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Welcome all seeking refuge from low carb dogma!

“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!)

Sunday, December 5, 2010

Fat Accumulation: Taubes v. Frayn ~ ASP in vivo in humans

This is actually a re-posting of the cited article, but I've updated the post significantly since the original.

Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period  Jumana Saleh,* Lucinda K. M. Summers,† Katherine Cianflone,1,* Barbara A. Fielding,†Allan D. Sniderman,* and Keith N. Frayn.  1998.

This paper demonstrated ASP actions in vivo for humans in the postprandial (post-meal) period.  ASP levels were measured locally to the adipocytes  (venous output side) and systemically in the arterial "supply" side.  This was important because many who would dismiss the action of ASP look at systemic ASP levels and claim no connection.  However, this paper demonstrated otherwise:

Abstract 


The objective of this study was to determine whether Acylation Stimulating Protein (ASP) is generated in vivo by human adipose tissue during the postprandial period.  After a fat meal, samples from 12 subjects were obtained (up to 6 h) from an arterialized hand vein and an anterior abdominal wall vein that drains adipose tissue. Veno-arterial (V-A) gradients across the subcutaneous adipose tissue bed were calculated.  The data demonstrate that ASP is produced in vivo (positive V-A gradient) with maximal production at 3–5 h postprandially. The plasma triacylglycerol (TAG) clearance was evidenced by a negative V-A gradient. It increased substantially after 3 h and remained prominant until the final time point. There was, therefore, a close temporal coordination between ASP generation and TAG clearance. In contrast, plasma insulin and non-esterified fatty acid (NEFA) had an early (1–2 h) postprandial change. Fatty acid incorporation into adipose tissue (FIAT) was calculated from V-A glycerol and non-esterified fatty acid (NEFA) differences postprandially.  FIAT was negative during the first hour, implying net fat mobilization. FIAT then became increasingly positive, implying net fat deposition, and overall followed the same time course as ASP and TAG clearance. There was a direct positive correlation between total ASP production and total FIAT (r 5 0.566, P , 0.05). These data demonstrate that ASP is generated in vivo by human adipocytes and that this process is accentuated postprandially, supporting the concept that ASP plays an important role in clearance of TAG from plasma and fatty acid storage in adipose tissue.—
Unfortunately, the "fat meal" was actually a somewhat balanced meal (although pretty low protein) relatively high in fat and carbs:  60 g fat, 85 g carbohydrate, and 13 g protein = 932 calories total   58% fat / 36% carb / 6% protein.  But this actually makes a more compelling argument for ASP regulating/controlling fat accumulation than for insulin when we look at the time course of "fat storage" here.  

Insulin and NEFA initially increased in the first 1-2 hr.  As stated above, fatty acid incorporation into adipose tissue (FIAT) was NEGATIVE in the first hour indicating net fat mobilization!  This seems an odd paradox, but this is not the first study I've read that demonstrated a release (at least initially) of fat from stores in response to a meal.  So early in the postprandial period, insulin does not suppress fatty acid release from the fat cells, nor does it send fats on a one way street into the cells.  So the high carbs in the meal do not lead to fat accumulation through the actions of insulin.  Other research I've blogged on here and here indicates that insulin can stimulate ASP production, although its action is much less potent than chylomicrons.  Later in the postprandial period ASP levels increased in the adipose tissue and correlated with triglyceride uptake and net fat accumulation.  

At the time of the original posting, I was not aware of who Keith Frayn was, and his name on this paper didn't really mean much to me.   Since that time, I've become aware that Taubes cites Frayn in GCBC and Taubes has consulted with him regarding fat metabolism at least in the intervening years since the publication of GCBC.  Frayn is "the English guy" who is described by Taubes as an expert in fat metabolism.  Indeed he is.  Searching the peer review literature that bears his name can rather overwhelm a person with the volume of work.  I've shared some of this and have more to come.  Thus, given Taubes' claims of rigorous scientific research, he should have been aware of this 1998 paper bearing Frayn's name.   This wasn't some obscure rodent study, or in vitro experiment.  This study looked at what ACTUALLY happens in live humans after consuming a large (~900 cal, high fat and high carb) meal.  The results demonstrate pretty well that Taubes' automaton fat tissue at the ready to accumulate fat in response to glucose and insulin is grossly inaccurate.  Instead, net fat accumulation occurs after the insulin response and correlates with ASP which is stimulated largely by the chylomicrons.   Yes, insulin can amplify ASP response, but fats stimulate it more.

I am increasingly convinced that Taubes deliberately maintains a state ignorance on such matters as ASP.  Because it pretty much demolishes his hypothesis.  

In a post entitled WHAT IF LOW CARB IS WRONG? DOES ASP PROVE THAT INSULIN DOESN’T MATTER AND THAT ITS CALORIES THAT REALLY COUNT?, Josef Brandenburg (June 30, 2009) wonders over the significance of ASP and asks Taubes about it.  Brandenburg cites the following articles as references for that post:  Purification and  Characterization of Acylation Stimulating Protein Katherine M. Cianflone,  Allan D. Sniderman, Mark J. Walsh,  Hai  T.  Vu, Jean GagnonS,  and  Miguel  A.  Rodriguez, 1989; and Metabolic response of Acylation Stimulating Protein to an oral fat load,K. Cianflone, H. Vu, M. Walsh,  A.  Baldo, and A.  Sniderman, 1989.  Notice anything?  These two 1989 papers were authored by folks whose names one begins to recognize as often associated with Keith Frayn.  

One wonders why the "obsessed" Josef Brandenburg (his description) didn't delve a little further into the topic.  I've included the authors for a reason, because just a little more intellectual curiosity on the topic would have led to the later works of this group in  its varying combinations.  But that's why we should always be skeptical of personal trainers peddling scientific theories.  Not saying they can't be trusted, but clearly here Brandenburg displays the "scholarly ineptitude" of which Taubes spoke of in our email exchange.  I can certainly forgive this of Brandenburg, I could care less unless I were to hire him as a personal trainer.  In any case, here were his two conclusions from the papers:
#1. “ASP is far more powerful than insulin in stimulating the creation of new body-fat.” (1)
#2. “ASP is released in response to an oral fat load.” (2)
Brandenburg asks Taubes for his take, from the "Take It Home Gary" section of the post:
“Nice to know you’re suitably obsessed Josef.
“One thing to keep in mind in all this is the need to explain the observations, not just work with possible mechanisms that can’t explain anything. So one of the observations is weight loss on a high fat diet — the Atkins diet.
“So if ASP was good at sequestering dietary fat away in the fat tissue without carbs being needed, why would people lose weight when they ate an Atkins diet?
Ummmm, if insulin was good at sequestering dietary fat away in the fat tissue, why would people lose weight when they ate a low fat diet?   As to his question why people lose weight on Atkins ... oh, perhaps ... because they spontaneously, and considerably, reduce caloric intake.  Just a thought.  
“Another observation we’re trying to understand, as I point out in lectures, is the obesity in poor populations eating low-fat, high carb diets. So there ASP would be irrelevant. Now if we had obesity in populations eating low-carb, high-fat diets, that would be telling and a reason to invoke ASP, but, as far as I know, no such populations exist.
Diverting attention.  But what populations get fat eating a low fat high carb diet?   
 “So maybe ASP plays a role in obesity in rats that are fed high fat diets, but we’re not all that interested in rats.”
I've stated this before in comments on another post, but it really exposes the hypocrisy of Taubes and, indeed, many low carb advocates.  That being that rodent studies are applicable when they seem to fit LC the(ory)ology, but not when they don't.   I would inquire of Taubes as to why he likes to use that fat rat slide in his lectures if we're not interested in rats after all?  

Clearly Taubes is aware of ASP, and if he were actually interested in getting the science right or making good on his "pledge" of sorts to hold himself to the same rigorous standards to which he holds others, he would have followed the names and delved into the research on ASP conducted in the intervening TWENTY YEARS between Brandenburg's articles and his blog post.  This is presuming he even bothered to read the 1989 articles.  So, how should I class his response in 2009?  Umm ... scholarly incompetence for starters. 

So the answer to Brandenburg's post title question is YES.  The insulin/carb fat accumulation theory is wrong.  Fat (net) accumulates when intake exceeds expenditure, and stores (net) diminish when expenditure exceeds intake.  Proveably so, and has been since before Taubes even wrote the Big Fat Lie article.   

78 comments:

Matt Stone said...

Excellent article again as always. Clearly insulin from carbohydrate ingestion is not the cause of obesity, otherwise the 99% of the several billion lean people in the world wouldn't be eating a low-fat, high-carb diet in comparison to the SAD - but they are.

Of course, there are plenty of high-fat eaters that are also not obese. The Masai were very lean and the composition of their diet was almost a complete opposite to the diets of those in other parts of Africa (note: I am getting sick of pointing out tiny microfractions of human civilizations as supposed proof of something... I think I might actually make myself vomit if I say "Masai" ever again, heaven forbid "Eskimo" or "Kitavan").

But I still think examinations of insulin vs. ASP are still not even close to taking in the breadth of perspective needed to understand human energy regulation over periods of months, years, decades, and lifetimes.

The root cause of obesity, if it is ever identified, will be a lot more subtle than "fat" or "carbs."

James Krieger said...

Matt,

When you say "the root cause", that implies that there is a single root cause. But why do we assume a single root cause? To me, this is one of the biggest mistakes people make in regards to obesity...assuming that the cause is univariate rather than multivariate.

Sanjeev said...

What really PO's me is that people who knew better didn't raise a (bigger) stink.

If Bray had included stuff like this I might have been more skeptical months & years earlier.

sigh ... maybe I'm trying to blame others for my shortcomings. I may have been then as many are now, brainwashed, in denial & unwilling to listen.

Sanjeev said...

>> But that's why we should always be
>> skeptical of personal trainers peddling
>> scientific theories. Not saying they can't
>> be trusted,

And writers. And MD's. And (some) PhD's ...

Some PTs are pretty darn good though .. I believe Alan Aragon & Anthony Colpo both refer to themselves as personal trainers.

James Krieger said...

CarbSane,

Taubes has made his first blog post:

http://www.garytaubes.com/2010/12/inanity-of-overeating/

Sanjeev said...

James beat me to it.

Mr. Taubes seems to be of the school that maintains

"
if you find yourself in a hole
stop digging
get rid of the shovel
hightail it down to the local Caterpilar place
and get yourself a backhoe.

This will make the digging so much more effective. "

CarbSane said...

Yeppers, saw it before this post and asked him in the comments if he thought Keith Frayn was among those he considers to be making a junior high school science mistake ;)

It's utterly hilarious that he highlights a piece by another science writer but says he's out of his area of expertise. That's really Taubes' only excuse for himself.

CarbSane said...

Sanjeev, I've been wondering a lot about Richard Hanson in this regard. He reviewed GCBC before it went to print and Taubes claims the G3P section went through a few drafts to essentially satisfy Hanson that it was accurate. I just can't imagine that Hanson agreed it was. Might be why he didn't specifically say carb was required to store fat in the book but worked it into (got skewed so he says) his lectures. Still any errors in fact or form remain his own (according to his book). One wonders why he felt the need to include that statement rather than just thanking them for their assistance. >:)

All I can think is that in the end, Taubes has not made as much of an impact on the mainstream, however large he seems to loom in the LC webosphere. Research scientists like Hanson and Frayn don't usually venture into the fray.

Frayn did apparently tell him he was wrong in a conversation, but I guess he left it to Taubes to set the record straight. I think it was having some of these guys in the audience of one of his lectures asking embarrassing questions that finally got him to fess up a bit. I wonder if he'll even link to his interview with Jimmy in his blog to discuss it. Doubtful.

As to the PT's it's why I used the word skeptical. Basically verify then trust ;) In the sports and nutrition realm there are too many peddling fads and gimmicks with, as you point out, all manner of initials after their names. I would even consider going to JB were I in the market for a trainer in his area if I liked his training methods and/or success of his clients. I don't know anything about the guy other than that blog post I found when I went looking for whether Taubes ever addressed ASP.

Jonathan said...

CarbSane,

I'm just tuning into your blog. Very interesting. I read the Brandenburg article and caught one point that I thought was key. Here is the quote:

"It is true the addition of ASP REALLY accelerated the creation of new fat (triglyceride) – it was faster than insulin. HOWEVER, both the ASP and the no-ASP cultures had insulin and carbs added to them. So the water is very muddy: Could the ASP be a way in which insulin accelerates its activity? Maybe the super deadly combo a high-fat and high sugar meal? Maybe the only thing to learn from this study is that frosting is more fattening than candy? Why not test ASP without insulin and carbs if your goal is to see what the difference between them is?

I have always thought that the real problem is not carbs alone or fat alone but the product of the two: "fat times carbs". Is it not possible that ASP is an acclerator of the effect of insulin, and vice versa? If so, that would explain why both a very low fat or a very low carb diet can be effective in weight loss, but the "typical American diet" (which has both) is a disaster.

If this is the case, then it can be true BOTH that insulin is necessary to promote fat accumulation and that ASP promotes fat accumulation. It doesn't have to be either/or.

Do you have any evidence that ASP can promote fat accumulation in the context of zero carbohydrate and insulin?

Your thoughts?

Jono

CarbSane said...

I agree James. The upset homeostasis models can never explain how eating disorders develop, and, as you know that was my route to obesity. Yet others certainly become obese without binge disorders, etc. Still, if one frequents weight loss blogs and discussion boards, it's far more the norm than the exception.

Matt, I share your feelings on those obscure cultures. They are instructive to the extent that they demonstrate no macronutrient is necessarily fattening, but the lifestyles of these remote cultures differ so dramatically from American culture be it in the 50's, 80's or today. So discussing them goes nowhere to identifying the causes of the obesity epidemic in our culture.

Just to clarify as well, when I point to dietary fat and ASP as driving fat accumulation I'm doing so only to apply Taubes' faulty carb/insulin logic to what actually occurs. I don't believe any macronutrient, hormone or peptide leads to spontaneous fat accumulation leads to obesity.

I believe it was your blog, or perhaps your comments on someone else's where you hit on the cause for many: Dieting! Not the diet phase, but the metabolic aftermath and going off the diet. Repeatedly. Diet mentality. Low carb approaches don't fix that, and many take it to extremes that seem even more extreme than low fat dieters.

CarbSane said...

@Jonathan: I've blogged quite a bit about why I believe fat + carbs are particularly fattening. I don't see that there's any mystery why Americans (the only folks I get to routinely observe in their natural habitats ;) ) keep getting fatter. If you pick up a menu from any chain restaurant like TGIFridays, Olive Garden, etc., one is hard pressed to find entrees and dinner salads under 1000 cals! Add in an appetizer, dessert or cocktail, let alone all three and it is easy to see how we "overeat". Yet if I were to post a picture of that meal it wouldn't look overly large. Even if it's once a week or once a month, without compensating for it, it adds up. I've blogged about separating fats and carbs here: http://carbsanity.blogspot.com/2010/08/separating-fats-carbs.html

So, I don't believe any hormone or peptide is responsible for "driving" NET fat accumulation. ASP is a potent agent in triglyceride clearance from circulation, insulin less so, although it can stimulate ASP. But this study did demonstrate that IF we are to point to fat accumulation, ASP is the big Kahuna. Insulin is not, as far as I know, directly involved in fatty acid uptake (as in transporting it). We primarily store the fats of our dietary excesses. That was true when the low fatties said so, and it remains true from everything I can tell no matter how many times some say otherwise. Now it is true that if carbs are a sort-of "metabolic bully" but it's the combo of both that lead to excess. It is EASY to get there without even realizing it eating processed foods or those prepared and served in portions decided by others.

I have a number of ASP articles I'm mulling over and will post more in the future. Stay tuned!

Welcome to my blog Jono and thanks for contributing :)

LynMarie Daye said...

It's been a while since I read any of the ASP studies, but in regard to Jono's comment, I believe insulin is added to the fat cells to promote growth and differentiation (pre-adipocytes -> adipocytes) but then is removed before the start of the actual study. Not in all cases but in some. As for adding glucose, this is done to provide a source of alpha glycerol phosphate which is needed if you want to study triglyceride synthesis. It would be interesting to substitute glucogenic amino acids for the glucose, but AFAIK that has never been done.

Nick said...

And it continues.... The more we learn the less we know.

Perhaps we can take a little bit form everyone here. What if it's not fat or carbs but an unknown combination of other nutrients in our food that our bodies are craving.

What if modern agriculture/factory farming has destroyed the nutrient dense and varied food that we use to have access to. The amount of nutrients we receive from any give food has diminished requiring a greater overall intakes to obtain them.

Maybe fat storage is the byproduct of over consuming macro-nutrients(protein, fat, carb) in a desperate attempt to obtain the micro-nutrients our food lacks.

I believe the solution lies in finding the most nutrient dense food possible. (Thus requiring less calories overall, and inducing weight loss) Maybe combined with an intentional reduction of calories to restore optimal weight.

As GT stated "We are not fat because were eat too much, we eat too much because we are fat" (substitute 'fat' for 'desperately searching for nutrients that aren't there')

In that sense I think he is on to something. The over-consumption is a symptom not a cause.

But he blames the over-eating on a high carb diet alone. I think it just so happens that the foods which tend to lack nutrients are for the most part higher carb. By looking at the macro-nutrients alone he came to a conclusion that we would all make:

Today as a culture we consume a significantly larger amount of crabs then historically, and as a result we have become obese. Eating carbs causes and insulin spike. Insulin's job is to store fat.

But as the ASP study points out that is only one half of the story.

Obviously its much more complicated then that.

It would seem that the easy answer would be to just cut out anything that wasn't available 100 years ago and base our diets on that. Unfortunately once again its not that simple.

The way our food is prepared and delivered has been changed. Genetically modified produce, animals being fed unnatural diets, plastics and other chemicals messing with our natural hormone balance. Government regulation and support of big business preventing easy access to high quality food. Subsidized farming making the least nutrient dense food the cheapest. We face many challenges.

d4rkboy said...

My impression was always that a low-carb, Paleo-style diet was more satiating/calorie than any high-carb, low-fat diet (http://www.nutritionandmetabolism.com/content/7/1/85). Thus it is generally easier to keep input in line with output.

dietconcepts said...

Actually, I think the why we get fat bit is pretty straightforward. Fat gets stored as fat, carbs is either burnt or stored temporarily (carb->fat can happen, but you have to eat ginormous amounts of carbs - more than 500g a day for quite some time), and protein gets used or discarded. If you eat carbs+fat and above your maintenance level, all the fat gets stored. If you eat carbs+fat below your maintenance, nothing gets stored. (This is a simplistic view - what happens is that some gets stored as fat, but less than what gets burnt as you're in a deficit). The key point is that as long as you're eating below your maintenance, you will loose weight. However, if you eat just a little below maintenance, say 100-200 cals, then it will take something like 2-3 weeks to loose a pound of fat. This is the real killer, as most peoples maintenance level is usually much lower than they think.

CarbSane said...

@Jono & LynMarie: I have come across at least rat in vivo studies that look at ASP response to a fat-only load and it does just fine. Will be putting more up in the next week or so on this topic.

@Nick: I've had a Nick comment before, not sure if that was you, if not, welcome to my blog and thanks for contributing to the discussion. I am in agreement that micronutrient deficiencies can drive overeating. I would add that, especially for women, the standard 15% protein reducing diet is woefully inadequate and probably explains a goodly portion of folks not being able to stick with them. But back to the micros, yeah, I think when someone is eating crappy foods their bodies may well tell them to keep eating to satisfy some need. However I don't see how this is at all analagous to Taubes' theory on fat accumulation which is that our macronutrient driven hormonal environment causes fat to accumulate, essentially robbing our tissues of access to it that then increases hunger and perhaps also causes lethargy for the same reason (lack of FA availability for energy).

My problem with this theory, aside from its flawed basis in insulin only, is that Taubes is a master at looking at short term metabolic occurrences which make insulin and carbs look pretty bad, while ignoring 24 hr and longer term balance. This is something that Frayn marveled at to an extent in Metabolic Regulation: how so many of us seemingly are able to maintain a long term homeostasis that would average out to changes in the 10-20 cal/day range while daily intake and to a lesser extent expenditures fluctuate far more wildly day to day. As far as I'm concerned, whenever the whole 3 meals a day "norm" came about is when humans ceased being homeostatic creatures and some sort of conscious or subconscious mechanisms have been at work.

Back to the insulin/ASP, both appear to be potent regulators of adipose tissue: ASP moreso for triglyceride formation, insulin moreso in suppressing lypolysis/FFA release. But these agents are stimulated by dietary intake and circulating substrates as well. Where the triglyceride/FA cycle is concerned, we know fats are constantly being esterified and hydrolyzed between the two forms, and as much as ~60% of released FA's are taken up and esterified in fat or peripheral tissues. What determines this? Oh ... rocket science? Nope (sorry for the sarcasm). Energy needs. In GCBC Taubes confuses the notion that energy surplus is required for weight gain with the notion that energy surplus is required at all times for any fat accumulation to occur which was never what the laws of thermodynamics dictate.

So I think dietconcepts put it well. The reason that the whole 100 cal/day differential has been supposedly "debunked" is not because it is invalid, it is because to maintain a 100 cal deficit consistently is difficult (if one shoots to have a 500 cal deficit, then perhaps one day it's 600, the next 400, etc. and if you're fairly diligent you probably average 500, but if one is shooting for just 100 cals, it would take meticulous record keeping to average this smaller increment) and the superslow results on the scale may not be sufficiently motivating. But ... it is probably the best way metabolically for our bodies to lose fat. It's simply not a very doable approach, especially for those who are not creatures of habit and/or have a lot of weight to lose. For example, I do know folks who have 2 eggs and 2 slices of toast for breakfast every day. Such a person could have 1 fewer egg or slice of toast on alternating days. But most of us don't eat nearly that regularly.

CarbSane said...

@d4rkboy: Welcome! I've been linked to that study a few times and plan to do a post on it. I have an issue with the classification of the diets in that study, but that's a subject for another day. Anyway, I agree that some low carb diets are definitely more satiating, especially initially. This is how I believe LC works: spontaneous (and often considerable) reductions in caloric intake. It certainly worked for me for a good long time.

What I guess becomes my question these days is if Paleo/Primal/Atkins/InsertLCPlanHere is so satisfying, insulin stabilizing, etc., and it was the insulin that made these folks accumulate fat to begin with, why do we see the familiar "on average" weight loss trajectory of rapid losses up to ~6 months followed by regain? Why do we see the reports of folks regaining even while adhering to low carb? Once this diet has supposedly lowered insulin levels, why do so many followers of these plans plateau out at significantly higher weights than ideal? That latter observation is anecdotal, of course, but with the exception of those who were never obese to begin with, or those who do some sort of diligent fitness training, I don't see many who are truly lean (especially the women).

Sanjeev said...

>> a low-carb, Paleo-style diet was more
>> satiating/calorie ... easier
>> to keep input in line with output

please add "for some", or "for most"

Certainly it's not more satiating just as one extreme example for those born with defective copies of the leptin gene.

And for those like me who have managed to put on weight on most diets ... all meat, all vegetable, all grain, low carb, high carb, high protein, you name it ... who for whatever reason don't seem to have the internal sense to know when to stop eating, but can control weight when the calories are carefully counted out and contolled.

In this regard, Taubes' diet is the worst diet possible.

If one overeats tremendously but following the rules laid out by Pritikin or Ornish, it's not possible to overconsume all that many calories.

If one takes Taubes at his word ("eat as much as you want, absent carbs you canNOT gain fat") and ... overeats zero carb, overeats fatty beef tongue & filet mignon & bacon (unlike what others write about feeling full & satisfied, I can eat this stuff til the cows come home ... and then I'll eat the cows) ... watch out. The number of calories will be just incredible. And, in fact, my heaviest ever weight was "achieved" on Atkins.

CarbSane said...

Sanjeev, if you download the PDF of that study, scroll to the end and take a gander at the dietary compositions and scatter plots of leptin and satiety scores for the individual participants. They are all over the map. Paleos averaged 130g/day carb amounting to just under 40% of total cals. Carb intake in grams on "Mediterranean" (I put that in quotes because this seems more like USDA food pyramid diet if anything) that amounted to just over 40% of total cals since they consumed more. I don't know that this is a fair Paleo v. Med comparison and I see a LOT more scatter in the Paleo dots for everything than I do with the Med group that was far more clustered. Interesting. I'll be blogging more on this one.

d4rkboy said...

Sanjeev, no "diet" will work for everyone. It is not fair to compare the merits of a diet with regard to how well it accommodates individuals with rare genetic defects. The primary principle, as has been stated, is that energy input must be in line with expenditure, end of story. The preference for carbs or fats has much more to do with their impact psychologically and how an individual responds to consuming them.

For instance, carbs do not satisfy me for more than an hour, so when I eat high carb I tend to eat constantly throughout the day and lose track of my energy intake. My energy levels assume the familiar peak and trough that comes with high GI foods. Of course, low GI carbs are another viable option that are usually much more satiating anyway.

Fats and protein, on the other hand, are always more filling to me. Energy levels are much more constant because of their slower absorption profiles. On top of that, protein has the greatest thermogenic effect of the three so that it actually comes in around 3.5-3.8kcal/gram, less than carbs or fat. Thus, high protein diets are likely to be the most filling while containing less usable energy.

In order to truly reap the rewards of a low-carb diet, the amount of carbs needs to drop below 100g, placing the average person in a state of ketosis. Long story short, ketosis involves the mobilization of body fat to produce ketone bodies, which supplement the low glucose levels in the blood. Ketone bodies are less efficient fuel sources, yielding only 7kcal/g as opposed to fat (9kcal/g). In other words, ketosis results in a less efficient mobilization of body fat stores, so more fat is used than if blood glucose levels were normal. In addition, ketone bodies blunt appetite (in average individuals).

CarbSane, I really cannot respond to your anecdotes except to say that I know of many who have been successful in losing all kinds of weight and keeping it off, mostly by restructuring their entire lifestyle so that food is not the sole object of their attention. We are both aware that anecdotes are incredibly unscientific, there are all kinds of reasons why the individuals you know may have followed a traditional weight loss profile.

Sanjeev said...

which paper? I noted nothing about Leptin the first time through "Coordinated Release of acylation ..." and & I'm not seeing anything about leptin in it now ... searching for satiety & leptin produces nothing.

I'll look at the other papers linked above as time allows

CarbSane said...

d4rkboy's Paleo v. Mediterranean link purported to demonstrated better satiety/calorie:

http://www.nutritionandmetabolism.com/content/7/1/85

Sorry about any confusion.

Nick said...

I am new to the board and a long time low Carb'er. 10 years and counting. Thank you for the warm welcome. I have experienced the problems you mention with the diet.

I apologize in advance if I make reference or suggest something that has already been discussed. I will come up to speed on the rest of the site eventually.

On that note; Have you read any of the research by Dr. Weston A Price? Way ahead of his time. I encourage everyone to visit www.westonaprice.org.

CarbSane said...

No problem needing to catch up Nick! I post a lot of stuff in no particular order, but find the labels function of blogging super helpful for organizing things. Also, it's one thing for me to have a hard drive full of PDF's of this or that study, any time I go to reference it, I would have to keep very organized bookmarks. This way I can search my blog, use the tags to find the posts, and have the links to the originals at the ready.

I would be interested in you sharing what problems you've had and how you've worked through them.

I've not read a whole lot at the website per se, but lots of stuff about his writings from numerous discussions.

Nick said...

Working through them! A little background. 10 years ago at Age 17 I was 290lbs at 5'11. Went on Atkins and dropped down to 215 in one year. Then slowly gained back (Up to 285 January of this year) despite severely low crabs at times. I must say the more crabs I ate the quicker I gained. Hard to say how much was fat gain as I also went from 5'11 to 6'4 and am considerably stronger. Right now I am at 260 and slowly dropping.

What have I been doing differently?

1. Low frequency heavy weight training. 1 time a week for about 20 min. Huge strength gains. Cardio strictly for enjoyment.

2. Cut out all artificial sweeteners and noticed joint pain is gone. Was a big diet coke drinker. Now Tea, Coffee (before noon only) and water.

3. Good quality water. It is 70% of our body right? Municipal water supply is badly contaminated. Bottled water is mostly filtered tap and the plastics mimic estorgen in our body. Just started to get my water from a wild spring near where I live. visit www.findaspring.com.

4. Organic produce, grass fed meats, wild fish, raw nuts and seeds. Raw milk, cheese, Pastured chicken, and eggs, 88% cocoa chocolate. Cocoa Nibs ect, oysters.

So far I feel way better and see results. To be honest all this stuff is fairly new so the long term results are not in yet but I will keep you posted on progress. May start adding in wild rice and potatoes(this would be a big change for me). Still will avoid gluten refined carbohydrates and most sugar.

Sanjeev said...

CarbSane said...
Sanjeev, I've been wondering a lot about Richard Hanson in this regard.
__________
I've come across this many times. The folks with day jobs, with their arms in their research up to their armpits, don't have the time to critique pop culture. May not even understand it either.

Like all the physics PhDs who leave it up to the James Randis of the world and assorted like minded folk to critique the misuse of quantum mechanics in the newage, among the Law of Attraction crowd, the "teach yourself ESP" courses, and so on, and so on ....

The researchers may not have some the skills (and certainly not the practice) for it too, the way a performer does. Or the stomach to handle some of the opponents' tactics.

Jonathan said...

CarbSane,

I'm posting back here after getting your reply over in the Taubes blog comment section (aka Jonathan, my full name). I'm still interested seeing the study (in rats?) showing the role of ASP in fat deposition in the context of fat-only meals. Did that study also monitor insulin and glucose levels during the meal? Was the high fat administered on an empty stomach or on top of a recent prior meal? What I have not seen yet (and maybe you have) is any evidence that one can get fatter on an extremely low carb or ketogenic diet.

My working model reading a lot of this stuff is a rough way to estimate the fattening potential of a meal is to multiply the total fat grams by (total carbohydrate grams + 0.5% total protein grams). If either of the two multiplicative factors is zero, the potential for fat accumulation is low, but if both are high (think ice cream and cheesburgers on buns) you are screwed if you want to lose weight. This "model" explains how you could lose weight on a really low fat diet or on a really low carb diet, but don't mix high fat and high carb.

Now if you could show me that a really high fat diet causes fat storage, I'd have to think about that. On the other hand, I've occasionally jump-started weight loss with a "fat fast" -- for example a "cream soda" made by diluting heavy whipping cream (HWC) with sparkling water (very refreshing in summer) or macademia nuts or the like. Not a sustainable diet, but it seems to jump start fat loss.

How can I square that personal observation with ASP or chylomicrons causing fat storage in the presence of zero carbohydrate?

CarbSane said...

I'll get back to you, but in the meantime, check out my latest post on ASP. I have a few thoughts on the fat fast to share, but right now I'm off to procure ingredients for dinner ;)

fredd said...

Hi,

You say:

"Insulin and NEFA initially increased in the first 1-2 hr. As stated above, fatty acid incorporation into adipose tissue (FIAT) was NEGATIVE in the first hour indicating net fat mobilization! This seems an odd paradox, but this is not the first study I've read that demonstrated a release (at least initially) of fat from stores in response to a meal. So early in the postprandial period, insulin does not suppress fatty acid release from the fat cells, nor does it send fats on a one way street into the cells. So the high carbs in the meal do not lead to fat accumulation through the actions of insulin"

and

"Instead, net fat accumulation occurs after the insulin response and correlates with ASP which is stimulated largely by the chylomicrons."

Is it not possible that the spike in insulin during the first 1-2 hours did in fact cause (or I should say, played a major part in) the FIAT that followed the insulin release, but that the response was not as quick as one would assume? I.e. just because large amounts of insulin was secreted during the first 1-2 hours does not mean that as soon as we see it spiking we should expect FIAT.

So instead of seeing instant FIAT ("ala Taubes" - instant fat deposition at the slightest whif of insulin), we are seeing delayed FIAT, albeit still caused (or heavily driven by) by insulin? As FIAT started ramping up after the 60 minute mark, possibly when insulin was heavily cirulating, causing cessation of fat mobilisation and starting fat storage?

Just thinking out loud here...

CarbSane said...

Hi Fredd, when I read comments like this I can't help but think they sound like trying to explain how the evidence could fit a pre-existing theory rather than looking at the evidence such as it is and then formulating a plausible theory that fits it. No doubt insulin has SOME role in fatty acid uptake and esterification. But the major part of that role may well be in stimulating ASP. Insulin has a relatively short halflife and when one looks at glucose and insulin profiles, peak insulin tends to coincide with peak glucose (more or less) and acts quickly to clear it. The glucose clearance doesn't occur an hour after the insulin peak through a delayed action. OTOH, we do see esterification coinciding with ASP. Why ignore the obvious (Occum's razor) there?

Welcome to my blog fredd!

Oh ... and I see I owe Jono a response!

Fred Hahn said...

Go to Frayn's Metabolism book:

http://www.amazon.com/gp/product/1855780488/ref=ord_cart_shr?ie=UTF8&m=A242BDZWH3O9ZO#reader_1855780488

Search "insulin" and page through the results until you get to page 98, Box 4.3, "Synthesis of fatty acids and choleserol from glucose."

Then check out page 117, figure 4:14. "Overview of Fatty Acid and Glucose Metabolism in White Adipose Tissue" and look at the role of insulin."

Read as much as you can of the section on fat storage.

Also, look on page 121 and you'll see that insulin restrains lipolysis. Insulin doesn't have SOME role - it plays a HUGE role in both storage and release.

Disputing a text book is OK of course and should be done if new information comes along but has it?

CarbSane said...

@Fred: On p. 131 of the version of Frayn's MR cited by Taubes it states: "The pathway of lipogenesis, although of interest from the point of view of metabolic regulation, is probably not of major importance as a route of fat deposition in humans on a Western type of diet. The evidence for this is reviewed in Box 5.4. That box cites several overfeeding studies and such. DNL accounts for a few grams of synthesized lipid. Also see:
http://carbsanity.blogspot.com/2010/06/excess-carbs-coverted-to-fat.html (discusses Hellerstein's work)
http://carbsanity.blogspot.com/2010/07/nutrient-fates-after-absorption.html (Jequier)
http://carbsanity.blogspot.com/2010/11/fat-futile-cycling-from-carb-excess.html

Also see what Frayn says in http://carbsanity.blogspot.com/2011/02/non-esteried-fatty-acid-metabolism-and.html

More at my DNL label.

Textbooks are notoriously outdated, especially in the biological fields. I still have my college bio texts. They make for good door stops or a fire hazzard. Not sure which.

Nobody disputes insulin's role in fat tissue. It is the taking out of context that is misleading. Postprandial insulin's immediate actions are not chronic. The fat cells don't go wild hording fatty acids and depriving other tissues of them just because someone ate an insulin provoking food.

Fred Hahn said...

I'm not understanding how the info in the text book I quoted on Amazon is out of date or wrong WRT how insulin affects lipogenesis or lipolysis.

Fred Hahn said...

James K said:

"When you say "the root cause", that implies that there is a single root cause. But why do we assume a single root cause? To me, this is one of the biggest mistakes people make in regards to obesity...assuming that the cause is univariate rather than multivariate."

That's because there is a root cause. Everything else is a derivative of excessive carbohydrate consumption like energy surplus, less energy expenditure, hormonal disruption, etc.

The root cause of lung cancer is smoking. There are reasons why people smoke but the root cause of the disease is the smoking itself.

Here's a question for you and Carbsane. Do you think it's possible for people to become obese eating fatty animal products, non starchy vegetables and drinking water only? If so what would the mechanisms be?

CarbSane said...

Fred, it's not wrong, it's just taken out of context. For example, fructose (no insulin BTW) is the most lipogenic carb - increasing DNL by several fold - but what is the ultimate consequence? 1. FA's are oxidized and not shipped out to the fat cells , or 2. FA's are so miniscule in amount (and require energy to synthesize) as to be irrelevant in the scheme of things.

We're talking couple of grams fat from 100-200g SURPLUS carb. Think about that!!

CarbSane said...

Fred: People will, and have, found ways to gain weight on VLC diets. Eating animal flesh cooked only in its own fat with leafy greens? No obesity. Eating Kitivan style? None either.

Sanjeev said...

>> possible for people to become obese eating
>> fatty animal products, non starchy vegetables
>> and drinking water only? If so what would the
>> mechanisms be?

ASP, g3p and calories in excess Fred. And if you convince people that with zero carbs they can eat as much as they want, many WILL eat excess calories. Guaranted that I would. Guaranteed because when I did zero carb and ate as much as I wanted I "achieved" the highest fat mass of my life.

Taubes already admitted he was wrong on g3p yet maintains the fantasy that without carb you canNOT gain fat mass. And he's still in ASP denial.

Sanjeev said...

> The root cause of lung cancer is smoking. There are reasons why
> people smoke but the root cause of the disease is the smoking
> itself.

I don't know whether to laugh at that or cry.

diagnostic X-rays
Asbestos
viruses
radon
Any radioactive material that can come near the lungs - isotopes of potassium, zinc, whatever ...

lung cancer in non smokers

lung cancer in animals - many of these are experimental animals but many are not

Sanjeev said...

"many of these are experimental animals but many are not "

should have been

"many of these are experimental animals exposed to smoke but many are not"

Sanjeev said...

> think it's possible for people to become obese
> eating fatty animal products, non starchy
> vegetables and drinking water only

quoting someone named FRED: if you think it's not possible YOU need to prove it.

With controlled experiments, not with theories(several of which have now been proved wrong) or with endless repetition of the mantra.

Fred Hahn said...

Sanjeev said:

"And if you convince people that with zero carbs they can eat as much as they want, many WILL eat excess calories. Guaranted that I would. Guaranteed because when I did zero carb and ate as much as I wanted I "achieved" the highest fat mass of my life. "

Prove that!

Sanjeev said...

What's to prove Fred -
"guaranteed that I would"

it happened to me, and I didn't claim it would happen to everybody, just to a few. Ask Lex Rooker. That's two. My point's proven.

Now, where's your mea culpa about smoking?

And where's your proof about "it's impossible to gain fat mass with only meat & non starchy vegetables?

Your standard of proof is far higher - you claim that's true for EVERYBODY. I made no such claim for my stance.

Sanjeev said...

And where's your proof about (paraphrased)

"it's impossible to gain fat mass with only meat & non starchy vegetables?

Sanjeev said...

Please duck your side Fred, as I've now discovered you always do.

Dwell on trivia, as you so frequently do

Ignore direct responses proving you wrong, as you frequently do

Demand from others what you have never satisfactorily provided.

IOW, be yourself Fred; don't ever change.

Sanjeev said...

Oh, yeah, AND prove there's only ONE cause of obesity.

I don't know how you propose to do that ... you would need to list every possible cause and refute every one.

Good luck; your attempt at proof via analogy to smoking and lung cancer was laughable, what are the odds you'll be able to do it rigorously, without analogy?

but you did make the claim.

To quote FRED: PROVE THAT
(!!! !!!!!!!!!!!!)

Fred Hahn said...

"Fred, it's not wrong, it's just taken out of context. For example, fructose (no insulin BTW) is the most lipogenic carb - increasing DNL by several fold - but what is the ultimate consequence? 1. FA's are oxidized and not shipped out to the fat cells , or 2. FA's are so miniscule in amount (and require energy to synthesize) as to be irrelevant in the scheme of things. We're talking couple of grams fat from 100-200g SURPLUS carb. Think about that!!"

Fructose is a separate issue and Taubes discuses this at length.

The bottom line is that by keeping your diet low in carbs, adequate in protein and making sure that you are eating enough veggies to meet the rest of your micronutrient needs not met by animal matter, you are not going to become obese or insulin resistant.

And if you are obese, assuming no hormonal abnormalities that require a physicians intervention (like Hashimoto's Thyroiditis), you will get lean without having to count calories.

What I don't understand is the underlying (and at times overt) sentiment from you, Krieger and others that Taubes, Feinman, Eades, Atkins, etc. are purposefully suppressing and hiding information that would reveal that its really all about calories in calories out.

How anyone can come away with this idea who has read their works either has a serious chip on their shoulder or doesn't fully understand what they are saying - IMHO.

Fred Hahn said...

Sanjeev what are you ranting on about? Please be specific. I never said there aren't other ways to get lung cancer nor did I say that eating too many carbs leading to insulin resistance was the only way to become obese.

Explain to us all what happened to you. I am truly interested to hear the story. So you started eating only meats and non starchy veggies and you became fatter than ever. Please explain how you managed this.

CarbSane said...

Fred: Do you have evidence that eating too many carbs leads to pathologic (e.g. I'm not talking transient IR due to things like a massive fructose incursion or fat meal) insulin resistance?

Also, do you read at all over at Jimmy's LLVLC forum or other places like the Active Low Carber or Low Carb Friends forums? There are literally hundreds of posts by present and former members indicating weight gain, regain and/or stalling out at a weight that is still overweight.

LC does not work for everyone that tries it. In the long run it seems to work for relatively few. Perhaps even a smaller percentage than other dietary approaches.

It's not so much what Atkins, Eades and Taubes hide, it's the gimmicky misinformation they perpetrate that the science DOES NOT SUPPORT. See my Toothpick post re: Taubes and his interview. But there are also omissions that are as intellectually dishonest when one seeks to educate others on a topic. To this day Taubes ignores ASP. It is not controversial that ASP is a potent stimulator of FA uptake/esterification, more potent than insulin. HOW can any treatise on fat metabolism in 2010/2011 fail to include its action?

Fred Hahn said...

"People will, and have, found ways to gain weight on VLC diets."

Carbsane can you please explain this - what do you mean?

CarbSane said...

I thought that was self-explanatory. Many MANY reports of low carbers gaining and/or regaining even while remaining low carb. Does the name Jimmy Moore ring any bells to you? How about Dana Carpender who has gained weight during recipe development for a low carb cookbook? There is also a recovered anorexic who contributes here who has followed a low carb approach to normalizing her weight (obviously upwards).

Fred Hahn said...

"Fred: Do you have evidence that eating too many carbs leads to pathologic (e.g. I'm not talking transient IR due to things like a massive fructose incursion or fat meal) insulin resistance?"

The evidence is indirect since lowering dietary carbohydrate is the only way to correct it. You cant do a preventive study on people.

"Also, do you read at all over at Jimmy's LLVLC forum or other places like the Active Low Carber or Low Carb Friends forums? There are literally hundreds of posts by present and former members indicating weight gain, regain and/or stalling out at a weight is still overweight."

No I haven't been to these sites. More than likely many of these people have developed hormonal disorders like my wife did and/or are drinking too much alcohol, artificial sweeteners, etc. Oh and then there's cheating of course.

"LC does not work for everyone that tries it. In the long run it seems to work for relatively few. Perhaps even a smaller percentage than other dietary approaches."

Q: How are you sure these folks are doing low carb correctly? Would you like to know how many of my clients think low cab means low fat even after I have explained it to them till I was blue in the face, not to mention the cheating that goes on. Jusat yesterday I asked a new-ish client what they had for breakfast and she said "Oatmeal." When I read her the riot act she said "Oh! I thought a bowl of oatmeal with a banana was healthy - you said a low carb diet was a healthy diet Fred." This is a VERY common occurrence in the low carb world. I deal with dozens of people on a daily basis about this and have for 10 years now.

When people finally get it right it works like a charm every single time. Never once have I seen it fail except when there are other serious health issues in play.

"It's not so much what Atkins, Eades and Taubes hide, it's the gimmicky misinformation they perpetrate that the science DOES NOT SUPPORT. See my Toothpick post re: Taubes and his interview."

Can you give me 2 examples of this? I know you have blogged on this before, but if you would please state 2 gimmicky pieces of information that Eades and Taubes have said I'd appreciate it.

"But there are also omissions that are as intellectually dishonest when one seeks to educate others on a topic. To this day Taubes ignores ASP. It is not controversial that ASP is a potent stimulator of FA uptake/esterification, more potent than insulin. HOW can any treatise on fat metabolism in 2010/2011 fail to include its action?"

Forgive me if I missed you already citing the references for this, but could you cite the specific references to support the idea that ASP is a more potent stimulator of FA uptake than insulin. What textbook states this? What scientist is teaching this? As far as I know and in talking many people about this, ASP is secondary at best.

Fred Hahn said...

From Frayn's:

"ASP is a potent stimulator of fatty acid esterification in adipocytes. Thus adipocytes act locally to regulate their own fat storage."

Nowhere in the textbook does it state that it is a more potent stimulator of FAE.

So I decided to contact Dr. Frayn personally. I am awaiting his response.

CarbSane said...

Fred said: The evidence [that carbs cause IR] is indirect since lowering dietary carbohydrate is the only way to correct it. You cant do a preventive study on people.

Firstly, you can at least do epidemiological studies and there's no evidence that folks like the Japanese have high rates of insulin resistance. Secondly, a high fat meal reduces glucose disposal but a high carb meal increases it by stimulating both non-oxidative and oxidative glucose disposal in the cells.

Secondly, instead of relying on shoddy analyses of Shai, look at the results for the diabetics (blogged on here. The highest carb consuming Mediterranean dieters faired better than the low carbers. There's simply no evidence that low carb is the only way to correct it!!

Carbs promote insulin sensitivity.

As to gimmicks: Taubes (1) that you can be a protein and fat glutton and you won't gain weight w/o carbs (since retracted reluctantly), and the whole premise to sell WWGF that carbs make us fat because they stimulate insulin. Eades: (1)we futile cycle off fat excesses and (2) metabolic advantage.

ASP is mentioned in Frayn's latest version of MR, but unfortunately texts are woefully outdated. They are NEVER considered better references than peer review journal articles. Read my latest blog on a Frayn article: http://carbsanity.blogspot.com/2011/02/non-esteried-fatty-acid-metabolism-and.html Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. and ASP is a more potent stimulus to fatty acid uptake and esterification in adipocytes than is insulin.. Search on Frayn here or look at the GCBC fact check label if you need more. Or, try the ASP label. Just a thought.

The low carbers are "doing it right", and as I've stated before, if folks can't be "purists" and stick to any plan what good is it? This is why strict diets ultimately fail -- ALL of them -- for most people.

This is my last reply to counter your claims. If you make a claim YOU need to substantiate it or there's not much point to a one sided discussion. It's not up to me and my readership to refute claims and provide you with our evidence. My blog content can be searched and is tagged so between those things I think you can find what you're looking for if it's there. So please be respectful of my time and do that sort of legwork before asking me to. I don't really have the time and I've gotten roped into wasting enough of it already.

CarbSane said...

Jeez Fred. If only you read this blog!

Fred Hahn said...

Another question Carbsane if I may - given all of the information in Gary Taubes GCBC as well as in his new book Why We Get Fat, are you suggesting that all of the scientists, doctors, hospitals, universities, etc. that promoted low carbohydrate diets for fat loss between 1901 and the late 1950's directly because it was the carbohydrate that was the fattening agent were ALL purposefully trying to hoodwink the public and were commuting intellectual dishonesty?

You realize that Gary over and over again in his books states quite clearly that none of this is his idea. He has never claimed to be the one who finally figured out that its the carbs that make us fat. He is merely reporting what the history is and summing it up.

To accuse him and the Eades of intellectual dishonesty is quite a thing to say.

CarbSane said...

No, but he is being dishonest misrepresenting his own references (Frayn's Metabolic Regulation, but more starkly, Newsholme & Start). It's plain as day Fred. N&H says there's no evidence to support the theory Taubes promoted up until a few months ago! He can't even keep his mea culpas straight.

Secondly, I don't care if there were 1000 references in GCBC or 2. The sections on obesity are sparsely referenced if at all and he states as fact, all too often, old theories as if no new evidence has come down the pike. In one case he even asserts no new measurement methods have been developed.

Eades stated as fact in his latest book that which he has only guessed at in his blog and that for which there is no evidence to support.

Unless provided with a free ebook copy, I won't be reading WWGF. I have better uses for my money.

There's nothing dishonest in promoting LC on its merits. It is dishonest to perpetuate myths.

Sanjeev said...

Fred wrote:
> Sanjeev what are you ranting on about? Please be specific. I never
> said there aren't other ways to get lung cancer nor did I say that
> eating too many carbs leading to insulin resistance was the only way
> to become obese.

That's exactly what you claimed. Please try, try in vain to spin your own words to mean something else. Show your writing to some 3rd parties that actually understand English and have them explain to you what you wrote.

I'll remind you, since you seem to have forgotten

> James K said:

> "When you say "the root cause", that implies that there is a
> single root cause. But why do we assume a single root cause? To me,
> this is one of the biggest mistakes people make in regards to
> obesity...assuming that the cause is univariate rather than
> multivariate."

> That's because there is a root cause. Everything else is a
> derivative of excessive carbohydrate consumption like energy
> surplus, less energy expenditure, hormonal disruption, etc.

The root cause of lung cancer is smoking. There are reasons why
> people smoke but the root cause of the disease is the smoking
> itself.

> Here's a question for you and Carbsane. Do you think it's possible
> for people to become obese eating fatty animal products, non starchy
> vegetables and drinking water only? If so what would the mechanisms
> be?

Sanjeev said...

+ > The root cause of lung cancer is smoking. There are reasons why
+ > people smoke but the root cause of the disease is the smoking
+ > itself.
+
+ I don't know whether to laugh at that or cry.
+
+ diagnostic X-rays
+ Asbestos
+ viruses
+ radon
+ Any radioactive material that can come near the lungs - isotopes of potassium, zinc, whatever ...
+
+ lung cancer in non smokers
+
+ lung cancer in animals - many of these are experimental animals but many are not

Here's my prediction you would try to evade providing explanations. The type of explanation you demanded I provide.

Sanjeev said...

+ Oh, yeah, AND prove there's only ONE cause of obesity.
+ I don't know how you propose to do that ... you would need to list every possible cause and refute every one.
+ Good luck; your attempt at proof via analogy to smoking and lung cancer was laughable, what are the odds you'll be able to do it rigorously, without analogy?
+ but you did make the claim.
+
+ To quote FRED: PROVE THAT
+ (!!! !!!!!!!!!!!!)


You declined to explain your absolute ignorance on lung cancer and the the ONE TRUE CAUSE of obesity.

AS I PREDICTED YOU WOULD. How does it feel to be more predictable than a box of rocks?

Sanjeev said...

Fred wrote:
> I never said there aren't other ways to get lung cancer nor did I
> say that eating too many carbs leading to insulin resistance was the
> only way to become obese

That's exactly what you claimed. One way.

Fred wrote earlier:
> That's because there is a root cause.

Know the difference between "cause" and "causes" Fred?

Again, please show your writing to someone who understands English.

Have them explain "plural" versus "singular".

Sanjeev said...

Google sometimes doesn't let me make one post ... sory for the multiple posts

Fred:
> nor did I say that eating too many carbs leading
> to insulin resistance was the

Again, learn to read. Again, here's what I asked for:

> Oh, yeah, AND prove there's only ONE cause of obesity.

> I don't know how you propose to do that ...
> you would need to list every possible
> cause and refute every one.

Nothing about you proving starches & fatty meats being the root cause, just asking for your proof that there is a "root cause".

you made the claim Fred,
FRED wrote:
> PROVE THAT !
right back atcha Freddy baby.

M. said...

James Krieger ->"When you say "the root cause", that implies that there is a single root cause. But why do we assume a single root cause? To me, this is one of the biggest mistakes people make in regards to obesity...assuming that the cause is univariate rather than multivariate."

Fred -> “That's because there is a root cause. Everything else is a derivative of excessive carbohydrate consumption like energy surplus, less energy expenditure, hormonal disruption, etc.”

CS -> "Fred: Do you have evidence that eating too many carbs leads to pathologic (e.g. I'm not talking transient IR due to things like a massive fructose incursion or fat meal) insulin resistance?"

Fred -> “The evidence is indirect since lowering dietary carbohydrate is the only way to correct it.

Not only bad science, but bad logic. The analogy that Dr. Harris uses is that just because someone with a bad gallbladder might have problems with fatty meals doesn’t mean that fatty meals damaged his gallbladder.

This all becomes kinda funny after a while. Taubes is the T. Colin Campbell of the low carb movement.

CarbSane said...

No worries Sanjeev. I delete dupes when I can and will post a line that I did so.

CarbSane said...

Amen M.!!

This is a huge issue with the lipid hypothesis being repeated with the carb hypothesis.

Sanjeev said...
This comment has been removed by the author.
Sanjeev said...

I write either completely passively, in atonal, boring 3rd person mode or EMPHATICally.

It's funny to read (It was funnier when I used to submit writing assignments at school in EMPHATIC mode, believe me. Good thing I had profs with a sense of humour).

heh ... someday I'll learn a happy medium.

Fred Hahn said...

Carbsane -

Would you like to know what Dr. Frayn said RE: Insulin vs. ASP? I bet you would. Well, tune into my latest blog (I should be done with it in a day or so) to find out.

"N&H says there's no evidence to support the theory Taubes promoted up until a few months ago! He can't even keep his mea culpas straight."

Gary Taubes is not offering HIS theory. When will you get that through your head? Gary like Atkins, Eades, Bruch, Donaldson, Banting, etc. is presenting what doctors and scientists have known for over a century about obesity. It's not GARY'S theory. He has never pretended to be the person who discovered the role insulin plays on fat regulation. He is reanimating an alternative hypothesis to the one that has pervaded the current dogma - a hypothesis that has been known for a long time and has been shown in research to be true.

I really have no idea what you and others keep going on about with this intellectual dishonesty nonsense. Did you actually read the book? I don't think you did.

CarbSane said...

I read GCBC. I read Newsholme & Start. Now you go read my Reference Check post on G3P and show me where I'm off base criticizing your bud.

It is his theory when he pulls it out of his nether-regions!

CarbSane said...

P.S. Care to forward me the email exchange?

Fred Hahn said...

Carbsane -

Could you please give me a direct link to the G3p post? And spare us all the inuendo.

And let me ask you this - aren't we all looking to find what science has to say on this subject? Why do you so adamantly state that certain people are purposefully committing "intellectual dishonesty" when you have no idea of the facts?

Why not first gather the facts instead of making stuff up to fulfill some sort of personal vendetta? That makes for bad science. Worse, it makes for no science at all and at the same time suppresses what we already know about obesity.

You and others set the solution back to the stone age with the calories in, calories out mantra.

Don't you want to know the why and how? Do you really not understand the difference?

CarbSane said...

Fred, I don't have time to find you every link. There's no innuendo for the "us" who actually read here.

http://carbsanity.blogspot.com/2010/11/gcbc-reference-check-part-iii-of-is.html

I'm not the one making stuff up.

Sanjeev said...

Fred:
> It's not GARY'S theory. He has never pretended
> to be the person who discovered the role
> insulin plays on fat regulation

So the Taubes claim (not in these exact words)

"without carbs one canNOT gain fat mass. It's simply impossible, regardless of excess calories."

Came long ago? Care to name several pre-Taubes sources for that? I predict you'll write that was Atkins's claim. Please cite work & page number. I know you won't (you keep fulfilling that prediction too ... demanding but never providing)

Fred:
> give me a direct link to the G3p post?

And how many direct questions have you honestly answered? Or even made a good faith attempt to answer?

There is this thing called a search engine. It took less than 10 seconds to find these

http://carbsanity.blogspot.com/2010/12/oh-nevermind-taubes-and-g3p.htmllink

http://carbsanity.blogspot.com/2010/05/glyceroneogenesis-v-taubes.html link

http://carbsanity.blogspot.com/2010/11/gcbc-reference-check-part-iii-of-is.html link

and down the right hand side there are these tags:

# Glycerol 3P (9)
# glyceroneogenesis (9)


Still waiting on your response to the ROOT CAUSE of lung cancer.

I predicted there would be no substantive answer. How does it feel to be so predictable? You'll try to avoid it again, or provide a non-responsive answer or otherwise sidestep the entire thing.

Your entire post is shot through, reeking and dripping of the attitude that you HAVE the answer, and you write:

> aren't we all looking to find what science has
> to say on this subject

Irony FRED ... learn it, know it, live it. Avoid doing it by accident.


FRED:
>You and others set the solution back to the stone age

If you're going to make wild, unsupported allegations to complement the accusatory, vaguely malicious tone you could do it with a sense of humour.

Like this: I wonder what you know about solutions Fred, considering you precipitated out of the solution long ago ... every solution to every problem, real or imagined, past, present or future, in this and all parallel universes, real or imagined.

FRED:
>You and others set the solution back to the stone age

Wrong blog FRED ... You probably meant to post that on Nikoley & Sisson's blogs.

Fred Hahn said...

"Fred, I don't have time to find you every link. There's no innuendo for the "us" who actually read here."

Thanks for the link.

http://carbsanity.blogspot.com/2010/11/gcbc-reference-check-part-iii-of-is.html

"I'm not the one making stuff up."

I am not accusing you of making anything up. I think you sincerely believe, for whatever reason, that Taubes and Eades are purposefully selling snake oil.

It's just that you are trying so hard to show that Taubes, Eades (my co-author) and others of their ilk are sheisters, that you are falling all over yourself and your facts. I won't go into the details here and now.

My blog on ASP should be done this week.

CarbSane said...

Did you read the link? No comment? He either didn't read his own reference or he lied about what it said. It says point blank "no evidence for the claim" then gives several pieces of evidence that would refute it. Still, Taubes repeated and repeated that you need carb to store fat (wrong) and G3P is rate limiting.

I do hope you'll be including the email exchange in its entirety in that post on ASP.

6WC was full of errors and unsubstantiated claims. So was GCBC.

Crilly Butler said...

"My guess is that you are right: insulin is the primary regulator of both fatty acid uptake and fatty acid release. The ASP story was a nice one but I don’t think it’s been substantiated."
Best wishes,
Keith Frayn

(From a 2011 email)

carbsane said...

There is no confirmation about that email. Call me skeptical on Fred Hahn. ASP plays a clear role in the clearance of dietary fat into adipose tissue. The evidence for this is substantial.

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