I'd like to open a new thread to disscuss Gary Taubes material. hi slecture can be found here

http://webcast.berkeley.edu/event_details....webcastid=21216

the gist of it is that carbs make us fat. but regardless of the gist, I'd like to disscuss the science presented there. his presentation style is fresh enough to merit attention. while I agree with some of his conclusions, I don't agree with others. I'll post my notes and thoughts later.

I'd just like to say that to be an expert you don't have to back your shit up with logic, you just have to go against the grain and shout loud anough. which he does.

those who read the book... is there anything there of any novelty over the lecture?

The book is dense and covers the same thesis as the lecture. It is not referenced which is annoying but its difficult to not come away with a real sense that the scientific support for what is commonly held nutritional wisdom (e.g. that fat is bad for you and makes you fat, that obesity is a function of caloric excess, that carbs are generally more healthy, etc) is seriously lacking and that is, I think, his point.

Hale and Anthony Colpo have criticised his writings. I think Hale did it on forums. Colpo did it in his "They're all MAD" book. You can download this ebook for free from his site.

for me the questions are

1. is the science presented by Taube legit and complete? (both his debunking of the caloric excess and supporting his carb-insulin hypothesis)
2. is the logic presented by Taube to support further deducation and observations legit?
3. what are the implications, beside leannes/obesity of diet as advocated by taube? (on brain, muscle, overall health and longevity). what is teh optimal form of such a diet?
4. if we cover up the holes in 1 and 2, what is M&M's alternative obesity hypothesis?




Here are some of the issues I have, vis-a-vis my points.


1. is the science presented by Taube legit and complete?
most of it is legit. WRT complecity, its obvious taht for clarity there is a cutoff point in terms of nuances and details. that said, thee are some major questions.

a. Taube mentions lypogenesis de novo alot, as if it is something that is fairly frequent in individuals. to my knowledge it is frequent only under certain conditions. VV, Spook, others has debated this alot . I will search more later, but it is a gross generalization IMO.

b. I quote Taube quoting some Edgar Gordon guy: "Lypogenesis is not possible without carbs". woah. this needs to be proved.

c. Taube keeps mentioning Alpha-Glycerol-Phophate as the rate limiting step in TG formation in the cell. he than goes on to say that AGP levels go up in the presence of glucose and that "AGP is directly derived from dierary carbohydartes", whatever the hell that means. again, this seems fishy to me.

d. Taube ignores completley Brain,Ras,HPA,Adipokines. well, he may be saying implicitly (Occam's razor) they being fucked may all be a squale of eating carbs, and may fixed by not eating carbs. this needs to be proved. one small example is:

e. visceral adipose tissue has plenty of fat turnover. if the problem is fat mobiliztion like taube says, how come abdominally obese people don't get thinner? how do they get fat at all? (short answer IMO is they don't oxidize enough of it, how does this sit with Taube's theory?)

2. is the logic presented by Taube to support further deducation and observations legit?
there were several leaps of logic and rhetorical stuff in teh lecture. this is generally fine as sometimes one assumes things are obvious are common knowledge, or plain forgets. some of it is gaping holes

a. antropomorphic obesity. Taube used it to debunk the excess calories hyopthesis but did not explain how it sits with his alternative hypothesis. is one part of teh body eating carbs while the other isn't? or maybe for him it doesnt matter(... stop eating carbs and you'll get thinner reagrdless of where you are fat.) I think this debunks his oversimplified hypothesis. we will get to that.

b. Taube mentioned research showing "Obesity rates going up in the US... in all classes, regardless of education of income". he than goes on to alot about how being poor, with access only to refined carbs, makes you fat. so why are the rich getting fatter? are they missinformed?

c. ancedotally, alot of people are/were on the atkins diet. if the science is so sound, why sin't more people jumping on teh bandwagon? compliance rates just observationally are not that high to something that presented as bulletproof, as are results. some people do get leaner, but to a point. according to taube they should continue to lsoe weight forever.

d. why do people have carb cravings?


3. what are the implications, beside leannes/obesity of diet as advocated by taube? (on brain, muscle, overall health and longevity). what is teh optimal form of such a diet?

a. muscle: ofcourse being diebetic is not optimal to build muscle. but eating VLCD and trying to build/maintain muscle?

relevant study posted by fitencise today - FFA's effect on muscle and insulin.



b. collorectal cancer anyone? (alot of carcinogens from cooked/burned animal protein and fat, not enough fiber and nutrients)

I'll keep coming back to this and update with more questions and answers resolving them

It seems silly to entertain that lipogenesis can't, under any circumstances, occur without carbs. Does Taubes ever explicitly argue for this? My understanding is that he believes carb ingestion is by far the most potent modulator of lipogenesis -- not necessarily the sole modulator. That is, a hypercaloric high carb diet in the sedentary individual will get him fatter faster than with a lo carb diet of the same cals. I think this is the question that ought to be debated here. Additionally, it is important to note that he stresses another facet of his "All calories aren't the same" argument: How different macronutrients effect thermogenesis and other baseline energy expenditure, making their functional caloric value variable according to the status of the whole organism.

Benson - I think you should read this

http://www.thefatlossbible.net/They_Are_All_Mad.pdf

Initially, He does a good job of showing the other side of the coin WRT high carb weight loss. taht said his crticism on Taune shows he missunderstands teh hypothesis presented by Taube. couple taht with the fact he has a book to sell which opposes Taube's theory and we are left with alot of rehotrics and only one scientific refernece throughout teh entire criticism. that's really bad.

BTW, FTR, I agree with Taube's assumption that obesity is a delta E probelm and somethign correlated with being obese causes you get hungry and sedentary, NOT vice versa.

Maybe we can get them both to answer some questions

True. But he also argues strongly that obesity is not a thermodynamic equilibrium issue but is rather a derangement of fat storage. This makes tremendous sense to me now that I think about it. The body has powerful homeostatic mechanisms for controlling energy expenditure and thinking that there will not be compensation for excess or reduced expenditure is a little silly.

I suspect Taubes would argue that if you simply switched someone from a high-carb to a low-carb diet without changing expenditure or caloric intake, they would lose weight. The clinical data support this as do my own N=1 studies...and most people who have really tried Atkins or any other no-carb diet would likely tell you the same.

the argument about causality is a little backward, as those two are tightly correlated (derangement of fat storageand thermodynamic equilibrium)




while what you are saying is true, its incomplete as pointed by me and apparentley by others. I could provide cilinical studies(just look at the link to the pdf) stating otherwise (people faring better on low fat diets) and in Israel where Atkins diet is popular, still there is (ancedotally) lack of consistent results in terms of health benefits, compliance and weight reduction, all 3 are a must for the theory to be valid.

empirical evidence can marely disprove, not prove, a theory.

In all seriousness I would want to abstain from teh low-vs high carb debate, becuase its way too simplistic IMO. and please refute the points I made to prove otehrwise. The namedropping of occam's razor is nice, but it doenst suffice WRT aforementioned issues.

I need to check the link you said before I can respond fully to Taubes' critics but the epidemiological evidence for his case is compelling.



The recent data almost all points in the opposite direction Liorhh...namely that low-carb diets are more effective at producing (and sustaining) weight loss in obese individuals and that they do not produce negative health effects and do, in fact, generally improve markers of chronic CVD. And this all must be considered in the light that it is still strongly contrary to the "party line" in the US to make the claim that fat intake is healthy and that Ancel Keyes was wrong...

This is what I took away from it, and it makes tremendous sense to me as well.

However, I think one problem with Taubes' argument has to do with set point; specifically, set point can only go up, not down (or if it can go down it is very difficult to achieve). So how does this work out for those individuals with a higher than normal set point?

Perhaps not a total aside, our good santa claus-looking doctor Andrew Weil likes the book a lot:
http://youtube.com/watch?v=aoQGRJqGQTs

And Hale keeps getting brought up, but I'd like to see his take on the research presented in the "low carb" thread in the diet forum regarding ASP. He claims that it's responsible for esterification in the absence of insulin but the studies seemed to indicate that it needed glucose to function fully. Of course, this is doubtful that he'd even leave his subforum; I've rarely seen him outside of that or the inner circle.

This is pretty much at the center of the debate...control the insulin and you largely control the deposition of fat. There may be other secondary mechanisms but they appear to also be insulin dependent to some degree or another and if you are not diabetic, the only way to control insulin is to control your carb intake.

The clinical data supports the effects in the real world, low-carb diets work for fat loss and, in general, improve other markers of health. It also makes sense from a developmental standpoint...our digestive systems developed long before agriculture brought us flour and sugar and would be optimized for a diet with nuts and animal fat/protein as the primary energy sources.

I got kind of interested in the Sat Fat thing and found some data online to chart in Excel (chart below). This is European sat fat intake data from 1998, plotted against CHD deaths. The ref I used for the raw data was: http://www.ehnheart.org/files/statistics%202005-092711A.pdf .

The R-squared wasn't monsterous, but this picture is quite different than what I think sat fat is portrayed to do w.r.t CHD risk. There are a lot of other variables that could be in play here as well, but interesting nonetheless.

France of course has long been known for higher levels of fat (and according to this data, sat fat) intake while maintaining very low CHD. This of course lead to the French Paradox discussions. Taubes might say there's no paradox at all.

Or, it could be the alcohol. The French are drinking more alcohol per capita than any other country: http://www.inra.fr/esr/publications/cahiers/pdf/bentzen.pdf. For the red wine arguments, Italy is drinking as much wine as France, but Greece is drinking half as much wine and still ranks respectably in the CHD department. Belgium and the Netherlands eat almost as much Sat Fat as France, drink less than a fifth as much wine (as France) per capita, and have among the lowest CHD risks, so maybe it's not just about the wine.



EDIT: chart should be "deaths per 100,000"

I listed in length my issues with Taube's stuff, please offer somethign new (and I don't want to hear anything about "real world results support". real world results don't support shit, they marely do not disprove).

go on and read colpo's little booklet.

god people, stop spamming the thread with posts containing some personal opinion on taube or with correlation research. this is the advanced hypothesis forum. where's frangible when I need some whiplashing.

I'd love to see him, post something coherent for a change

Colpo's booklet is full of inaccuracies and ignores probably a dozen clinical studies done in humans over the last five years that demonstrate that low-carb diets are generally more effective than low fat diets for weight loss, even independently of energy restriction. Which is why Krieger, et al concluded after a 2006 meta-regression analysis of 87 clinical diet studies that "Low-carbohydrate, high-protein diets favorably affect body mass and composition independent of energy intake, which in part supports the proposed metabolic advantage of these diets."

He does have impressive abs...

About the only thing he got right was that mice and rats are bad proxies for man for studying weight loss...its only in rats and mice that low-carb diets do not work which makes sense given that rodents evolved on a diet of plants and grains.

there is no equality here

controlling insulin is the key to controlling fat deposition = wrong, incomplete

diagram = true, proves nothing really.

this is my point Taube's deduction is half assed, at best.


my points listed above are holes in the logic and science of this theory.

BTW, this "this is what our bodies evolved for" stuff is irrelevant beyond telling some nice stories. our bodies evolved to have average mortality of 17. the past does not equal the present and the world today is not the paleolithic age nor are our epigenetics teh same. its funny how people use this "this is how our body naturally does things" at one time and than say we need to progress and change nature and natural is only to die in the first year of life (more than 50% in paleloithic communities)

You keep saying that but have thus far failed to demonstrate it.

What is the alternative insulin-independent mechanism and why doesn't it work for Type I diabetics?

Colpo's attack on the metabolic advantage people has merit, though I'm not sure if anyone here is arguing that, insolong as insulin is kept in check, that fat storage doesn't happen. It's a very narrow view to a smaller portion of the data presented by taubes in his lecture.

I'm interested in the human data that can be observed, especially the bit about obese people eating under 2000 calories/day. It's science; we can check these facts.

Hold on

if something is not insulin depenent it doesn't mean its insulin independent. it coudl be multi faceted.

anyway I'm wasting time on this. I'm going to address those points myself.

Okay lets make it simpler. Is fat storage in humans accomplished in the absence of insulin? If so, what is the mechanism?

If there is not an insulin-independent mechanism, then if you can control insulin, you can control fat storage and you can control insulin by choosing foods that invoke a minimal insulin response when consumed. That is Taubes' central thesis and I have yet to see anyone put a substantial hole in it.

I agree.



About DNL:

http://www.mindandmuscle.net/forum/index.php?showtopic=31581

Am J Physiol Endocrinol Metab. 2002 Jan;282(1):E46-51.

Increased hepatic lipogenesis but decreased expression of lipogenic gene in adipose tissue in human obesity.

Diraison F, Dusserre E, Vidal H, Sothier M, Beylot M.

Institut National de la Santé et de la Recherche Médicale Unité 499, Faculté RTH Laennec, 69008 Lyon, France.

To determine whether increased lipogenesis contributes to human obesity, we measured (postabsorptive state), in lean and obese subjects, lipid synthesis (deuterated water method) and the mRNA concentration (RT-competitive PCR) in subcutaneous adipose tissue of fatty acid synthase (FAS) and sterol regulatory element-binding protein (SREBP)-1c. Before energy restriction, obese subjects had an increased contribution of hepatic lipogenesis to the circulating triglyceride pool (14.5 +/- 1.3 vs. 7.5 +/- 1.9%, P < 0.01) without enhancement of cholesterol synthesis. This increased hepatic lipogenesis represented an excess of 2-5 g/day of triglycerides, which would represent 0.7-1.8 kg on a yearly basis. The lipogenic capacity of adipose tissue appeared, on the contrary, decreased with lower FAS mRNA levels (P < 0.01) and a trend for decreased SREBP-1c mRNA (P = 0.06). Energy restriction in obese patients decreased plasma insulin (P < 0.05) and leptin (P < 0.05) and normalized hepatic lipogenesis. FAS mRNA levels were unchanged, whereas SREBP-1c increased. In conclusion, subjects with established obesity have an increased hepatic lipogenesis that could contribute to their excessive fat mass but no evidence for an increased lipogenic capacity of adipose tissue


Am J Clin Nutr. 2001 Feb;73(2):253-61.

Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men.

Marques-Lopes I, Ansorena D, Astiasaran I, Forga L, Martínez JA.

Departments of Physiology and Nutrition and of Food Science, University of Navarra, Pamplona, Spain.

BACKGROUND: Adjustments of carbohydrate intake and oxidation occur in both normal-weight and overweight individuals. Nevertheless, the contribution of carbohydrates to the accumulation of fat through either reduction of fat oxidation or stimulation of fat synthesis in obesity remains poorly investigated. OBJECTIVE: The objective of this study was to assess the postprandial metabolic changes and the fractional hepatic de novo lipogenesis (DNL) induced by a high-carbohydrate, low-fat meal in lean and overweight young men. DESIGN: A high-carbohydrate, low-fat meal was administered to 6 lean and 7 overweight men after a 17.5-h fast. During the fasting and postprandial periods, energy expenditure (EE), macronutrient oxidation, diet-induced thermogenesis, and serum insulin, glucose, triacylglycerol, and fatty acids were measured. To determine DNL, [1-13C]sodium acetate was infused and the mass isotopomer distribution analysis method was applied. RESULTS: After intake of the high-carbohydrate meal, the overweight men had hyperinsulinemia and higher fatty acid and triacylglycerol concentrations than did the lean men. The overweight group showed a greater EE, whereas there was no significant difference in carbohydrate oxidation between the groups. Nevertheless, the overweight men had a marginally higher protein oxidation and a lower lipid oxidation than did the lean men. DNL was significantly higher before and after meal intake in the overweight men and was positively associated with fasting serum glucose and insulin concentrations. Furthermore, postprandial DNL was positively correlated with body fat mass, EE, and triacylglycerol. CONCLUSION: After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional hepatic fat synthesis than did lean men.


and other studies.

All that matters is if you think you are healthy.


Self-rated health showed a consistent association with serum HDL-cholesterol in the cross-sectional Oslo Health Study.Tomten SE, Høstmark AT.
Norwegian School of Sport, Physical Education, Box 4014 Ullevål Hageby, 0806 Oslo, Norway. sissel.tomten@nih.no

OBJECTIVE: To examine the association between serum HDL-cholesterol concentration (HDL-C) and self rated health (SRH) in several age groups of men and women. STUDY DESIGN AND SETTING: The study had a cross-sectional design and included 18,770 men and women of the Oslo Health Study aged 30; 40 and 45; 69-60; 75-76 years. RESULTS: In both sexes and all age groups, SRH (3 categories: poor, good, very good) was positively correlated with HDL-C. Logistic regression analysis on dichotomized values of SRH (i.e. poor vs. good health) in each age group of men and women showed that increasing HDL-C values were associated with increasing odds for reporting good health; the odds ratio (OR) was highest in young men, and was generally lower in women than in men. Odds ratios in the 4 age groups of men were 4.94 (2.63-9.29), 2.25 (1.63-3.09), 2.12 (1.58-2.86), 1.87 (1.37-2.54); and in women: 3.58 (2.46-5.21), 2.81 (2.23-3.53), 2.28 (1.84-2.82), 1.61 (1.31-1.99). In the whole material, 1 mmol/L increase in HDL-C increased the odds for reporting good health by 2.27 (2.06-2.50; p<0.001), when adjusting for sex, age group, time since food intake and use of cholesterol lowering drugs. Chronic diseases, pain, psychological distress, smoking, alcohol, length of education, and dietary items did not have any major influence on the pattern of the HDL-C vs. SRH association. CONCLUSION: There was a consistent positive association between HDL-C and SRH, in both men and women in four different age groups, with the strongest association in young people.

ofcourse DNL happens in fatties.

but does it happen in non-obese individuals. how does this pertain to antropomorphic fat deposists i.e pear vs apple.

Benson, check this hole:

visceral adipose tissue has plenty of fat turnover. if the problem is fat mobiliztion like taube says, how come abdominally obese people don't get thinner? how do they get fat at all?
VAT is insulin resistance, so according to Taube one who has VAT should get fat in one's insulin sensitive tissue first (legs). but guess what. there are people who will show vains in their legs while still adding VAT like a mofo.

what the hell does it have to do with this topic?

He mentions the issue of people with screwy fat deposition patterns in the Berkely lecture and points out that its difficult to explain why people get fat in one part of their body and remain lean in others...I'd guess this has more to do with individual gene expression.

But carbs pack on VAT, especially for men...they don't call it a beer belly for nothing.

I would think that people with beer bellies tend to exhibit some insulin resistance in general, assuming they don't put on fat anywhere else.

of course, as you like, say.
(but it is not a question of coming to hasty conclusions)

same thread

post 5
http://www.mindandmuscle.net/forum/index.php?showtopic=31581

Obes Res. 2003 Sep;11(9):1096-103.

Effect of carbohydrate overfeeding on whole body and adipose tissue metabolism in humans.

Minehira K, Bettschart V, Vidal H, Vega N, Di Vetta V, Rey V, Schneiter P, Tappy L.

Institute of Physiology, University of Lausanne, Lausanne, Switzerland.

OBJECTIVE: To evaluate the effect of a 4-day carbohydrate overfeeding on whole body net de novo lipogenesis and on markers of de novo lipogenesis in subcutaneous adipose tissue of healthy lean humans. RESEARCH METHODS AND PROCEDURES: Nine healthy lean volunteers (five men and four women) were studied after 4 days of either isocaloric feeding or carbohydrate overfeeding. On each occasion, they underwent a metabolic study during which their energy expenditure and net substrate oxidation rates (indirect calorimetry), and the fractional activity of the pentose-phosphate pathway in subcutaneous adipose tissue (subcutaneous microdialysis with 1,6(13)C2,6,6(2)H2 glucose) were assessed before and after administration of glucose. Adipose tissue biopsies were obtained at the end of the experiments to monitor mRNAs of key lipogenic enzymes. RESULTS: Carbohydrate overfeeding increased basal and postglucose energy expenditure and net carbohydrate oxidation. Whole body net de novo lipogenesis after glucose loading was markedly increased at the expense of glycogen synthesis. Carbohydrate overfeeding also increased mRNA levels for the key lipogenic enzymes sterol regulatory element-binding protein-1c, acetyl-CoA carboxylase, and fatty acid synthase. The fractional activity of adipose tissue pentose-phosphate pathway was 17% to 22% and was not altered by carbohydrate overfeeding. DISCUSSION: Carbohydrate overfeeding markedly increased net de novo lipogenesis at the expense of glycogen synthesis. An increase in mRNAs coding for key lipogenic enzymes suggests that de novo lipogenesis occurred, at least in part, in adipose tissue. The pentose-phosphate pathway is active in adipose tissue of healthy humans, consistent with an active role of this tissue in de novo lipogenesis.






there is no only one cause for everything.
(but if, for the first step, fat accumulation; carb overfeeding)


by me at:
Visceral fat.
http://www.cuttingedgemuscle.com/Forum/sho...?threadid=18252


Clin Endocrinol (Oxf). 2007 Mar;66(3):440-6.

Intra-adipose sex steroid metabolism and body fat distribution in idiopathic human obesity.

Wake DJ, Strand M, Rask E, Westerbacka J, Livingstone DE, Soderberg S, Andrew R, Yki-Jarvinen H, Olsson T, Walker BR.

Endocrinology Unit, Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Scotland, UK.

OBJECTIVE: Causes of visceral fat accumulation include glucocorticoid excess or decreased oestrogen/androgen ratio either in plasma or within adipose tissue. In obese subjects, the intra-adipose cortisol-generating enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is increased, but information on sex steroid signalling is sparse. We aimed to test associations between body fat or fat distribution and mRNA transcript levels for androgen and oestrogen receptors and for enzymes metabolizing sex steroids in adipose tissue. DESIGN: A cross-sectional study. PATIENTS: Forty-five healthy men and women with body mass index (BMI) 21-36 kg/m(2). MEASUREMENTS: In subcutaneous adipose biopsies we measured mRNAs for enzymes metabolizing local oestrogens (aromatase) and androgens [5alpha-reductase type 1; AKR1C2 (3alpha-HSD3); AKR1C3 (17beta-HSD5, 3alpha-HSD2)] and for sex steroid receptors [oestrogen receptor (ER)-alpha and androgen receptor (AR)]. We related these to body fat mass and distribution. RESULTS: Generalized obesity (BMI) was associated with increased aromatase mRNA (r = 0.35, P < 0.05). Central obesity (waist : hip ratio) was associated with mRNA for AKR1C2 (r = 0.28, P < 0.05) and AKR1C3 (r = 0.38, P < 0.01) but not aromatase (r = 0.06). 5alpha-Reductase type 1, ER and AR mRNA levels did not predict fat amount or its distribution. CONCLUSION: These data on transcript levels suggest that, in idiopathic obesity, increased intra-adipose oestrogen generation by aromatase predicts peripheral fat distribution, while androgen metabolism by AKR1C isoforms predicts central fat distribution, supporting the hypothesis that intra-adipose sex steroid metabolism is a determinant of gynoid vs. android patterns of body fat.


Glucocorticoids and Mineralocorticoids play its role also, again incremented by visceral fat.

Int J Obes (Lond). 2007 May;31(5):864-70.

Adipocyte-derived products induce the transcription of the StAR promoter and stimulate aldosterone and cortisol secretion from adrenocortical cells through the Wnt-signaling pathway.

Schinner S, Willenberg HS, Krause D, Schott M, Lamounier-Zepter V, Krug AW, Ehrhart-Bornstein M, Bornstein SR, Scherbaum WA.

Department of Endocrinology, Diabetes and Rheumatology, University Hospital Düsseldorf, Düsseldorf, Germany.

read:

http://www.cuttingedgemuscle.com/Forum/sho...?threadid=18252




.

.



Less oxidation, because of reduced of levels of adiponectin (Caused by Cytokines).
Increased lipolysis cos of TNF-a and IL-6 (Cytokines) increased levels (secreted by visceral fat)
Il-6 cause directly, insulin resistance at the liver.
TNF decreases Periplin concentrations (Perilipins are phosphoproteins found in adipocytes on the surface of triacylglycerol droplets that act as gatekeepers, preventing lipases from hydrolyzing triacylglycerol to facilitate the release of FFAs) consecuently promote insulin resistance.




.

duh oswaldo. (close but no cigar)
I'll rephrase the obvious - does lipo de novo happen when not carb overfeeding?

regarding VAT you're missing AT/Cortisol ofcourse

VAT and SAT are different. in people like you and me (and fatties), one is IR, one is not

not missing.
post 29 in this thread.



read:
by me at:
http://www.cuttingedgemuscle.com/Forum/sho...?threadid=18252

and

http://www.mindandmuscle.net/forum/index.php?showtopic=27508



.

.









i answered your question.

or do you like, endless rephrasing ?







laughs.......... but the answer is yes, again !










.

That's what I was saying. People who are (relatively) thin but have a large amount of VAT are probably IR.

hmm I thought it was well known that carb overfeeding causes DNL otherwise the low fat fad would have worked. you bothering to answer the obvious (and than spam about it), great.

does DNL of any significance happen when eating small amounts of carbs?

not really (think a bodybuilder)

I'm not sure you can so casually discount developmental biology....don't you find it somewhat telling that although there are essential fatty acids and essential amino acids, there is no such thing as an "essential carbohydrate"?

A human can live forever on a diet of animal flesh with a little supplemental vitamin C but the same human, given a multivitamin and a diet of unlimited bread, sugar beets and casava root and no fats or complete proteins, would be seriously ill in one month and dead in three even though there would be calories to spare. This tells me something about the relative value of carbohydrates to our digestive systems. Cows are designed for carbs, we are not.

.






rephrasing again ?

High fat diets prevent ampk activation in muscle. bad for fat loss, inslins sensetivity of msucle, etc.

Which is, of course, why they are more effective than low fat diets at inducing fat loss and improving insulin sensitivity...

PMID: 15616799
PMID: 15817850

thanks for the info and feedback, lets keep this going.

lets see:

15616799
I dont' see how this research dispells my concerns with blankHF reccomendations. HF may have some advantages over HC?I'm not advocating HC. I don't see what it adds to the always no carb argument. furthermore, check it, from the abstract
ouch. PS thsoe researcehrs are stupid and their conclusions are dumb. reduce saturated fatty acids even more on a HC diet? lunies. anyway. you see I do agree with you that some of teh low carb ideas are good intial gudielines but they are no panacea and cureall, taube sciecne is dubious and is logic is full of holes, they are problematic in many scenarios and shold be tinkered with according to the phenotype and goal.

15817850
dude the HF diet here is 37% carbs. you were saying?

you're like that car from the transformers movie which only can only talk by quoting others.

In this case, that's only during endurance activities. Says so in the title.

Solution: HIIT

bolocks. hiit is not for faties. tehy need ampk all the time, not alot of it for short periods. hiit is good for when you are leaner. anyway teh breaks put on by the brain prevent faties from really hiit.

"dude" I can't keep doing this.

You know how to use PubMed as well as I do and I have no idea how you can come away from a review of any of the dozens of studies done on the relative merits of high fat vs high carb diets done in the last seven years without an understanding that they are better for short and long term fat loss and improve insulin sensitivity and and triglyceride levels.

Which makes sense because there is no insulin-independent mechanism for fat storage that is worth a tinker's dam in terms of effect. If this is incorrect, please post some reference that shows it to be.

fat storage is not the prblem with fat people. its working just fine, its not in any sort of over drive like Taube's tries to epxlain, on the contrary in certain tissues and cases they don't creat new fat cells when they are too fat as angiotensin supresses diffrentiation and increases prolifferation... there is plenty of fatty acid turnover in fatties, much more than lean people. how can that be the problem? a very simple pubmed or search of MnM will remind you that. why are you resorting to rhetorics? I'm using clear explanation and logic. the reductionism from those research to the real world is not working. why should research saying very obese people got a little leaner on 37%C, 45%F, apply to you and me, or other people, to eliminate all carbs, jsut because?

every time I ask you to explain how the results prove a theory, you come up with dubious scinece, every time I ask you the explain the dubious scinece, you come up with unrelated results. and add a little rhetorics like "can't you see", "it makes sense", "real world results"... this could go on and on. obviously I'm tired of it so start backing your stuff with something better.

I have provided a least half a dozen studies that support the proposition that low/no carb diets are more effective for weight loss than low fat under various caloric conditions and another half dozen showing that they improve lipids (triglycerides), inflammation markers and insulin sensitivity. It should come as no surprise that most of the diet studies were done in obese people.

You have yet to produce one reference to refute Taubes central idea that controlling insulin will control fat deposition and that, in the absence of insulin, fat deposition is essentially impossible. If Taubes is wrong, you have yet to explain why diabetics, lean or otherwise, will lose body fat if provided with insufficient exogenous insulin. And given that a low-carb diet reduces serum insulin levels by greater than 1/3 in normal weight men (PMID: 12097663) we can extrapolate that such a diet would also reduce the rate of fat deposition even in the face of a caloric excess because insulin is, for all intents and purposes, required for fat deposition.

But even beyond fat control, the ability of low-carb diets to favorably influence TAG and CRP levels in obese and normal weight men and women alone should recommend them over high-carb.

I don't agree with the idea that a person can eat unlimited calories in so long as they keep carbs low; eat enough protein and you're going to get a fair amount of glucose generated. ASP is there and imparts esterification, though I've yet to find a study that indicates this happens in the absence of insulin or to the same degree (dose/response).

That said, type 1 diabetics dying without insulin, no matter the amount of calories, is too important to ignore. I also believe that, as evidenced, low carb is individual and ketosis is likely not needed to reap the benefits of such a diet. As much as I hate to agree with the midget, Polquin's notion that very few athletes (and most every weekend warrior) needs more than 1g/lb of carbs has some level of merit.

I don't udnerstand why is this rehashed. who said its not true. insulin is part of the storage pathway when its not fucked up. seriuosly I'm not sure why you think its a new idea of some sort. but from this to "all weight loss and metabolic sydromes, CV stuff, is solved just by removing carbs, not related to exercise, food selection, micronutrients, with no regard to phenotype, fattiness, regards to perfomance (cognitive, immune, sports, etc)" this is ridiculous. where is the science supporting thsi simplistic bullshit. there is no science. I have many more things to say about this but will hold, I'm workign on a grander project that will answer thsoe questions as well, so unless you have some new sciecne to contribute or other input, hold put.