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Author Topic:   Good Calories, Bad Calories, by Gary Taubes
molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 309 of 451 (629177)
08-16-2011 9:14 AM
Reply to: Message 307 by purpledawn
08-16-2011 8:22 AM


Re: Triggers for Fat Storage or Use
You didn't show me how Taubes mangled the papers.
1. He neglected to mention leptin.
2. He neglected to mention 81% carbohydrate intake.
3. He neglected to mention the Pima were lean on a carb diet.
I see you've chosen to ignore the evidence.
You just restate Taubes' erroneous claims. To wit:
5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.
6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
The point is that their total energy expenditure is inhibited on diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue.
I addressed each of these in the last post.
You just quoted Guyenet and Guyenet didn't provide any quotes from the book to match his comments. I don't intend to debate Guyenet.
You just provided the quotes!
And I am using Guyenet to support the very same arguments I made upthread.
PD: Obesity is a disorder of excess fat accumulation.
Guyenet: 2. Insulin decreases the release of fat from fat cells.
PD: Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.
Guyenet: 1. Insulin increases appetite.
PD: Diets that are carbohydrate-rich because significant amounts of energy are being lost into their fat tissue.
Guyenet: 3. Carbohydrates increase body fat.
I'm not going to repost the cites.
Either refute the evidence or concede the point.

This message is a reply to:
 Message 307 by purpledawn, posted 08-16-2011 8:22 AM purpledawn has replied

Replies to this message:
 Message 310 by Percy, posted 08-16-2011 9:23 AM molbiogirl has replied
 Message 324 by purpledawn, posted 08-16-2011 5:31 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 311 of 451 (629185)
08-16-2011 9:40 AM
Reply to: Message 310 by Percy
08-16-2011 9:23 AM


Re: Triggers for Fat Storage or Use
The comments from Guyenet seem to be congruent with PD's comments, but with varying degrees of relevance.
???
PD just restated Guyenet's summary of Taubes' hypothesis, using Taubes' quotes.
She didn't address Guyenet's evidence refuting said hypothesis.

This message is a reply to:
 Message 310 by Percy, posted 08-16-2011 9:23 AM Percy has replied

Replies to this message:
 Message 312 by Percy, posted 08-16-2011 9:54 AM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 313 of 451 (629195)
08-16-2011 10:10 AM
Reply to: Message 312 by Percy
08-16-2011 9:54 AM


Re: Triggers for Fat Storage or Use
OK.
PD & I agree re: Taubes' hypothesis.
1. Insulin increases appetite.
2. Insulin decreases the release of fat from fat cells.
3. Carbohydrates increase body fat.
Insulin decreases appetite.
Guyenet writes:
Insulin infused into the brains of baboons causes a suppression of appetite and fat loss, which is consistent with the well-established fact that insulin and leptin have overlapping functions in the brain (10, 11). ... Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13).
Insulin does not inhibit fat release from fat cells.
Guyenet writes:
Knocking out insulin receptors in the brain leads to increased fat mass in rodents, suggesting that its normal function involves constraining fat mass (12).
Guyenet writes:
Insulin is also co-secreted with amylin, which suppresses food intake and body weight (13).
Guyenet writes:
At least two studies have shown that higher fasting insulin is associated with a higher resting energy expenditure, independent of body fatness, not a lower expenditure (14, 15).
High carb diets are not associated with obesity.
Guyenet writes:
New Guinea highland tribe at Tukisenta 1960s and 70s. West Nile district, Uganda, 1940s. Northern Cameroon, 1980s. Most of Asia, 20th century. Kitava, 1990s. Pima, 20th century.
Each of these groups had a diet of ~80% carbs. Each of these groups was lean (until the Westernization of their diets).
Edited by molbiogirl, : sp
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 312 by Percy, posted 08-16-2011 9:54 AM Percy has replied

Replies to this message:
 Message 316 by Percy, posted 08-16-2011 2:02 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 314 of 451 (629212)
08-16-2011 11:15 AM
Reply to: Message 307 by purpledawn
08-16-2011 8:22 AM


Amylin & insulin decrease appetite
Insulin decreases appetite.
Pliquett,R et al The Effects of Insulin on the Central Nervous System - Focus on Appetite Regulation, Horm Metab Res 2006; 38(7): 442-44
Among its many well-known functions, insulin is also a potent anorexigenic hormone, and insulin receptors are widely distributed throughout the central nervous system.
Nirmala, G et al Appetite Regulating Hormones, Veterinary World, Vol.2(6): 242-24
Insulin applied intra-cerebro-ventricularly (icv) inhibits food intake and body weight in rats.
Leptin and insulin are important anorexigenic hormones acting on the hypothalamus.
Encyclopedia of Molecular Pharmacology, Volume 1, Stefan Offermanns, Walter Rosenthal
In the hypothalamus, insulin reduces appetite and stimulates energy expenditure.
Leptin is produced by adipose tissue in direct correlation to the quantity of adipose tissue. Insulin and glucocorticoids also stimulate secretion of leptin. In the hypothalamus, leptin increases satiety, decreases appetite and food intake, increases energy expenditure and stimulates thermogenesis.
Insulin is co secreted with amylin.
Naeve S, et al 2005 Amylin’s inhibitory effect on food intake is not due to malaise in rats. Appetite 44:369
Collectively, the aforementioned effects of amylin (e.g. decreased fat mass, preservation of lean mass, no decrease in EE, and increased POMC) resemble those observed after leptin administration (15).
In summary, our studies demonstrated that peripheral administration of amylin reduced food intake, slowed body weight gain, and selectively reduced body fat in a rodent model of obesity.
Mack C et al Pharmacological actions of the peptide hormone amylin in the long-term regulation of food intake, food preference, and body weight American Journal of Physiology 293:1855
The ability of amylin to reduce acute food intake in rodents is well established. Longer-term administration in rats (up to 24 days) shows a concomitant reduction in body weight, suggesting energy intake plays a significant role in mediating amylin-induced weight loss.
Wielinga, P et al Central amylin acts as an adiposity signal to control body weight and energy expenditure, Physiology & Behavior, 101:45
Amylin (2 pmol/h) significantly lowered body weight compared to saline after 2 weeks of infusion, independent of whether prior body weight was decreased by fasting, increased by voluntary overfeeding or unmanipulated.
Chronic amylin also reduced RQ, implying a preferential oxidation of fat.
There are literally dozens of papers. Care to comment?

This message is a reply to:
 Message 307 by purpledawn, posted 08-16-2011 8:22 AM purpledawn has replied

Replies to this message:
 Message 325 by purpledawn, posted 08-16-2011 6:26 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 315 of 451 (629224)
08-16-2011 12:40 PM
Reply to: Message 307 by purpledawn
08-16-2011 8:22 AM


Increased FFAs in the obese
Guyenet writes:
In obesity, fat tissue is insulin resistant. How do I know? Because the fat tissue of obese people doesn't suppress fatty acid release in response to experimentally elevated insulin or mixed meals as effectively as the fat tissue of a lean individual (18, 19).
Guyenet writes:
There is no defect in the ability of fat cells to release fat in obesity, the problem is that the fat that is released is not being oxidized (burned) at a rate that exceeds what is coming in from the diet, therefore it all ends up back in the fat tissue. Hypothesis falsified (#2).
Fat people release more fat from fat cells, not less.
F. Xavier et al, The Obesity Epidemic: Pathophysiology and Consequences of Obesity, Obesity Research (2002) 10, 97S—104S
The increased levels of free fatty acids (FFAs) found in obese individuals also contribute to the defects in glucose use and storage. As body fat increases, the rate of lipolysis rises, leading to increased FFA mobilization and consequently to increased FFA oxidation in muscle and liver.
Jensen, M et al, Influence of body fat distribution on free fatty acid metabolism in obesity, J Clin Invest. 1989 April; 83(4): 1168—1173.
Plasma free fatty acids (FFA), originating from the release of adipose tissue triglyceride fatty acid, represent virtually the only route by which these fat stores can be transferred to nonfat tissue for net loss via oxidation.
Both types of obesity were associated with impaired suppression of FFA turnover compared to nonobese women.
In summary, the basal release of FFA from adipose tissue to meet lean body mass energy needs is greater in obese women than nonobese women.
Groop, L et al. Effect of insulin on oxidative and nonoxidative pathways of free fatty acid metabolism in human obesity, AJP - Endo July 1992 vol. 263 no. 1
1) Lipolysis in uncomplicated obesity is normally sensitive to insulin; the enhanced FFA flux is simply a consequence of the increased fat mass. 2) Nonoxidative FFA disposal expressed per lean body mass is enhanced in obese subjects and correlates with the increase in plasma FFA concentration and fat mass. 3) Enhanced oxidation of intracellular lipids contributes to the enhanced rate of total lipid oxidation in obese subjects.
There are over 400 cites of this paper alone that support increased FFA levels in fat people. If carb --> insulin --> increased fat storage, how is this possible?

This message is a reply to:
 Message 307 by purpledawn, posted 08-16-2011 8:22 AM purpledawn has not replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 318 of 451 (629240)
08-16-2011 2:36 PM
Reply to: Message 316 by Percy
08-16-2011 2:02 PM


Taubes: All carbs are bad
I've summarized Taubes' thinking accurately.
From GCBC:
[qs]This alternative hypothesis of obesity constitutes three distinct propositions. First, as I've said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of energy intake and expenditure. The second is that [color=red]insulin plays a primary role in this fattening process, and the compensatory behaviors of hunger and lethargy[/color=red]. The third is that carbohydrates, and particularly refined carbohydrates-- and perhaps the fructose content as well, and thus perhaps the amount of sugars consumed-- are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity. [/qs]
He condemns all carbs, not just refined. Particularly refined, not only refined.
Guyenet writes:
At this point, I know some people will be insisting that Taubes is talking specifically about refined carbohydrate, not carbohydrate in general. Taubes does repeatedly suggest in both of his books that all carbohydrate is fattening, but he also suggests that refined carbohydrate and sugar are more fattening.
I have yet to mention yet another problem with Taubes' hypothesis.
Protein raises insulin too.
Guyenet writes:
The II is simply a measure of how much eating a food increases insulin, per unit calorie (28). It turns out, it doesn't correspond with the carbohydrate content of the food very well.
Guyenet writes:
In particular, protein-rich foods such as beef can increase insulin secretion as much as certain starch foods such as pasta, or more. High-protein diets, as many of you know, aid with weight loss.
And unrefined carbs raise insulin as much as refined.
Guyenet writes:
The other problem is that refined and unrefined carbohydrates often have a similar II.
These are well established facts. I can post plenty of supporting research.
But I'm getting the feeling that you disagree with the overall premise about carbohydrates and obesity.
His hypothesis is indefensible. I said it 3 years ago, I'll say it again.
He's just another "expert" who decided the fleece the American public with a fad diet.
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 316 by Percy, posted 08-16-2011 2:02 PM Percy has replied

Replies to this message:
 Message 326 by Percy, posted 08-16-2011 7:43 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 319 of 451 (629241)
08-16-2011 2:38 PM
Reply to: Message 317 by Aware Wolf
08-16-2011 2:12 PM


Internal starvation
Just an FYI.
While we're on the subject, let's address the idea of "internal starvation". Taubes suggests that people overeat because they can't access their fat stores due to elevated insulin. However, obese people have equal or higher circulating free fatty acids and glucose (22, 23), so how is that possible? It's not. The internal starvation model was interesting at the time it was proposed, however the evidence has refuted it since then. If anything, obesity is a condition of "internal excess". This information is readily available in the scientific literature, and I'm sure the numerous obesity researchers he interviewed would have been happy to explain it to him, so it doesn't make sense that he instead relied on his own speculation here.
The whole post is worth a read.
Whole Health Source: The Carbohydrate Hypothesis of Obesity: a Critical Examination
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 317 by Aware Wolf, posted 08-16-2011 2:12 PM Aware Wolf has replied

Replies to this message:
 Message 322 by Aware Wolf, posted 08-16-2011 4:20 PM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 321 of 451 (629247)
08-16-2011 3:27 PM


Where's the genetic evidence, Taubes?
If, as Taubes suggests, obesity is the result of a defect in fat metabolism (carbs --> insulin --> fat), where's the genetic evidence?
There's plenty of genetic evidence that implicates the leptin signaling pathway in obesity, but nothing re: "obesity and insulin action on fat cells."
Guyenet writes:
There are enough proteins that regulate insulin secretion in the pancreas and insulin signaling in fat cells that one would expect genetic variability in these proteins to turn up if it were an important regulator of fat mass, just as genes that regulate leptin signaling and reward sensitivity turn up in these studies. But this is not observed.
Where are the mutations that support Taube's hypothesis? The variant alleles?
There are over 20 single gene disorders that implicate leptin (which affects the hypothalamus, not adipose tissue). There are lots of alleles that implicate leptin.
Guyenet writes:
Of the numerous common gene variants that have been found to associate with BMI variability, and whose function is known, the large majority are expressed in the brain, particularly the hypothalamus, and some are in the leptin signaling pathway (41, 42).
Taubes even mentions one of the genetic studies which implicate leptin, not insulin.
It's also the system that is mutated in the genetically obese rodents he discusses (2, 3).
He just forgets to mention the leptin!

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 323 of 451 (629252)
08-16-2011 4:32 PM
Reply to: Message 322 by Aware Wolf
08-16-2011 4:20 PM


Re: Internal starvation
I imagine your caloric intake is down. That tends to happen with most this-is-to-blame-so-stop-eating-it diets.
Caveman diet, eat right for your blood type diet, atkins diet, low fat diet, low carb diet, zone diet, south beach diet.
Eat all you want, just don't eat this!
And I didn't think you were advocating Taubes' silliness.

This message is a reply to:
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molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 330 of 451 (629368)
08-17-2011 9:01 AM
Reply to: Message 324 by purpledawn
08-16-2011 5:31 PM


Re: Triggers for Fat Storage or Use
So I quoted from the book where I felt Taubes covered the idea where all calories are not equal and what supported my understanding of what Taubes wrote.
I don't intend to debate Tuabes. I intend to discuss the science underlying his hypiothesis.
Please provide cites to support your argument. Not Taubes' quotes. Cites.
What do you think Taubes' central thesis is?
I've already posted it twice. I've even supplied the original quote from GCBC.

This message is a reply to:
 Message 324 by purpledawn, posted 08-16-2011 5:31 PM purpledawn has replied

Replies to this message:
 Message 341 by purpledawn, posted 08-17-2011 11:37 AM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 331 of 451 (629371)
08-17-2011 9:09 AM
Reply to: Message 325 by purpledawn
08-16-2011 6:26 PM


Re: Amylin & insulin decrease appetite
That idea is that processed carbs and sugar cause some people to store too much fat.
As I stated in the last post, I have posted the original GCBC source for Taubes' central thesis.
I haven't claimed anything concerning insulin.
You're arguing Taubes' position on this. Taubes claims it's insulin.
I'll say it again. I care about the underlying science.
Provide the cites to support your argument.
From what I can tell you and Guyenet are upset because Taubes didn't get specific on a cellular level.
Oh. He gets plenty specific. The index is an inch thick, full of cites. Why don't you use the index to support your argument?

This message is a reply to:
 Message 325 by purpledawn, posted 08-16-2011 6:26 PM purpledawn has seen this message but not replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 332 of 451 (629372)
08-17-2011 9:12 AM
Reply to: Message 326 by Percy
08-16-2011 7:43 PM


Re: Taubes: All carbs are bad
Your comments and citations of research seem as full of misrepresentations, misinterpretations, misstatements and errors...
If you want to support that with some quotes, I would be more than happy to discuss it.
There are other factors.
That's not Taubes' position. Carbs = obesity. Period.

This message is a reply to:
 Message 326 by Percy, posted 08-16-2011 7:43 PM Percy has replied

Replies to this message:
 Message 336 by Percy, posted 08-17-2011 10:25 AM molbiogirl has replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 333 of 451 (629373)
08-17-2011 9:29 AM
Reply to: Message 327 by Percy
08-17-2011 6:13 AM


"Insulin increases appetite."
Taubes never says or even suggests anything as simplistic as, "Insulin increases appetite,"
I suggest you look at his discussion of Wilhelm Falta's work. Chapter 22. Page 379. Taubes noted that injecting insulin increased the appetite specifically for carbs.
Edited by molbiogirl, : No reason given.
Edited by molbiogirl, : sp

This message is a reply to:
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molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 334 of 451 (629374)
08-17-2011 9:42 AM
Reply to: Message 327 by Percy
08-17-2011 6:13 AM


that insulin doesn't play a role in fat uptake...
I never said insulin doesn't play a role. I said it's not responsible for shutting down the body's ability to release fat from fat cells, which is Taubes' argument. I said it doesn't increase appetite, as Taubes claims.
...but she wants PD and me to defend a position that neither of us have taken, that Taubes is correct to blame insulin.
Fruit of the poisonous tree. You buy Taubes' argument. Taubes' blames insulin.

This message is a reply to:
 Message 327 by Percy, posted 08-17-2011 6:13 AM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2641 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 335 of 451 (629376)
08-17-2011 10:06 AM


"Insulin increases appetite."
What if It's All Been a Big Fat Lie? - The New York Times
Taube's NYT Magazine article:
Taubes writes:
The science behind the alternative hypothesis can be called Endocrinology 101, which is how it's referred to by David Ludwig, a researcher at Harvard Medical School who runs the pediatric obesity clinic at Children's Hospital Boston, and who prescribes his own version of a carbohydrate-restricted diet to his patients. Endocrinology 101 requires an understanding of how carbohydrates affect insulin and blood sugar and in turn fat metabolism and appetite.
David Ludwig on Endocrinology 101 in the same article:
Ludwig writes:
This, he says, is effectively what happens when we eat carbohydrates...As Ludwig explains, your body effectively thinks it has run out of fuel, but the insulin is still high enough to prevent you from burning your own fat. The result is hunger and a craving for more carbohydrates. It’s another vicious circle, and another situation ripe for obesity.
Taubes' argument: Carbs --> insulin --> increased appetite --> carbs.
Boo yah.

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