter the details of why. To those, if they are reading this, I would say that any objective view of my arguments would lead to the conclusion that these are NOT minor details, they are the sum total of Taubes' evidence in support of his hypothesis. Not only has he NEVER debunked the calorie-based theories on obesity, but almost all evidence in support of his "alternate" theory HAS been.
I will not be referencing this post, it's all been done before here, and I don't have the time to trace down every link etc.
So, what do the four prongs of the fork stuck in the potato above represent?
1. Carbohydrates stimulate insulin which stimulates fat storage and/or traps fats in our fat cells so fat accumulates.
2. Carbohydrates are converted to fats that accumulate in our fat cells.
3. Carbohydrates stimulate insulin leading to hyperinsulinemia, eventually leading to insulin resistance starting in muscles and only far down the line reaching the fat cells.
4. Carbohydrates provide the backbone molecule, glycerol 3 phosphate, for the process by which fats are "fixed" or "trapped" in the fat cells. Therefore the more carbs, the more G3P, the more fat accumulates. We can't accumulate much if any fat without carbs.
Taken somewhat out of context, the first prong of Taubes' theories is the only one remaining intact. It is correct that insulin stimulates esterification (deposition) and suppresses lipolysis (release), thus where fat cells are concerned, insulin's net action favors fat accumulation. The problem with this is that Taubes focuses on immediate actions and not what occurs over the course of 24 hours. Further, this simplified theory ignores a major player in post-prandial esterification, ASP, and fails to explain why insulinogenic proteins do not promote fattening. So, we'll return to this at the conclusion of this post.
As to the rest?
The whole excess carbs turned to fat promote fattening is simply not true for humans. The amount of lipid synthesized from carb-derived acetyl CoA is on the order of single digit grams, even when stimulated or magnified several-fold. Granted this is something Taubes does not focus on too much in GCBC, and he did scale back on this through the years in his lectures, it was nonetheless an additional means by which Taubes pegs the carbohydrate as fattening. (And, in my opinion it was one of the more harmful of the theories in getting good scientific arguments started vis a vis weight gain because it has been picked up and perpetuated by "primal" voices and other pseudoscientific messengers in the name of science.)
The only carbohydrate implicated in the development of insulin resistance is fructose, the only one that does not stimulate insulin. Furthermore, transient peripheral insulin resistance is also attributed to dietary fat intake, again, the macro that does not elicit an acute insulin response. There is no evidence that I've seen implicating carbohydrate induced insulin "spiking" leading to insulin resistance, peripheral or of the fat cells. If anything, carbs improve insulin sensitivity. Hyperinsulinemia - genetic conditions, disease or injury aside - does not result from postprandial secretions of insulin, but rather by chronic stimulation most probably by the direct action of NEFA on the pancreas. The half-life of insulin alone, which is around 5 minutes, argues against the possibility that dietary carb can lead to chronically elevated insulin. Lastly, as I've blogged on repeatedly, it has been pretty well established that it is elevated NEFA and/or accumulation of lipid (or concurrent build up of intermediates such as diacylglycerols and ceramides) in ectopic (non-adipose) tissue cells that causes chronic IR. Furthermore, the elevated NEFA are the result of the loss of insulin sensitivity of larger (filled) fat cells indicating that the condition initiates in the fat and progresses outward, not the other way around.
Lastly, I've spent enough time on this blog on the whole G3P issue so I won't repeat it further. Suffice it to say that there is not now, nor has there ever been, any evidence to support this theory. G3P is not rate-limiting. What controls the esterification rate seems to be, in the end, the levels of lipids in circulation. Oil and water don't mix so when levels get too high, things are set in motion to clear the fats from the bloodstream, and the primary facilitator of this, particularly dietary fat, appears by all indications to be ASP.
Left with just the first prong, Taubes is having a rough time of it explaining away such things as the Japanese. He's trying to fall back on glycemic index arguments on that topic (and misrepresenting their diet), but that gets him in trouble when trying to explain why nuts and cheese are common "agents of stalling" on low carb diets. No, nuts and cheese must somehow be unusually insulinogenic. He might want to get with Dr. William "Butter is fattening because it provokes an insulin response" Davis on that one. And now going totally into calorie denial about 50% of the time, he has to resort to trying to convince people that all diets work when they do because they restrict carbohydrates. I'm not getting why so many are falling for that one, especially since the totality of the Shai study results negate the argument, but I digress...
So ... If you break three tines off of a 4-tined fork, what are you left with? A toothpick. Listening to and reading GT's recent interviews one can see how ineffective this one remaining theory is in explaining the evidence ... much as a toothpick is an inefficient tool for eating.
It is, however, perfect for cherry picking! {evil grin}
CHEERS!!
Comments
Nonetheless your statement "Not only has he NEVER debunked the calorie-based theories on obesity, but almost all evidence in support of his "alternate" theory HAS been." again shows me that you mix two things together that are not related: The "biochemistry/insulin/g3p/etc." issue and the "overeating/1st-law/cause-and-effect/etc." issue.
@Jeremy: What page is that on? I don't recall reading that version on the 600 calories. If he did say that in absolute terms that would be wrong from everything I've read. Also, keep in mind, where Taubes' position is concerned he's implicating DNL as one route for increasing fat mass, and that is not the case except in massive overfeeding.
@Christian, I'll address the last statement when I get around to responding to the other comment. As to Taubes' retraction on G3P, I'll take perhaps a little credit for his finally doing so in interviews. But its a prong of his theory that should have never been propagated to begin with by his own references!!!!!!!!!!. He still hedged his retraction in the Jimmy interview, and went a bit further in another interview. The man needs to use his blog - an avenue of communication he lamented not having in the JM interview - to set the record straight on this, in print. Ideally he would explain why he misrepresented the whole issue as it was presented in Newsholme & Start, the 2003 Reshef paper and countless other works from Hanson's group. My description of this as a broken tine is not altered by the fact that Taubes has now admitted it. An major issue I have with his work is that it should never been part of the discussion to begin with.
You are a marvel!
You have provided the most pertinent fact about insulin: it has a half-life of FIVE MINUTES.
The pancreas' pulsatile secretions are as result of blood glucose or aminos, and there is clearly a quick feedback. Hyperglycemia resulting from a failure to store glucose in the glycogen stores of liver or muscle results in in BGs higher than the level desired by the brain and the pancreas responds!
It is to my intellectual shame I was never aware of this. I have had enough experience in researching stimulus response effects in pharmacodynamics to understand the singular importance of half-life in dynamic modelling and yet I failed to enquire about it in the case of insulin.
Jeremy
It is generally acknowledged that absent high performance athletes, that over the course of a day, a human body, utilises 80-90% fat fuel vs 20-10% glycogen/glucose. The oxidative content of either fuel depends on the oxidation demand one places on one's body and whether it can respond.
I am like you in that I do not believe the hype.I have been low carbing decades when even Atkins was unheard of though he did already write his first book.The first low carb book I found did not mention induction flu and so every time I tried it I would feel sick by day 3 and gave up not knowing that if you cut carbs you need to flush them out of your system for the body to switch to ketosis.
Lately I have been saying that we went wrong in the low carb world when someone stated that it must be a high fat diet.This went against my common sense but I fell for it and Atkins never worked for me again.Lately I am doing a low carb diet in that I eat meat and leaner meats when I want to be leaner...so simple but lost in the "gotta get the fat higher mindset".
There are days I eat 700cal and days I eat around 1500 and some 2500.I do not count and just eat some meat when ever I am hungry.
As for carbs,I use BBQ chicken,fried chicken,fried chciken cutlets etc at times.Most times I eat a huge salad with some grilled chicken when I wanna get leaner.I also subscribe to eating whatever I want once a week and find it keeps me sane while adding a bit of fat back on.Like you pointed out in an older post its what you do as a percentage and not the one huge splurge that accounts for what we weigh.I also at times eat a bagel or whatever when I feel really down and depleted.
This is working brilliantly for me I must say.Face is lean,muscular and just have a belly to lose.This is where the dieting even when low carb comes into play.I eat less calorie meals by substituting fatty meats for lean.
Here is a link to a video from the BBC that did a study on why the Atkins diet works yet your allow to eat all the high calorie foods you want....hint...the Atkins dieters eat less calories.Its in 5 parts but was what opened my eyes to the idea that maybe it is all calories.
That said when I eat same amount of food with carbs I look like my skin breaks down as in aging.Everyone is of course different and for me,I believe,its my hyperinsulemia.
http://www.youtube.com/watch?v=2d_wxJageqw&feature=related
Would you agree that to boil this all down simplistically for the layman, given that it's the protein that accounts for the success of the Atkins (or other "low carb" diets) because it results in overall lower calorie consumption, one of two things is really the problem:
1. Fat in the diet can result in overconsumption of carbohydrate when they are present together in foods (as in the experiment mentioned)
2. Sugars in the diet can result in overconsumption of both carbohydrate and fat (think ice cream, or sweetened beverages, i.e. passive overconsumption)
I don't see a whole lot of evidence that whole grain carbohydrates will cause weight gain because fiber acts to increase satiety.
In other words, biochemistry aside, the main issue with weight control is appetite control. Right?
@Wolfstriked - I think this is one of, if not the major, reason plateaus, stalls, or weight regain is so prevalent in the LC community. Of course every other "diet" plan's maintenance rates are deplorable, but of all the macros to make the center stone of one's diet, why on earth would you make it the most calorie dense one?
I fell for it, and I see so many others struggle with the same problem. It's as if after saturated fat was demonized by the health community, Atkins had to come to its rescue.
What I don't understand is why Atkins didn't advocate a high protein, med fat, low carb diet? Did he believe that fat was the most satiating macro or something?
Don't get me wrong, I like fat and don't fear eating it; however, as Wolfstriked said, if you're trying to lose "fat", common sense should dictate that maybe "fat" shouldn't be the cornerstone of your plan.
so it's not insulin resistance in the liver the first step but in the adipocyte?
I think you nailed it with the quote that Muata cited, and it all boils down to that we won't NET burn fat from body stores if we keep adding a ton of it from the diet.
Muata, I think that the whole "high protein" is bad for the kidneys and such stigmas led to LC advocates steering away from characterizing such diets that way. But originally Atkins described his diet as "high calorie" and NOT high fat. In his 1972 book (of which I got a new copy of but have since misplaced), there's nothing in there about being sure to select the fattiest cuts of meat or avoiding low fat. Seems to me that it was quite possibly the Kim Kins fraud that caused the over-reaction to this form of the diet. I've always been puzzled by folks who dip a leaner cut of steak in butter, fry two eggs in two tablespoons of butter, or add more fat to skin-on fried chicken because it is notoriously low fat. In the recipes in that book his serving sizes for dressings were 1-2T, he used like 1/2T butter to fry a 3-egg omelet, etc. This whole "eat more fat" advice truly baffled me to where I really wonder if I would have lost the weight at all had I followed such advice.
Just because sat fat is not the devil doesn't mean we should consume 75+g of it in a sitting. It is not healthy to have our blood swimming with lipids under any circumstance!!
I'm thinking that muscular IR is more to do with activity (or the lack of it!) than diet.
@Muata,I think Atkins did start out calling his diet a high protein diet.He didn't really know why his diet worked so when he was attacked with the kidney issues he started to tweak it.Then Kwasnieski came around with the fact that a low carb diet should be very high fat.I'm not sure but I think that this may of been when Atkins started promoting higher fat(not even sure if he did though).I tried to believe in the Optimal diet as it made a ton of sense but every time my hunger was thru the roof from cutting protein and the high fat seemed to go right to my love handles.I felt great but I would be ravenous at night and drinking cream does nothing but add belly fat.Muata I also feel that fat should not be front and center and have a saying that protein is "the missing link".It went from high carb to high fat and now maybe the truth is high protein.
@CarbSane thanks for the welcome and yes I was a Livin La Vida blog visitor and still am.Is that where I heard CarbSane before. lol .
I wanna point out something I feel you may agree with and it is about the standard calories we as humans should eat.People tell me all the time"just eat 2500cal and exercise" as a standard male response while females get the "never go below 1200cal" tip.Yet the only time in my life I had abs was before hitting 15yrs old and again at around 25.I went down to 900cals to achieve them and here I am at 40 wondering if I should eat 2500cal.I think that obese people just have %#$&#% up metabolisms and just require less food.This is where I agree with you that when your thin its not time to go bananas and start eating like crazy again.You have to eat less for life but you can go out and splurge though.I do every saturday.I also use the high glycogen in my muscles to have an outstanding full body workout.The post workout meal is very high in protein and I still find myself hungry a little bit later where I take another large protein meal.Other than that I eat meat to hunger with a little carb for flavor.
James Kreiger had a depressing article on regain a while back: http://weightology.net/weightologyweekly/?page_id=415
In a nut shell my body at a reduced weight of XX burns less than it would have had I weighed XX all along. Since I've now been roughly this same weight (slightly less) for over two years now, it seems my metabolism is coming back a bit. I don't count calories but it seems I'm able to get away with a bit more (maybe 1-200 cal/day) w/o gaining. Of course this is not controlled because I've also added back in a few more carbs on a regular basis and do purposely "move more" albeit not with formal exercise.
I think that don't go <1200 thing is a farce and probably why "women of a certain age" seemingly *can't lose weight*. I maintain in the 1600-ish range but keep in mind that although I'm not large, I still weigh close to 200 lbs. All of those tables say I should be able to eat 3000 calories. Ha ha hahaha!!
Perhaps since I haven't been VLC'ing for a while, a stint might produce some results again, perhaps combined with IF so I could sustain like 800 cal/day for a stint. We'll see. Thanks so much for your input. I linked to that special. I'm surprised nobody ever mentioned it before .... well, actually not b/c it fries the proverbial golden goose (with skin and slathered in mayo of course ;) )
Insulin Degrading Enzyme deals with proteins involved in the pathogenesis of Alzheimer's. One theory is that when insulin is constantly high, IDE has it's hands full with degrading insulin and therefore cannot properly break down these AD-related proteins. Do you happen to know if IDE has more 'break down jobs'? What I try to say is that some unfavorable condition ('MetabolicSyndrome') may put a very high burden on IDE (and other enyzmes?), with chronically elevated insulin as one result.
I have to read more of your posts about it. I read Taubes/Frayn. So too many insulin spikes don't lead to insulin resistance. What doctors/media says it's wrong then.
http://www.drbriffa.com/2010/08/06/high-starch-diets-associated-with-increased-risk-of-type-2-diabetes/
What causes diabetes then? Sorry if my question is silly, like I've been asleep during the lesson.
If it's the NEFAs what can we do about it and how can it be diagnosed in its first stages?
Are you sure about this ? I think this statement is completely false. Have you heard of the upregulation and downregulation of receptors ? Different tissues downregulate their insulin receptors at different rates.
I think it is inconceivable that your comment is true.
http://en.wikipedia.org/wiki/Downregulation_and_upregulation
When I had an insulin stress test on my pituitary gland in 2005, I was injected with 10 units of fast-acting insulin. This did its funky stuff for several hours (by which time my BG had fallen to 1.5mmol/L or 27mg/dL).
@lightcan. Association does not prove causation. A high-starch, high-calorie diet in active people (e.g Kitavans & Okinawans) is fine. In sedentary people, it can cause obesity. Obesity increases the risk factor for type 2 diabetes.
Fructose barges its way into the liver, as Glu-T5 is insulin-independent. Once liver glycogen stores are full (resulting in insulin resistance), the liver disposes of further fructose intake by lipogenesis (eventually resulting in home-made liver paté).
There is no down-regulation of Glu-T2. Also, fructokinase has a much higher affinity for fructose than hexokinase has for glucose.
I'm not trying to say Dr. Briffa is right. I'm saying exactly the opposite that generally we're told that excessive insulin over time leads to insulin resistance. I gave that reference for his reasoning/interpretation not for the study as such. Stephan Guyenet talks about the Kitavans a lot so I have heard about them. You don't need to tell me that association does not prove causation. But thanks anyway. Some people think that obesity is only related to T2, not a cause and that it is protective up to a certain point. I don't want to argue with you as I don't have the knowledge or the studies at the tip of my finger. I'm just trying to figure it out. OK? The fact that I'm posting here shows that I'm questioning my position and that I'm open to change.
Carbsane
You might like this if you haven't seen it.
http://high-fat-nutrition.blogspot.com/search/label/Weight%20loss%20when%20it%27s%20hard%201.
@Nostril Damus: Welcome to the Asylum! Yes, I've heard of up and down regulation of receptors. Your point? Once someone develops IR and/or hyperinsulinemia then postprandial insulin spikes from carbs can exacerbate the problem, but they are not the cause. Taubes actually discusses one study demonstrating that carbohydrates improve insulin sensitivity of fat cells. He does this in the context of further evidence that carbs are fattening, but if this is the case, it would actually be something we want. We do not want insulin resistant fat cells, that's at the root of it all where chronic IR/Metabolic Syndrome/T2 is concerned.
Just a comment to Nigel: The half life of injected insulin is much higher than endogenouse insulin. Insulin aspart(rapid) has a half life of 81 minutes, regular 141 minutes and detemir (basal) 5-7 hours,
Yeah, I think Briffa is simply wrong with this statement: "This situation is described as ‘insulin resistance’, and the more insulin one secretes over the course of one’s life, the more likely one is to become insulin resistant. " I would have to take a look at those studies, but my gut is that they simply CAN'T control for other dietary factors, type of starch, etc. I also note that sugar consumption showed NO association, in direct opposition to fructose's known effect on insulin sensitivity in acute excesses.
Here's part of an email I sent to Krieger last month:
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In "Why Is It So Easy To Regain Weight?" you explain that the Leibel study demonstrates a sustained decrease in NEAT (and to a lesser extent REE) following weight loss. It occurs to me, however, that this study is potentially subject to a fairly severe selection bias. Because the RMR & NEAT numbers for the weight loss subjects are measured only post-diet, it doesn't rule out the possibility that the differentials in RMR & NEAT preceded the weight loss.
In other words, this study is consistent with the hypothesis that it was the low NEAT (and/or low REE) that caused those individuals to gain the excess weight in the first place, and that the lower levels measured post weight loss are just reflecting those initially lower levels, and were not caused by the weight loss itself.
The Wake Forest study you discuss in "Physical Activity and Weight Regain" lends at least some support to this hypothesis. In that study, which included both pre and post weight loss measurements, there was no measured decrease in RMR relative to lean body mass. This suggests that the decreased REE measured in the Leibel study could very well be a result of selection bias.
The Wake Forest study did measure a lean body mass adjusted decrease in NEAT, so this appears to be a real effect, but it still seems very possible that the NEAT decrease in the Leibel study is overstated due to selection bias. I note that in the Wake Forest study, participants lost on average (if I'm doing the math right) 15% of their body weight, and averaged a 162 calorie NEAT decrease. In the Leibel study where particpants had lost >10% of bodyweight, there was a 298-334 calorie NEAT decrease. To the extent that there is a discrepancy (unclear because of the ">10%") it might be accounted for by selection bias in the Leibel study.
Taken together these studies seem consistent with the following hypothesis:
1) weight loss does not cause a decrease in RMR (adjusted for lean body mass)
2) weight loss does cause a sustained decrease in NEAT, but the effect is modest
3) individuals with lower RMR & NEAT (regardless of the underlying cause) are more likely to gain/regain weight
As an aside, some of the commenters on your "Why Is It So Easy To Regain Weight?" piece found its results depressing. I saw it differently. A substantial decrease in RMR would be depressing, because there is very little you can do about it. To the extent that the Leibel study showed a decrease in RMR, this is a little depressing. But a decrease in NEAT seems much less disappointing, because NEAT can be targeted through specific behavioral changes. To the extent that decrease in energy expenditure is due to NEAT rather than RMR, that strikes me as good news. If my speculation above is correct about the measured RMR decrease being an artifact of the study, then that would be even better news.
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I would love to see this issue addressed by someone who's familiar with the literature.
"Just a comment to Nigel: The half life of injected insulin is much higher than endogenouse insulin. Insulin aspart(rapid) has a half life of 81 minutes, regular 141 minutes and detemir (basal) 5-7 hours."
Thanks for that. So there's insulin, insulin, insulin and insulin.
@lightcan: I wasn't having a go at you. I'm nerdy, so sometimes I state the bleedin' obvious!
It seems to me that strides have been made in dosing/delivery of insulin therapies, with longer acting insulin, insulin pumps, etc. that better simulate the behavior of endogenous insulin in the non-diabetic. In this regard I do find the demonization of insulin per se to be misguided. While I don't think high carbs and insulin to "cover" it are the best strategy, I'm skeptical of keeping overall insulin too low as it certainly has multiple functions in the body aside from glucose transport ... not the least of which being amino acid transport/metabolism. So were I a T1, or a researcher, knowing all I've learned, I would embrace insulin and seek the form of therapy that best imitates normal physiological function. Science has a way to go there, but I'll leave you with this: Hypothyroid folks pretty gladly take medications to normalize their thyroid hormone levels because of thyroid's role in metabolism , etc. So, too, I believe the ultimate hypo-cases (none) where insulin is concerned may want to rethink too low carb an approach simply because it keeps insulin low.
As a formerly obese person I would note that I'm pretty sure my NEAT was very low when I was most obese. You just don't feel like moving around much when it causes so much discomfort. Although I've been within 10 lbs of my current weight for 2.5 years now, I still find myself sometimes taking a seat at social functions, when wearing high heels, or just when chatting with my hubby while he's standing. I'm aware of this and make very deliberate efforts to move more. It may well be that the formerly obese are somewhat conditioned to sedentary behavior and its not so much the metabolism as habit. It does seem that since I've made these deliberate efforts, I'm able to maintain rather effortlessly eating what seems like a bit more these days. I'm a poor n=1 experiment for that, however, as I have not tracked nor kept intake records, etc. Still, I do know I was maintaining at around 1500 cal/day walking briskly for 1 hour 3-4 days a week in Summer 09. Doing no formal exercise these days but deliberately moving more, I would put my caloric intake perhaps 1-200 calories more. Maybe it just takes time for our bodies to recognize we're no longer in "famine".
You might find this of interest:
http://carbsanity.blogspot.com/2010/04/effects-of-aerobic-exercise-and-dietary.html
About the gaining weight back when resuming normal eating....3to4Kcal per day is not normal eating,at least for me and from what I see many people with extra fat on their bodies.There is the fat setpoint thrown around nowadays with leptin and other hormones being in the mix.What ever happened though to the old theory of the fat setpoint where the body would adapt to a set weight and that became the new fat setpoint.Its great that you have maintained for 2 yrs and I believe even if you gain some you can easily lose it as the body likes homeostasis and will speed up to burn off the excess.I have been stuck at 190 for yrs and now its dropping rapidly and I will not resort to old ways and gain it all back easily.
There is also something to a once a week binge in that it keeps you carbSane and what I find is the next day the appetite drops considerably as if the body wants to burn it off.Lyle Mcdonald says that as you get leaner you actually require more refeeds.I could do two per week no problem!! :)
1. You eat carbs.
2. Your blood sugar spikes.
3. Insulin is released, in a large dose.
4. The various tissues in your body downregulate the number of insulin receptors they have.
5. Your various tissues gradually become IR. Note that you do not become IR after one slice of bread. It takes time and each tissue does it at its own rate. Something like: Liver first, then muscle, then fat tissue with various other tissues in between.
Therefore I hold that the statement "The only carbohydrate implicated in the development of insulin resistance is fructose, the only one that does not stimulate insulin." is totally false.
There's not even an hint of an evidence that eating carbs causes an abnormal release of insulin leading to cells shutting down their receptors.
The amount of insulin released is strictly linked to the amount of carbs and proteins you introduce and hence need to process. If you eat more, more insulin is released, short term, but it takes almost the same amount to return to baseline levels. And even those low-carbers who eat no more than 20g of carbs a day, still have high levels of insulin after a meal and average levels of baseline insulin (not lowers than high-carbers) The increase in insulin levels after a meal is perfectly normal and harmless mechanism which has nothing to do with IR even when insulin levels are very high (if they're very high it's just because the meal was very big and hence more insulin is needed)
So the whole concepts that eating carbs might create an abnormal insulin surge causing the downregulation of receptors and leading to IR is nothing but a fantasy of certain LC authors, but nothing like that happens in real life, neither short term or long term.
P.S
There are people who suffer from hyperinsulinemia, but there are not many of them and they were born like that and no amount of carbs or even sugar caused them to become hyperinsulinemic and an LC diet is not even a good approach to solving their problem.
How does this link fit in with your view that "So the whole concepts that eating carbs might create an abnormal insulin surge causing the downregulation of receptors and leading to IR is nothing but a fantasy of certain LC authors, but nothing like that happens in real life, neither short term or long term." ?
http://www.nutritionandmetabolism.com/content/3/1/39
And how does this fit in with your view:
"Mechanism: The Insulin Receptor
The process of downregulation occurs when there are elevated levels of the hormone insulin in the blood. When insulin binds to its receptors on the surface of a cell, the hormone receptor complex undergoes endocytosis and is subsequently attacked by intracellular lysosomal enzymes. The internalization of the insulin molecules provides a pathway for degradation of the hormone as well as for regulation of the number of sites that are available for binding on the cell surface. At high plasma concentrations, the number of surface receptors for insulin is gradually reduced by the accelerated rate of receptor internalization and degradation brought about by increased hormonal binding. The rate of synthesis of new receptors within the endoplasmic reticulum and their insertion in the plasma membrane do not keep pace with their rate of destruction. Over time, this self-induced loss of target cell receptors for insulin reduces the target cell’s sensitivity to the elevated hormone concentration. The process of decreasing the number of receptor sites is virtually the same for all hormones; it varies only in the receptor hormone complex.
[edit]"
http://en.wikipedia.org/wiki/Downregulation_and_upregulation
It does not of course because you are wrong. Downregulation & upregulation occur at even trivial & normal levels of hormones.
Unreferenced speculation. There is some evidence that CHRONIC hyperinsulinemia can further exacerbate the IR state. Your piglet study speaks nothing of receptors. The poor things likely ate more of the cereal diet, hence the fattening, due to protein deficiency of the diet.
As Leo points out, there's no evidence that pp insulin "spikes" lead to long term downregulation of receptors. My research indicates that NEFA and lipid infiltration of ectopic (non-adipose) tissues are the culprit agents of IR (again, chronic, not transient) in these tissues.
That paper is just speculating. It's clear that the authors are Paleo supporters who got the chance to publish a paper. You know, most of those hyped Paleo and LC authors get papers published where they repeat the same exaggerated or wrong claims made in their books or articles. Just because it's published in journal it doesn't mean it is more scientifically sound that those articles and books.
It seems pretty evident to me that the Paleo diet had a reduced caloric intake, leading to weight loss which is what leads to more insulin sensitivity. Also the Paleo diet had an improved protein intake, which is where most of the benefit of Paleo and LC comes from.
That wikipedia article could have been written by someone who read GCBC and thought the science was sound enough. But physiology textbooks don't say that an higher insulin levels due to a greater amount of proteins or carbs to process causes downregulation of receptors and chronic insulin resistance. This is just an inverse-correlation speculation.
Actually, high body fat causes Insulin Resistance and Insulin Resistance causes high levels of insulin because the body releases more trying to bypass the downregulation of receptors. Those are indeed high insulin levels who are disproportionated to the amount of food consume.
But if you don't have Insulin Resistance, then whatever insulin release is proportionated to the amount of food you eat. If you eat more, more insulin is going to be released and this is not an excessive insulin spike, it's high but it's the right amount to process the food we have eaten. Once insulin has done its job it quickly falls back to average levels, shared by both high-carbers, junk food eaters and low-carbers. Not much difference there. In fact both high-carb, low-carb and junk food diets lowers Insulin Resistance and insulin levels, if they lead to weight loss. That's where the insulin sensitivity comes from.
This comment means that you do not have the faintest idea what up and downregulation is about.
Some big picture understanding of this process and why it occurs in all tissues for all hormones at all levels will improve your understanding of how this all fits together.
Unfortunately for you, Taubes did not invent, discover, nor popularise the concept of regulation. It just happens and any person with basic understanding of endocrinology knows this.
So you are back to hanging your hats on a totally false statement: "The only carbohydrate implicated in the development of insulin resistance is fructose, the only one that does not stimulate insulin."
Effect of sustained physiologic hyperinsulinaemia and
hyperglycaemia on insulin secretion and insulin sensitivity in man
S. Del Prato 2, F. Leonetti I , D.C. Simonson 3, P. Sheehan I , M. Matsuda I , R.A. DeFronzo 1
In summary, the present results indicate that
chronic, sustained, physiologic euglycaemic hyperin-
sulinaemia for as little as 48-72 h is capable of in-
ducing significant insulin resistance affecting the gly-
cogen synthetic pathway. If this insulin resistance
were to persist indefinitely, then hyperinsulinaemia
should be considered, not only a compensatory
response to the presence of insulin resistance, but a
self, perpetuating cause of the defect in insulin
action.
I'm going to run up against length limits on comments with HTML so I'll be continuing this reply in another posting.
Here's a link to the abstract http://www.ncbi.nlm.nih.gov/pubmed/7851681
Excerpts from abstract followed by commentary:
Two study protocols to examine the effects of chronic (72-96 h) physiologic euglycaemic hyperinsulinaemia (+ 72 pmol/l) and chronic hyperglycaemic (+ 1.4 mmol/l) hyperinsulinaemia (+ 78 pmol/l) on insulin sensitivity and insulin secretion were performed in 15 healthy young subjects.
I note that these were CHRONIC infusions that are in no way relevant to post prandial levels. So these healthy men were being subjected to something that would never occur in them under ANY dietary situation.
Subjects received a three-step euglycaemic insulin (insulin infusion rates = 1.5, 3, and 6 nmol.kg-1.min-1) clamp and a hyperglycaemia (6.9 mmol/l) clamp before and after chronic insulin or glucose infusion.
Following 4 days of sustained euglycaemic hyperinsulinaemia whole body glucose disposal decreased by 20-40%.
Whole body glucose disposal.
During each insulin clamp step,the defect in insulin action was accounted for by impaired non-oxidative glucose disposal (p < 0.01).
So, there was no downregulated insulin receptor action going on. The reduced glucose disposal was due to a reduction in glycogen synthesis (aka non-oxidative).
to be contd. ...
So hyperinsulinaemia did NOT cause insulin resistance in the liver!!! This is pretty solid evidence that postprandial insulin spikes don't lead to hepatic IR if 4 days of sustained elevated insulin didn't manage to do the trick.
Following insulin infusion the ability of hyperglycaemia to stimulate insulin secretion was significantly diminished.
There's quite a bit of evidence that insulin via some feedback mechanism impairs glucose stimulated insulin secretion. That's probably what was going on here due to insulin levels being artificially elevated for a sustained length of time.
Following 72 h of chronic glucose infusion (combined hyperglycaemic hyperinsulinaemia), there was no change in whole body glucose disposal. However, glucose oxidation during each insulin clamp step was significantly increased and there was a reciprocal decline in non-oxidative glucose disposal by 25-39% (p < 0.01)
So the glucose, aka the "carb ingestion" did not alter glucose disposal. Glycolysis increased, glycogen synthesis decreased. But again:
suppression of hepatic glucose production by insulin was unaltered by chronic hyperglycaemic hyperinsulinaemia.
No liver IR.
Chronic glucose infusion increased the plasma insulin response to acute hyperglycaemia more than twofold.
This might be expected in someone with normal beta cell function subjected to the environment resulting from impaired beta cell function.
These results demonstrate that chronic, physiologic hyperinsulinaemia, whether created by exogenous insulin infusion or by stimulation of endogenous insulin secretion, leads to the development of insulin resistance, which is characterized by a specific defect in the non-oxidative (glycogen synthetic) pathway.
These findings indicate that hyperinsulinaemia should be considered, not only as a compensatory response to insulin resistance, but also as a self-perpetuating cause of the defect in insulin action.
Yes, there is evidence that hyperinsulinemia exacerbates itself. Nothing about receptors there, and the effect seems to be due to impaired metabolism so less uptake rather than insulin sensitivity per se.
Chris Masterjohn had post a while back where he hypothesized that the epidemic of NAFLD could be a result of choline deficiency. Is it possible that NAFLD might be more a cause of IR than a result of?
Basically, excess calories and/or excess fructose and/or excess omega-6 in combination with choline deficiency disrupt liver function leading to NAFLD -> lipotoxicity -> IR. (or something like that…)
I'm not saying that dowregulation doesn't exist or is something Taubes invented. I'm saying there's no evidence that pathological downregulation can be triggered by a non pathological and perfectly normal process.
There's nothing abnormal about a big insulin release, it's perfectly normal and actually necessary to survival according to the amount of food the body needs to process and it's not something leading to disease. So the body doesn't have any reason to pathologically downregulate its receptors when the right amount of insulin is released for the right amount of food to process (and of course if the food was abundant, the insulin will be abundant)
The downregulation occurs only when something abnormal and risky is going on within the body, something like excessive visceral fat storage.
The body signals a danger and stop the cells from welcoming the nutrients. But the body has no reason to stop the cells from welcoming the nutrients just because the right amount of insulin was released in response to a normal consumption of a carby or proteic food.
Foods that spike insulin in the way that rice, bread, spuds, sugar etc do were not abundant for the most part of our evolution (at least not without incidental exercise that burnt most of the blood sugar off at the same time).
So what you consider a non pathological insulin spike that may only slightly downregulate receptors (boy I am glad we agree on that now) I consider a pathological spike that gradually leads you to IR.
Anyway you don't have to agree with me - we must each find our own way. As Peter of Hyperlipid says: "Make the choice. Pay the price."
You have yet to provide a single piece of hard evidence to support your statements. Making a hypothetical statement about evolution does not support your assertion. Second, rice, bread, etc. have been around long before insulin resistance and metabolic syndrome became prevalent in Western societies.
There is very little scientific evidence that regular physiological insulin surges due to food intake will downregulate insulin receptors.
@M.: I would say that's certainly a plausible path. By the time someone develops the "fatty liver" they are already past the point of lipotoxicity though. But there's no doubt many routes to the lipotoxicity. The "backup" of lipid oxidation in cells, not just the lipid content, seems to be at the root of insulin resistance vis a vis glucose disposal.
@ND: Again, there's no evidence to support your theory, so if you want to believe it as fact, it seems there's nothing we can do about that. All I can say is that just because someone writes it on a website, in a regular book or even in a textbook does not make it true.
Listened to Jimmy's interview with Gary?
I'm still convinced Gary Taubes has his heart on the right place. I also find your questions valid. What a pity that a decent, factual discussion between the two of you seems to be impossible.
It just struck me as interesting how you could possibly prevent lipotoxicity from "manifesting" (fatty liver) in a particular organ (arguably the most important organ).
Do you think if you could stop lipotoxicity from “manifesting” in the liver (preventing fatty liver via adequate choline consumption) that it would have any important effect on the rest of the body?
I also find it interesting on how important the liver seems to be to everything and how people cut back on egg yolks (choline) at about the same time the obesity slope got steeper.
Yeah, the demonization of probably one of the most perfect foods, the egg, was a HUGE mistake. It's sad that so many reasonably intelligent beings could be convinced that a carton of EggBeaters is somehow more "healthy" than an egg baffles me.
Choline aside, eggs are also rich in leucine, the amino acid strongly involved in appetite signaling and glucose metabolism.
If a cell is desperate for glucose (e.g. a muscle cell lacking in glycogen and undergoing intense activity, or a fat cell lacking in G-3-P), Glu-T4 up-regulates to increase glucose uptake.
If a cell is full of glycogen/TGs and can store no more, Glu-T4 down-regulates to reduce glucose uptake.
Full cell = Insulin Resistant cell.
"The only carbohydrate implicated in the development of insulin resistance is fructose, the only one that does not stimulate insulin."
Now I am confused :/
So the one minute glucose is not implicated in IR and now it is critical for it ?
Like most people I just seek out things that confirm my own biases. Which biases I have absorbed mainly from this great piece of old literature and other work by the same author:
http://www.diabeteshealth.com/read/2008/01/13/5617/insulin-leptin-diabetes-and-aging-not-so-strange-bedfellows/?isComment=1
Unfortunately I'm starting to think that Jimmy invited you to the podcast just to give Gary something to talk about.
I thought Jimmy was objective and didn't have bias but I was wrong. From the way he describes his interview with Gary you can say that he thinks Gary is right and is excited he is going to prove his critics wrong. I'm losing respect for Jimmy I'm afraid.
"Only isn't Nigel's point exactly the opposite of your view Carbsane, namely that:
"The only carbohydrate implicated in the development of insulin resistance is fructose, the only one that does not stimulate insulin."
Now I am confused :/"
See my reply to you on Jan 25th.
Both glucose & fructose can enter the liver. The liver can "say no" to glucose when its full (by down-regulating Glu-T2) but it can't "say no" to fructose (as Glu-T5 is insulin-independent).
Therefore, fructose is a problem for people on high-calorie, high-carbohydrate diets whose livers are permanently full.
Thanks for the clarification Nigee (you're my hero now because GT called you out! LOL). I didn't see how your comment conflicted with mine in the first place.
"Thanks for the clarification Nigee (you're my hero now because GT called you out! LOL)."
Er, WHAT?
I have seriously annoyed somebody else, though. He doesn't like you, either!
Oh, wow!
Jeremy
> Paul Jaminet (Perfect Health Diet) alleges that the body can only
> use around 600 calories a day in glucose.
...
> measured at 8 micromole/kg/min, which for a typical adult equals 120
> to 160 grams
I assume the blog carries their current thinking better than the book and on the blog their major rationale for recommending 600 calories of glucose equivalent (starch) is for mucus production.
They do NOT claim any amount greater than 600 calories gets turned to body fat.
Christian
> Gary Taubes already acknowledged that he made a mistake there.
part of the Jimmy Moore interview "retraction" of his G3P claims was Gary Taubes (phrased to imply that Hall & Chow agree): (paraphrased)
> It was a slight technical error, in the book or the slides or
> somewhere & I never made a huge deal out of it, but it's moot
> because Insulin so powerfully stimulates fat accumulation
GT: (paraphrased again)
"I was wrong but in fact that's incorrect"
me: (paraphrasing myself)
Best ever "Mea Culpa" (sans any actual Culpa).
Christian:
> shows me that you mix two things together that are not related: The
> "biochemistry/insulin/g3p/etc." issue and the
> "overeating/1st-law/cause-and-effect/etc." issue
Taubes: (paraphrased)
> 1st law does not apply because insulin drives fat storage
Carbsane: (paraphrased)
> I mostly follow low carb because it spontaneously reduces my intake.
> I don't need to believe fantasies about insulin trumping
> thermodynamics for it to work
Also read the above entry re: Hall & Chow.
From what I've just presented, your statement is exactly the opposite of the truth. Carbsane clearly differentiates, Taubes does not.
LeonRover:
> about insulin: it has a half-life of FIVE MINUTES
A point of curiousity for me is, how much insulin does most of the body actually see? Insulin's mostly destroyed in the liver and insulin's 1st delivery point is the the portal vein (INTO THE LIVER), so how much insulin do the muscle cells and adipocytes actually see?
Margaret:
> I don't see a whole lot of evidence that whole grain carbohydrates
> will cause weight gain because fiber acts to increase satiety.
I've seen enough negatives on whole grains to avoid them. All I can give is opinion at this point: I didn't notate & track the studies I've read, sorry. Vegetables & tubers do me fine for carbs, and lack many of the same issues.
Wolfstriked:
> wrong in the low carb world ... must be a high fat diet
the primary fault? doubtful.
My suggestion for the primary fault: "without carbs you CANNOT put on fat mass, it's just IMPOSSIBLE, so EAT EAT EAT EAT, as much as you want, but no carbs".
Nigel Kinbrum:
> When I had an insulin stress test on my pituitary gland in 2005, I
> was injected with 10 units of fast-acting insulin
Hey Nigel - first, as others point out, they're not the exact same molecule.
and 2nd, physiological insulin's delivered directly to the point where it's mostly destroyed. I wrote the above response to LeonRover before I read your post.
http://www.medbio.info/Horn/Time%203-4/homeostasis_2.htm
Lightcan: You might like this if you haven't seen it.
http://high-fat-nutrition.blogspot.com/2008/05/weight-loss-when-its-hard.html
Yeah, Petro was the 2nd or 3rd author I read bout ASP, something like 2 years (!!!!) (TWO YEARS!!!!) after I read Lyle McDonald writing about it.
http://forum.bodybuilding.com/archive/index.php/t-601375.html
And Lyle didn't take 5 highly publicized years out to research his magnum opus. Too bad I didn't listen to Lyle at the time & chose to follow certain others. What can I say. My BS detector was poor. Still is, but better.
Interestingly, in that post Petro agreed with Carbsane and did quite a bit of bloody violence with sharp (some dull) un-sterilized instruments to GT's ASP "thesis".
Nostril Damus:
> 4. The various tissues in your body downregulate the number of
> insulin receptors they have.
ONLY to show that
"more hormone -> (hormone resistance) or (reduced receptors)"
is not a universal law (and to show I can pick cherries too, but since I feel bad about it, my cherry picking's superior), from:
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2002.tb04202.x/abstract
> In early RA a significantly lower GR expression was found compared
> to controls. Interestingly, cortisol levels were also significantly
> lower
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WG0-48BBY1M-4&_user=10&_coverDate=06%2F15%2F2003&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1626091932&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=0a4f9164400a61fcea9c672a6138c26a&searchtype=a
> There was significantly higher hepatic GR mRNA abundance, despite a
> drop in GR protein content in the liver of cortisol-treated fish
I don't know exactly what this means: less protein but more gene expression - the tissue responds to high cortisol by trying to make MORE receptors, but despite the lower overall number of receptors, the liver is trying to
> esponses evident in the liver of trout imply changes favouring
> tissue responsiveness to glucocorticoids
so "more hormone" MAY lead to "fewer receptors" (that's what I take "less receptor protein" to mean). BUT "more hormone" actually led to "better sensitivity to the hormone", DESPITE lower receptor numbers.
Nostril Damus:
> Foods that spike insulin in the way that rice, bread, spuds, sugar
> etc do were not abundant for the most part of our evolution
Spuds and relatives (starchy tubers) have been in most human diets, in large amoounts, forever plus a day. Human saliva contains amylase, which breaks down STARCH. Pretty hard to evolve a starch-digesting enzyme with no starch in the diet.
Please read some of the more flexible, observation-not-ideology-driven paleo folks - Don Matesz, for example. As far as I know the Inuit, Yupik & relatives are the only ethnic/racial groups that have miniscule amounts of tubers. From what I've read, even high mountain tribes whose climate resembles the north pole (sans the seafood) seek out tubers whenever they can.
The penny has dropped. I just listened to Gary Taubes Responds To His Critics (Episode 439-Part 1)
______
What the ... ??? He claims you're a perpetual critic?
Didn't you support Taubes on Monkey Island for quite a while? Or am I confusing you with someone else?
Gary has kudos for Petro.
Seems Gary never felt the incisions (and blunt force trauma) to Gary's corpus administered in Petro's ASP post. Petro calls ASP a jewel, to Gary it "does no nothing", like Deusberg used to say about retroviruses.
@ the 13 minute mark: on low carb your body burns 1,000 calories of body fat per day so you spontaneously eat fewer calories. Funny thing: I've never read a low carb advocate claim that after a certain amount of body fat's gone, their appetite up-regulated to provide 1,000 calories per day (that USED to come from the fat but no longer can).
So everyone on low carb must, after some time, be losing 1,000 calories per day of something else: muscle tissue? Pancreas? liver?
Another case of calories don't count? I mean, if you've worn that groove into the laws of physics, it should be easier to do it the 2nd time.
Is this in the new book? Who vetted this - Hanson again?
ooooof: explanations of today's US obesity must be rejected as they don't explain obesity in Trinidad in the 50s.
DANG. bad case of MONO (causal) thinking. That insulin's some great & useful stuff - stores fat & makes great
http://en.wikipedia.org/wiki/Blinders
I'd hate to see what Martha Stewart could do with some Insulin.
more cortisol, higher sensitivity (NOT A RAT STUDY that cannot be extrapolated to humans)
In response to higher hormone levels, there is less actual receptor protein but more gene expression for the receptor protein so the tissue is trying to MAKE MORE receptors. The receptors have not been down regulated - the tissue's trying to make more.
In addition, despite the lower number of receptors, the tissue is less resistant
> esponses evident in the liver of trout imply changes favouring
> tissue responsiveness to glucocorticoids
so "more hormone" MAY lead to "fewer receptors". BUT "more hormone" actually led to "better sensitivity to the hormone", DESPITE lower receptor numbers.
"Nigel Kinbrum said...
The penny has dropped. I just listened to Gary Taubes Responds To His Critics (Episode 439-Part 1)
______
What the ... ??? He claims you're a perpetual critic?
Didn't you support Taubes on Monkey Island for quite a while? Or am I confusing you with someone else?"
You're confusing me with someone else. When I joined Monkey Island in 2005, I thought that "calories sort-of count". Then I read Lyle's articles and rapidly came to the conclusion that "calories count". :-D
>> Good to "see" you again
Thanks
I've been reading from a library but hate to type passwords at public terminals
Good to see you're raising consciousness. I've been noting some more skepticism in a few places I had not seen it before
You might like this post on Paleo Runner:
Why We Get Taubes, and what to do about it
http://paleo-runner.blogspot.com/2011/01/why-we-get-taubes-and-what-to-do-about.html
He ends his post:
"In my experience, quitting Taubesianism cold turkey is easier said than done. That's why I've provided the following three easy steps for other victims, who would wish to follow in my footsteps:
Realize you're addicted to Taubes. Stop studying his books like they were the Old and New Testament. Just read something completely different for a while, like 'Perfect Health Diet' by Jaminet and Jaminet.
Avoid following his new blog, which is also very boring. Subscribe to his archrival My Carb Sane-Asylum instead. I'm not saying she has all the answers, but it's refreshing to expose your mind to controversial views, and she's fun to read.
Don't take my word for it. For a second opinion, read this excellent review of WWGF by Yoni Freedhoff. Breath deep, relax, and feel Taubesianism leave your body (LOL).
Good riddance bodyfat, sedentary lifestyle and GT!"
This describes what I'm feeling quite well, except that I have not really made up my mind yet.
The interesting thing is, most of the more scientific bloggers in the paleosphere really don’t but Taubes’ Carb/Insulin thing.
They try to point people in the right direction, but they usually don’t come out and say explicitly that Taubes is wrong unless pressed on the issue.
I don't know how well this works though. There seems to be a lot of surprise whenever someone well-respected like Guyenet or Harris comes out and explicity says they disagree with Taubes' Carb Theory.
Yes, I've noticed that too. I guess this polite reluctance is born out of awe for the huge amount of work Taubes must have put in writing the tome. I'm still very impressed by all the information he dug up and the way he organized and presented it. I also highly admire his courage to think outside the box and tot propose an alternative hypothesis. I don't hink it's fair to call all of his work a fantasy, as some here do. We should not be afraid to point to obvious flaws in his reasoning, though. I really wonder why Gary ignores/belittles his critics. It's not enough to just call them obsessed stalkers. Still hoping for a civil debate.
Seems to me he's close to, if not already, past the point of Reductio ad absurdum.
Everything he now says and writes PRESUMES he's correct & unassailable. And obviously to his fans he is.
He pretends to want a debate ("forging stronger arrow heads") but ALL he talks about is how his critics WILL NOT LISTEN, and how he didn't WRITE to convince them (your critics rely on the data Gary[1], not on your WRITING; this emphasis admits and betrays that you wrote to push an agenda, not as an open minded exploration or exercise in critical thinking), about how he's now reading Frayn and finding stuff he could have used to support his argument (but he's found NOTHING, I mean ZERO, material to think about - to genuinely explore, only stuff he can use)
[1] all the data that which supports AND debunks your theories, not only your cherry pickings [2]
[2] I am SO tempted to make a droppings joke
Gary Taubes own theories might not be perfect, however he is RIGHT that the caloric bank account model has overwhelming evidence against it.
My own blog SHOWCASES ALL OF THIS.
The observation that Gary's own theories
on the etiology of obesity might be less perfect, is not a criticis .
NO ONE has figured out obesity yet Science DOES NOT CURRENTLY UNDERSTAND THE CHEMICAL BEHAVIOR OF FAT CELL RECPETORS.
The caloric bank account model of obesity is WRONG, and has NUMEROUS strong contradictions with mice models , Siberian Huskies fat retention, etc.
I think had GCBC focused on the fact that fats and sat fats in particular were being demonized inappropriately, that low fat diets calorie restricted diets tend to not work in the long run and propose why low carb was a healthy alternative, w/o ginning up some "everyone in the past 50 years got it wrong but I'm right" hypothesis on this all, I wouldn't have an issue with him at all.
Have you seen The Adventures of Chris “Razzi” Razwell and Other Assorted Internet Psychos?
You're (in)famous. Infamy! Infamy! They've all got it in for me! :-D
Nige.
My blog features even more of my names. :)
Wolfstriked said (paraphrased) was that what went wrong with LC was when it became an obligatory high fat diet.
You said: the primary fault? doubtful.
My suggestion for the primary fault: "without carbs you CANNOT put on fat mass, it's just IMPOSSIBLE, so EAT EAT EAT EAT, as much as you want, but no carbs".
I'm going to suggest that these two seem to go hand in hand. I remember WS from Jimmy's forum circa Spring/Summer 2009 when I first found that discussion forum. In response to questions about stalls, the almost universal advice doled out by members was "up the fat". Some were careful to say up the % fat, but the boilerplate message that came through was to eat more fat and calories. Cut carbs more if you're eating any.
I began following Jimmy's menus here and there at the time and discovered he was gaining weight eating pretty darned low carb and was shocked at the portions. Then this video just stuck in my mind: http://www.youtube.com/watch?v=Mhe2Y9CikrA
Purity bread was low fat (as almost all bread is). But Jimmy had it in his message that the fat-free nature of the bread needed "fixing" so you want to put butter on it. Forget that cheese & pepperoni will add plenty of fat to a pizza, no, he added what looks like at least half a stick of butter. More recently Jimmy discussed adding lots of fat to chicken wings because chicken is low fat.
Use HWC not half and half in your coffee, smother berries in whipped cream because the fat will blunt the insulin thing. Never ever eat a plain chicken breast or tuna that is not made into a salad swimming with mayo.
Atkins, himself, never advocated this. Indeed his super high fat diet - the fat fast - was to be done short term (although Silver Cloud diet extends it several weeks) and was CALORIE RESTRICTED at very low levels (1000-1200). I have pointed this out and asked if eating more fat and calories or just higher fat was the key to weight loss, why did Atkins limit calories? The answer is, you can easily overconsume fat (especially in the form of mayo, dips, dressings, dairy) ad libitum.
Also, between his attitude about Jillian Michaels and the fact that he had to mention I was a "female" anonymous blogger (and I thought I was verbose ... why not just use CarbSane or just CS), I do believe GT has a special disdain for his female critics.
"... reduces hunger, thus letting you spontaneously eat fewer calories ..."
> attitude about Jillian Michaels and the fact that
> he had to mention I was a "female"
I noted that as well ... but my posts were already getting rejected for length ; )
Like others have written, I am impressed you still answer posts, considering the time and effort it takes to put together the regular posts plus a full time job. Whenever I write longer presentations with serious analysis it takes me 10 times as long to put together the kind of posts you do.
PS - I was hoping if GT were lurking the Duesberg reference would "encourage" him to post. No such luck I guess ...
I am having a hard time following what you think he is doing wrong, and would like to understand your POV.
If you can formulate a question rather than "I still don't get it", I'll do my best to answer.
"The whole excess carbs turned to fat promote fattening is simply not true for humans."
This is just so divorced from my experience of reality that I can't follow your chain of thought and hence "don't get it".
> not true for humans."
> This is just so divorced from my experience of reality that I can't
> follow your chain of thought and hence "don't get it"
Rats and mice can turn carbs directly to fat. Humans rarely do, but it can LOOK that way -
Here's an explanation that is supported by current biochemistry
how we get fat
>> What part / which one of Taube's Hypothesis
>> do you think are wrong and why ?
(this is my take, no one else's)
He got the diet wrong (higher protein makes it "work" but he's now gone whole hog for the low carb thing)
He got the biochemistry wrong (wrong on carbohydrates causing insulin resistance, wrong on how strongly insulin stores fat, wrong on how strongly insulin suppresses fat mass loss, wrong on how hungry insulin makes you, wrong on ASP, wrong on g3p, wrong on calories)
He ignores almost all the evidence that casts doubt on his idea. Quoting scientists for example only for their supportive words and not for the opposite.
He spins and distorts mildly supportive data (the Shai study for example) badly. Combine that spinning with the rest of his corpus and in the end he's badly mutilated that mild support beyond reason
His rhetoric encourages people to throw caution to the wind and eat excessive calories ("if you stay low carb you can eat as much as you want"), perhaps massively in excess. Even a person who might do well on the diet if they were to do it in moderation will do extremely badly if he listens to Taubes and eats as much as he wants (as opposed to the reasonable "eat until you feel reasonbly full, and if you still gain weight, count calories")
Concomitantly he expresses no caution for the long term consequences - metabolic or chemical. You can find some studies that indicate caution is warranted in the right hand column -search for NEFA or FFA.
To get the specifics on WHY he's wrong on each of these, read many of the articles on this blog
>> "if you stay low carb you can eat as much as you want"
Notice that word - WANT?
If your body does not respond to a high protein diet like a lot of bodies do (by reducing calorie intake by itself, without much willpower) and you actually eat as much as you want, and you LOVE steak (yum, insert Homer Simpson sound effects here) and bacon (yum squared) and 5 year old raw-milk cheddar cheese(try to keep me away) and splenda-flavored ice cream made with real eggs, heavy whipping cream and zero carbs(If you want mine you'll have to pry it from my cold dead hands and frozen tongue and teeth)
how many calories do you think you could take in?
"The whole excess carbs turned to fat promote fattening is simply not true for humans."
This is just so divorced from my experience of reality that I can't follow your chain of thought and hence "don't get it".
http://carbsanity.blogspot.com/2010/07/nutrient-fates-after-absorption.html
http://carbsanity.blogspot.com/2010/06/excess-carbs-coverted-to-fat.html
It's a pathway alright but a minor one in terms of body weight.
I kept off the 135 lbs I lost for 3 years, fairly easily, living la vida very low carb. I thoroughly enjoyed (and still do) eating that way. I didn't have any desire to increase carbs. Then I put 20 lbs on for the sake of a sport I got into and maintained that weight until November 2010. I never counted a single calorie during my weight loss and maintenance (9.5 years). I kept out carbs (save the holiday meal) and just ate til full. That way kept me at 185 lbs through November 2010.
I took an opportunity in November last year (time off from sport) to find out my TDEE and to confirm the weight of the evidence I was finding in the research. I went omnivore (after 9.5 years of VLC), found my average TDEE to be 2500 kcals, and quickly/easily just cut calories to lean out to 165 lbs. My TDEE did not change from the 20 lb weight loss and I'm 3 months along easily maintaining the new lower weight. The surprise to me is how much I can actually eat at maintenance. 2500 kcals/d doesn't sound like much, but it is (if you're not eating it all as candy, highly processed food, and restaurant meals).
I'm straight up honest about myself, too. I'm sedentary. I dare say I'm lazy. I don't try to force myself to increase my NEAT. I know that as I age my TDEE will likely lower. I'd rather not artificially inflate how much I can eat now and then find myself in life circumstances (job, kids, moved, etc.) that lower my TDEE causing me to start to gain weight unwillingly again. My response to the Weightology link is that this N of 1 offers hope rather than despair. I'm 34 days away from a full decade since I started my weight loss and I didn't gain it back. There is hope!
I wish REE measurement, the 10 minute breath test, were more accessible. It would at least provide people with an individual number to start with.
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Its likewomen and mendon't seem to beinvolvedunlessit issomethingtoaccomplishwithWomangaga!Your personalstuffsoutstanding.All the timedeal withit up!"Stick a Toothpick in It? Taubes' 4-pronged Carb/Insulin "Fork"
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Most of the people who are truly wedded to the Taubes theory are people who are totally unwilling to MM. People who actually MM eventually figure out that it just doesn't work in real life.
The author replies to people in the comments, and there are also remarks from some other people who tried the diet, although you have to wade through a lot of "carbs are evil," "raw vegan is the answer," "just avoid processed food" type comments to find them unless you do a search (the author's name is "RichardDoughty".
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Really at a loss here as to why Ketosis is so bad, but yet it produced the desired results, which for 99% of people is fat loss?
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