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Author Topic:   Good Calories, Bad Calories, by Gary Taubes
molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 97 of 451 (466013)
05-12-2008 12:04 PM


British obesity on rise since the mid 1800s.
Lifestyle-related diseases such as obesity have come to prominence in the recent past, but the advocacy of regimen to promote health and longevity dates back centuries, if not millennia.
In the second half of the nineteenth century optimistic assumptions about the health benefits of material progress were challenged by medical practitioners who noted a rise in obesity among their middle-class patients due to the combination of an ever more abundant diet and an increasingly sedentary lifestyle.
Modern urban and suburban lifestyles emerged in Britain between the 1870s and 1930s as a result of the combined effect of rapid rates of urbanization, the development of suburbs, a rise of sedentary occupations, and the expansion of rail, urban, and motor transport.
Living standards increased dramatically with rising real incomes and abundant food supplies. Growing access to cheaper food coincided with shorter working hours, less demanding work due to mechanization, and more sedentary jobs.
According to Offer, eating habits failed to adjust to the lighter workloads and, indeed, households shifted toward a richer diet. Opportunity to exercise was frequently limited as walking and physical exertion at work declined, and many followed sport primarily as spectators.
Apart from a brief downturn during and immediately after the First World War, consumer expenditure in real terms continued to grow until the end of the 1930s despite the depression and massive unemployment.
For the middle classes the 1930s represented a "dawn of affluence" characterized by the emergence of a lifestyle more commonly associated with the postwar consumer boom of the 1950s.
The 1921 report singled out "our faulty habits and customs in respect of dietary," which led to a range of ailments amounting to "a substantial degree of impairment of physique-over-feeding-which results in incapacity and invalidity."
The 1926 report highlighted "excessive and unsuitable food combined with lack of fresh air and exercise which sow[ed] the seeds of degeneration."
In 1931, Newman accepted that "some persons no doubt are under-fed, but many are over-fed-giving their poor bodies little rest, clogging them with yet more food, and disregarding the imperative necessity to health and appetite of a thoroughly cleansed alimentary tract."
Zweiniger-Bargielowska, Ina: The Culture of the Abdomen: Obesity and Reducing in Britain, circa 1900-1939
Journal of British Studies (44:2) [Apr 2005] , p.239-273.
In 1910, Americans were eating 210 pounds of wheat flour every year. The commercial bread-slicing machine was invented in 1912 by Otto Rohwedder, and unveiled in 1928.
By 1971 consumption of white bread had dropped to around 110 pounds per year.
We didn't have a "1970s-1990s" like spike in obesity early in the 20th century.

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 99 of 451 (466553)
05-15-2008 2:36 PM
Reply to: Message 98 by Percy
05-12-2008 9:05 PM


Re: Looking for More Country Obesity Data
Poking around in Google Scholar a bit, apparently the French paradox is their low rate of CHD (obesity wasn't mentioned) in light of their high intake of saturated fat (carbohydrates weren't mentioned).
For many decades now, scientists have wondered about the “French paradox.” Despite a high intake of dietary fats (35% to 40% of daily energy), cardiovascular mortality in France appears surprisingly low compared with the other developed countries of Europe and the United States.
Nutrition and Health in France: Dissecting a Paradox
Journal of the American Dietetic Association, Volume 105, Issue 12, December 2005, Pages 1870-1873
France Bellisle
What do you suppose makes up the other 60%?
This is from Recent national French food and nutrient intake data
Key word? Recent.
The French rate of obesity doubled in the last 2 years.
They currently eat low quantities of carbs.
How does that help Taubes?
The falsity of your claim that carbohydrates are somehow associated with the French paradox is consistent with many of your other claims.
How do you suppose researchers figured out that 35-40% of French dietary intake was fat?
They measured total dietary intake. Total includes carbs, Percy.

This message is a reply to:
 Message 98 by Percy, posted 05-12-2008 9:05 PM Percy has replied

Replies to this message:
 Message 101 by Percy, posted 05-15-2008 2:55 PM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 100 of 451 (466558)
05-15-2008 2:54 PM


Well. Now I see why you quoted the same 6 sentences over and over.
Taubes makes mention of LDL (and VLDL) for a total of 3 pages. 170-3.
And, as I've shown, he gets the biochemistry all wrong.
And it's no wonder.
Look at the bibliography, Percy.
The first page. Of 17 cites, 12 are 1970s or older.
The second page 14/22.
The third page. 25/30.
The man doesn't cite recent work!
It's just as I said.
He ignores the vast majority of research. I just had no idea it was this obvious.

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 102 of 451 (466648)
05-16-2008 1:35 AM
Reply to: Message 101 by Percy
05-15-2008 2:55 PM


Let's take a look at a specific example.
On page 156, Taubes makes the claim that "carbohydrates elevate VLDL".
The source of this revelation?
Research from 1958 and 1963.
Current research, however, clearly shows that the insulin response to carb intake inhibits VLDL.

This message is a reply to:
 Message 101 by Percy, posted 05-15-2008 2:55 PM Percy has replied

Replies to this message:
 Message 103 by Percy, posted 05-16-2008 8:44 AM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 104 of 451 (466719)
05-16-2008 1:49 PM
Reply to: Message 103 by Percy
05-16-2008 8:44 AM


What the abstract is saying is that an LF/HC diet reduces VLDL clearance while having no effect on VLDL production. If this research from 1999 holds up then it neatly explains how carbohydrates contribute to increased VLDL levels, since reducing the expulsion rate of VLDL while maintaining the production rate will obviously increase VLDL levels.
There's a problem with your hypothesis.
From the paper:
By contrast, reduced clearance of VLDL-TG does not increase the flux of cholesterol into the plasma.
And there's this:
If increases in dietary carbohydrate elevate de novo lipogenesis, this increase in fatty acid availability to the liver could drive hepatic TG overproduction.
Most previous studies examining the kinetic mechanisms of carbohydrate-induced hypertriglyceridemia have used either short-term (<10 (28).
And this:
All subjects experienced significant elevations in fasting TG concentration on the LF/HC diet.
Significant reductions in LDL, HDL cholesterol, and elevations in VLDL cholesterol were observed.
And this:
LF/HC feeding was associated with significant, 2-fold increases in both the apo B-100 and apo B-48 content of the TG-rich lipoprotein fraction.
As I pointed out earlier, it is the apo particle levels that increase, not TAGs or FFAs.
And this:
Glucose flux data were obtained and showed no effect of diet on glucose production or the sources of endogenous glucose production. The 2 groups did not respond differently to the diets with respect to fatty acid flux or glucose oxidation.
And this:
This conclusion reveals a difference in the underlying mechanism from hypertriglyceridemia observed on higher-fat diets.
First, the transport rate of VLDL-TG (as assessed by the kinetics of TG palmitate) was not increased on the LF/HC diet.
Second, the half-life of VLDL-TG was prolonged, and the clearance of VLDL-TG was significantly reduced.
Third, fasting apo B-48 concentrations were elevated.
Finally, de novo lipogenesis was not increased.
That last line is important. The test subjects did not make more fat.
So. A high carb diet:
(1) Does not increase VLDL production.
(2) Does not increase cholesterol plasma levels.
(3) Does not increase fat biosynthesis.
(4) Reduces LDL levels and cholesterol levels.
(5) Merely increases the time the VLDL particles are in the blood (their half life).
Again. Taubes' conclusions about the biochemistry of carb metabolism is clearly wrong -- recent research does not support his arguments.
Which is why he cites stuff from 60 years ago.

This message is a reply to:
 Message 103 by Percy, posted 05-16-2008 8:44 AM Percy has replied

Replies to this message:
 Message 106 by Percy, posted 05-16-2008 8:44 PM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 105 of 451 (466720)
05-16-2008 1:56 PM


Taubes seems to think that diabetes is the result of dietary carb intake.
As I pointed out earlier, he's got a tough row to hoe, considering it's been around for millenia.
So. Let's take a look at diabetes. Specifically, adult onset diabetes.
Type II diabetes (T2D) has a genetic origin. Studies suggest that the risk varies widely across populations, from 5% or less in White and Asian populations to 50% or more among Pima Indians and South sea Island populations (Elbein et al. 2002). Lifetime concordance rates among identical twins approach 100%.
The genetic status of T2D is being sorted out as we speak. In just the last 2 years, 3 very strong candidate genes have been identified: PPARG, KCNJ11 and TCF7FL2. It was only in 2006 that TCF7FL2 was identified as a T2D gene. Since then, 20 studies have confirmed its association with the disease.
The pertinent question is whether genetic influences are exerted by few “major genes”, each with relatively large effect, or by a large number of “polygenes”, each with relatively minor effect (Stern 2000). Theoretical studies also have emphasized that as few as 20 susceptibility variants may suffice to explain as much 50% of the disease (Yang et al. 2005).
(As few as 20 genes. Huh. And Taubes seems to think that somehow carbs upregulate 20 genes. That's ... remarkable.)
Furthermore, studies have shown that both impaired insulin secretion and insulin action seem to be inherited and could represent the primary defects in glucose metabolism in those at genetic risk of developing T2D (Vauhkonen et al. 1997).
The studies from Lyssenko et al. (2007) confirm earlier findings and establish that the predisposition to T2D is the result of reduced insulin secretion rather than reduced insulin action.
In fact, most of the reliable candidate genes like PPARG, KCNJ11 favor impaired insulin secretion, not insulin action (Damcott et al. 2006; Florez et al. 2006; Saxena et al. 2006; Scott et al. 2006; Chandak et al. 2007).
Now. Here’s the fun part.
The magnitude of the TCF7L2 effect is much higher than any other confirmed T2D candidate. The individual effects of the other variants are modest, ranging from 10 to 30%.
TCF7L2, however, doubles your risk of T2D (Florez et al. 2006). At the same time, tho, it dramatically increases the effectiveness of both exercise and caloric restriction.
And yet Taubes would have us believe that if one eats carbs, one develops diabetes. Bada bing, bada boom. From page xxiii:
They will assume, rightfully perhaps, that the mechanisms of weight regulation and disease are complex, and then make the incorrect assumption that the fundamental causes must also be complex.
Translation: I can’t explain the mechanisms, but I have the answer!
Clearly, this brief outline of current research shows that this is not the case. There is no one “fundamental cause” of diabetes, any more than there is one “fundamental cause” of cancer.
If you’d like to watch a wonderful talk given last year by the guy who discovered the TCF7L2 gene, here it is:
The New Yorker
Elbein SC 2002. Perspective: The search for genes for
Type 2 Diabetes in the Post-Genomic Era.
Endocrinology, 143(6): 2012-2018. 1186-1191.
55: 3630-3634.
Stern Michal P 2000. Strategies and prospects for finding
insulin resistance genes. J Clin Invest, 106(3): 323-
27.
Yang Q, 2005. How many genes underlie the
occurrence of common complex diseases in the
population? Int. J Epidemiol. 34: 1129-1137.
Vauhkonen IIkka,
1997. Defects in Insulin Secretion and Insulin Action
in Non-insulin dependent Diabetes mellitus Are
Inherited. J Clin Invest, 100: 86-96.
Lyssenko Valeriya, 2007.Mechanisms
by which common variants in the TCF7L2 gene
increase risk of type 2 diabetes. J Clin Invest, 117:
2155-2163.
Damcott CM, 2006.
Polymorphisms in the transcription factor 7-like 2
(TCF7L2) gene are associated with type 2 diabetes
in the Amish: replication and evidence for a role in
both insulin secretion and insulin resistance.
Diabetes, 55: 2654 - 2659.
Florez JC, 2006. TCF7L2 polymorphisms and
progression to diabetes in the Diabetes Prevention
Program. N Engl J Med, 355: 241 - 250.
Chandak GR, 2007. Common variants in the TCF7L2
gene are strongly associated with type 2 diabetes
mellitus in the Indian population. Diabetologia,
50: 63-67.

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 107 of 451 (467090)
05-19-2008 2:51 PM
Reply to: Message 106 by Percy
05-16-2008 8:44 PM


But Taubes didn't say that high carbohydrate intake increases VLDL production.
Yes, he does.
P. 177.
It's the journey from VLDL to LDL that explains why most men who have high LDL cholesterol will also have elevated VLDL triglycerides. "It's the overproduction of VLDL and apo B that is the most common cause of high LDL in our society."
That's wrong.
From message 103.
Taubes is not saying anything about the cause of the elevated VLDL levels, only the correlation with carbohydrate intake.
That's not true, Percy.
Page 170-3. Your favorite 6 sentences. He is explicit in his (erroneous) interpretation of the metabolic pathway.
Your argument that an increased VLDL half-life is what Taubes is referring to is suspect. Nowhere in the book does Taubes mention the half-life of VLDL particles.
He does, however, spend 3 pages describing a fictional metabolic process for the production of VLDL particles.
Second. Even if I were to concede for the sake of argument that Taubes may have been referring to the VLDL half-life, of what use it that?
The VLDL particles are NOT converted into LDL particles. The LDL levels fell! Cholesterol levels fell! Nothing happens while the VLDL particles are in the blood.
Half-life simply means the VLDL particles are in the blood for 25 minutes instead of 12.
And finally. Re: your point that Taubes doesn't mention insulin.
Taubes harps on insulin and carbs ad nauseum. From your favorite 6 sentences, page 173.
After we eat a carbohydrate rich meal, the bloodstream is flooded with glucose...
From page 394.
Carbohydrates are singularly responsible for prompting insulin secretion.
There's a darn good reason why Taubes neglected to mention insulin in his fictional account of the metabolic pathway re: carbs and VLDLs (p. 170-3).
The research contradicts his hypothesis.
Krauss and Taubes discuss Taubes' ideas on NPR here:
Not All Calories Are Created Equal, Author Says : NPR
At 7:44, Krauss scolds Taubes to "not oversimplify the science" regarding carbs and body weight regulation.
Krauss goes on to say "There's an awful lot of regulation ... that determines obesity, involving organs like the brain, the intestines, the liver and muscle and involve integrated circuits and are not simply responding to insulin." "Regulation is much more complex than just insulin or no insulin."
Krauss does not agree with Taubes re: carbs/insulin and weight.
Krauss also mentions his research re: sdLDLs and specifically points out that it is those who are already overweight and those that have metabolic syndrome that have elevated levels of sdLDLs.
Variations in the size and density distributions of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles have been related to risk for cardiovascular disease. In particular, increased levels of small, dense LDL particles, together with reduced levels of large HDL and increases in small HDL, are integral features of the atherogenic dyslipidemia found in patients with insulin resistance, obesity, and metabolic syndrome.
Krauss paper.
He immediately goes on to dispute Taubes' simplistic notions re: sdLDLs and carbs.
From the Krauss paper you cited (immediately following what you quoted):
Thus, LDL subclass phenotypes may result from interaction of multiple genetic and environmental determinants, and the trait can be viewed as a marker for the mechanism underlying these effects.
Multiple genetic determinants. Multiple environmental (one of which is dietary intake) determinants.
Immediately preceding your quote:
Estimates of heritability of LDL particle size have ranged from 35-45% (148), indicating the importance of non-genetic and environmental influences. In addition to age and gender, effects on LDL particle size and density distribution have been shown for abdominal adiposity (149), estrogen (150), and oral contraceptive use (151).
And the final sentence of that paragraph and the following paragraph:
On the basis of the strength of the relationship between insulin resistance and the pattern B, small dense LDL has been added to the list of abnormalities that characterize the "metabolic syndrome" (158).
It is noteworthy that a predominance of small dense LDL is commonly found in conjunction with familial disorders of lipoprotein metabolism that are associated with increased risk of premature coronary artery disease. These include familial combined hyperlipidemia (159), as well as hyperapobetalipoproteinemia (160) and hypoalphalipoproteinemia (161). There is evidence that the inheritance of familial combined hyperlipidemia involves at least two major gene loci responsible for increased plasma apoB levels and the second for LDL subclass pattern B (162, 163). Such interactions of the genes underlying pattern B with other genes or environmental factors may contribute to familial dyslipidemic syndromes that are commonly found in patients with coronary artery disease (161).
Metabolic syndrome, hyperlipidemia, hyperapobetalipoproteinemia and hypoalphalipoproteinemia. Not normal folks. Those that suffer from metabolic syndrome, hyperlipidemia, hyperapobetalipoproteinemia and hypoalphalipoproteinemia.
Krauss does not agree with Taubes re: carbs/insulin and weight nor does he agree re: carbs and sdLDLs. He makes that abundantly clear in the interview. He repeatedly chastises Taubes for oversimplifying the science.

This message is a reply to:
 Message 106 by Percy, posted 05-16-2008 8:44 PM Percy has replied

Replies to this message:
 Message 108 by Percy, posted 05-19-2008 3:42 PM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 111 of 451 (467566)
05-22-2008 1:08 PM
Reply to: Message 108 by Percy
05-19-2008 3:42 PM


The NPR link is in the message, Percy.
Always has been.
Krauss was polite but stern with Taubes.
And he made the same points I have been making (repeatedly) in this thread.
The metabolic pathways are extraordinarily complex and interlinked (he calls them integrated circuits).
The metabolic pathways are very tightly regulated.
The metabolic pathways do not have a single trigger, like carbs or glucose or insulin.
And finally, Taubes is oversimplifying the science and doing a disservice both to the science and the public.
btw.
Weight loss plateau = all the water weight gone.
2 weeks = 1 pound lost = ~1500 calories/day is the appropriate caloric restriction level. Not 1200.

This message is a reply to:
 Message 108 by Percy, posted 05-19-2008 3:42 PM Percy has replied

Replies to this message:
 Message 113 by Percy, posted 05-22-2008 2:05 PM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 112 of 451 (467572)
05-22-2008 1:56 PM
Reply to: Message 109 by Percy
05-19-2008 9:09 PM


Re: Getting Back to the Main Point
...but the two are largely in agreement
No. They are not. He contradicts Taubes on every point Taubes tries to make. Taubes brushes him off by saying "Ron's in the public health business".
At 7:35.
If I may say, I think one of the issues that this highlights is that the tendency to oversimplify -- and, for your sake Gary, misinterpret -- the science ... the data you assembled and reviewed clearly reminds us of all that's been done to support the carbohydrate insulin fat connection, but there's an awful lot of regulation that you mention in fat tissue and systems that determine obesity involving organs like the brain, intestine, the liver and muscles that all involve integrated integrated circuits that are not simply responding to insulin and I think we are in a very exciting time scientifically where we are beginning to unravel these networks and realize how tightly controlled they are so that intervening with anything, be it low fat or low carb sets off a whole series of reactions that tend to keep body weight loss from occurring or at least minimizing it...
Krauss does not agree with Taubes. Nor does he support the way Taubes butchers the science.
Krauss writes:
So our research kind of started to resonate with other studies pointing to carbohydrates as being the culprit for much of what is associated not just with these particles but also with a whole constellation called the metabolic syndrome which is triggered by overweight and is influenced by carbohydrate intake among other things.
Metabolic syndrome. Again, allow me to remind our readers that this is not applicable to normal folks.
Once you have metabolic syndrome, yes, carbs play into that. But if you do not have the disease condition, carbs do not have that effect.
These metabolic pathways -- fat metabolism, carb metabolism, etc. -- are very tightly regulated. Very precise. Very functional.
If a disease condition interrupts or disturbs or redirects these processes, then of course things go haywire.
Krauss writes:
Our evidence is that it doesn't affect the dense LDL at all, and in fact substituting carbohydrate for fat, which is a natural consequence of those recommendations, will actually increase levels of the small LDL.
"Substitute carbs for fat". Let's unpack that.
Dr. Krauss mentions (earlier in the interview) the cheap, highly caloric carb snacks that folks gobble up when they go on a low fat diet. Those are the carbs Dr. Krauss is referring to.
He is suggesting that folks cut out the substituting stuff. He also suggest veggies and whole grains.
He does not support the wholesale reduction of carbs and he makes that point repeatedly throughout the interview.
At 19:35.
It's potentially an adverse consequence and an unintentional one...
At 24:04.
First, as Gary pointed out, it's the process of refined starches and sugars that are most deleterious metabolically and the corollary is that foods that contain lots of insoluble fiber and have a low density of energy -- that is, they have a lot of bulk but not a lot of carbohydrate calories are those that have a lot of insoluble fiber -- and a lot of vegetables and whole grains fit into that category...
What happens is people end up eating too many of the other kind of starches...
And Dr. Krauss' sdLDL reference is regarding those who suffer from metabolic syndrome.
Krauss writes:
Variations in the size and density distributions of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles have been related to risk for cardiovascular disease. In particular, increased levels of small, dense LDL particles, together with reduced levels of large HDL and increases in small HDL, are integral features of the atherogenic dyslipidemia found in patients with insulin resistance, obesity, and metabolic syndrome. Increased dietary carbohydrates, particularly simple sugars and starches with high glycemic index, can increase levels of small, dense LDL and HDL, primarily by mechanisms that involve increasing plasma triglyceride concentrations. Low-carbohydrate diets may have the opposite effects. Diets with differing fatty acid composition can also influence LDL and HDL particle distributions.
From here.
In folks with metabolic syndrome!
Taubes' insistence that this happens in normal folks is akin to my suggesting that all smokers will develop lung cancer.

This message is a reply to:
 Message 109 by Percy, posted 05-19-2008 9:09 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 115 of 451 (468025)
05-26-2008 1:50 PM
Reply to: Message 113 by Percy
05-22-2008 2:05 PM


Molbiogirl is claiming it's water loss, as if weight loss will now cease until I cut calories further.
Percy, this is silly. Why would your weight loss stop? Why should you cut you caloric intake further? 1 pound a week or every other week will continue and that is a perfectly acceptable weight loss. It just means it will take a year to drop that remaining 30 lbs, that's all.
(btw. 1#/week is the weight loss you will see with any caloric restriction diet.)
Contradicting her characterization of Dr. Krauss in the NPR interview...
Dr. Krauss repeatedly contradicted Taubes. He even went so far as to tell Taubes "You are misinterpreting the data."
Taubes response? "Huh uh."
From 109:
Krauss writes:
And I think some people, Gary I think has made this statement in his book, that the large LDL particles are not hazardous. Well, it's not all or none...
Translation: Taubes, you are misinterpreting the data again.
From 109.
So our research kind of started to resonate with other studies pointing to carbohydrates as being the culprit for much of what is associated not just with these particles but also with a whole constellation called the metabolic syndrome which is triggered by overweight and is influenced by carbohydrate intake among other things. So that the cholesterol paradigm based upon measuring LDL and worrying about saturated fat has now shifted, or is starting to shift, although we're still not practicing this in terms of our public health recommendations. The rationale is going to need to shift in the direction of lower carbohydrates.
Krauss is talking about carbs in the context of metabolic syndrome, not normal intake.
Krauss isn't the only scientist whose work Taubes mangled. And he's not the only one to speak up.
Scientist #1.
Ask Stanford endocrinologist Gerald Reaven. He's best known for calling attention to "Syndrome X," a cluster of conditions that may indicate a predisposition to diabetes, hypertension, and heart disease. Among Reaven's recommendations for lowering the risk of that syndrome is to reduce consumption of highly refined carbohydrates such as those present in soft drinks and table sugar. But that's where the overlap with Atkins ends.
"I thought [Taubes'] article was outrageous," Reaven says. "I saw my name in it and all that was quoted to me was not wrong. But in the context it looked like I was buying the rest of that crap." He adds, "I tried to be helpful and a good citizen, and I ended up being embarrassed as hell. He sort of set me up."
“The article was incredibly misleading,” says Gerald Reaven, the pioneering Stanford University researcher, now emeritus, who coined the term Syndrome X. “I was horrified.”
Scientist #2.
The very person with whom Taubes chose to end his article, Stanford's John Farquhar, was as livid as Reaven. ... "I was greatly offended by how Gary Taubes tricked us all into coming across as supporters of the Atkins diet," he wrote in an e-mail he broadcast to reporters and to colleagues who were stunned that Farquhar might actually hold the beliefs Taubes attributed to him. "We are against the Atkins Diet," he wrote, speaking for himself and Reaven. "I told him [Taubes] there is the minor degree of merit" to the idea that "people are getting fatter because too much emphasis is being placed on just cutting fats," Farquhar told me. But "once I gave him that opening -- bingo -- he was off and running, even though I said about six times that this is not the cause of the obesity epidemic."
“What I was referring to wasn’t that low-fat diets would make a person gain weight and become obese,” explains Farquhar.
“I meant that in susceptible individuals, a very-low-fat [high-carb] diet can raise triglycerides, lower HDL [”good’] cholesterol, and make harmful, small, dense LDL,” says Farquhar.
"I was greatly offended by how Gary Taubes tricked us all into coming across as supporters of the Atkins diet," says one such source, Stanford University cardiologist John Farquhar. "I think he's a dangerous man. I'm sorry I ever talked to him."
Big Fat Fake
Scientist #3.
“He knows how to spin a yarn,” says Barbara Rolls, an obesity expert at Pennsylvania State University. “What frightens me is that he picks and chooses his facts.”
She ought to know. Taubes interviewed her for some six hours, and she sent him “a huge bundle of papers,” but he didn’t quote a word of it. “If the facts don’t fit in with his yarn, he ignores them,” she says.
Australia's leading consumer advocacy group | CHOICE
Scientist #4.
According to Taubes, Harvard University’s Walter Willett is one of the “small but growing minority of establishment researchers [who] have come to take seriously what the low-carb-diet doctors have been saying all along.”
“There’s a clear benefit for reducing cardiovascular risk from replacing unhealthy fats”saturated and trans”with healthy fats,” explains Willett, who chairs Harvard’s nutrition department. “And I told Taubes several times that red meat is associated with a higher risk of colon and possibly prostate cancer, but he left that out.”
Australia's leading consumer advocacy group | CHOICE
Scientist #5.
It’s not clear how Taubes thought he could ignore ” or distort ” what researchers told him. “The article was written in bad faith,” says F. Xavier Pi-Sunyer, director of the Obesity Research Center at St. Luke’s-Roosevelt Hospital Center in New York. “It was irresponsible.”
Australia's leading consumer advocacy group | CHOICE
Taubes is thoroughly dishonest.
For example, The Post asked Taubes why he made no mention of a review of nearly 50 studies on weight loss in the National Heart, Lung, and Blood Institute’s 1998 Clinical Guidelines on treating obesity. The panel of experts was chaired by Columbia University’s Pi-Sunyer, who has served as president of both the American Society of Clinical Nutrition and the American Diabetes Association.
“Anything that Pi-Sunyer is involved with, I don’t take seriously,” said Taubes. “He just didn’t strike me as a scientist.”
Australia's leading consumer advocacy group | CHOICE
Dr. Dean Ornish and Dr. Barbara Howard kicked the snot out of Taubes on Charlie Rose.
Take a look.
https://www.youtube.com/watch?v=JPyme62niYM
And who are the scientists that publicly support Taubes? Andrew Weil and Mehmet Oz. Birds of a feather!
Edited by molbiogirl, : cite
Edited by molbiogirl, : No reason given.

This message is a reply to:
 Message 113 by Percy, posted 05-22-2008 2:05 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 116 of 451 (468029)
05-26-2008 3:09 PM
Reply to: Message 114 by Percy
05-23-2008 9:49 AM


Krauss believes Taubes oversimplifies the science, he agrees that carbohydrates plays a far more significant role in obesity, diabetes and heart disease than previously believed.
Percy, how you can hear Krauss correcting Taubes over and over again and still come up with this ... interpretation ... is beyond me.
Maybe you're not used to scientist-talk. Krauss was harsh in his criticism.
Concerning metabolic syndrome, we're coming to understand that while some people are more genetically predisposed than others, there is a progression from normal to metabolic syndrome to type 2 diabetes in which carbohydrate intake, particularly refined carbohydrate intake, plays a significant role.
Please don't butcher the science.
It is simplistic to suggest that one is "genetically predisposed" to disease. That is true of nearly every disease.
Carb intake does not play a significant role in the development of metabolic syndrome. If that were true, it would be all over pubmed.
Do the pubmed search yourself, Percy. You will find nothing. Nada. Squat.
Taubes' important contribution is in calling to our attention to the fact that during the precise period when nutritional experts where telling us to reduce fat intake (which means increasing carbohydrate intake, since we have to eat something), the nation got dramatically fatter and more diabetic and atherosclerotic.
Taubes ignores the uptick in caloric intake over the past 2 decades.
And obesity (from increased caloric intake) leads to diabetes and heart disease.
Whenever prosperous folks get their hands on lots of food, they get fat. That has been true for millennia, not just the last 2 decades here in the States.
Over 150 years ago, when Britain's industrial revolution created a middle class, those folks got fat.
The Chinese, South Pacific islanders, Mexicans, South Americans and some African tribes have historically prized obesity (obesity = sign of wealth) and overfed their children (and their women) to plump em up.
* Nauru at 80.2 percent
* Federated States of Micronesia at 70.7 percent
* Tonga at 65.9 percent
* Cook Islands at 65 percent
* Niue at 43.8 percent
http://tojou.wetpaint.com/...y+Trends+by+Geographic+Location
"There were obese people all the way down the ages in the upper classes," Cummings said.
And fat was often revered as a sure sign of good health and prosperity.
The Venus of Willendorf, an ancient carving unearthed in 1908, depicts a robust woman's body with large hips, full breasts and a fleshy belly.
"She's just outright fat," Cummings said.
Percy writes:
We're omnivores with a carnivorous evolutionary background, not glucose processing machines.
I've ignored your anthro stuff so far, but this is too much.
We do not have a "carnivorous evolutionary background".
Where on god's green earth did you get this idea?
This paper presents a review of the fossil evidence for the diets of the Pliocene hominids Anlipithecus ruimidus, Australopithicus anamensis, Australopithicus afarensis and Australopithicus africanus.
The dietary shift from apes to early hominids did not involve an increase in the consumption of tough foods, and so the australopithicenes were not adapted for eating meat.
Mark Teaford and Peter Ungar
Diet and the evolution of the earliest human ancestors
Proceedings of the National Academy of Sciences of the United States of America, Vol. 97, No. 25 (Dec. 5, 2000), pp. 13506-13511

This message is a reply to:
 Message 114 by Percy, posted 05-23-2008 9:49 AM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


(1)
Message 118 of 451 (468109)
05-27-2008 9:24 AM
Reply to: Message 117 by Percy
05-26-2008 7:47 PM


Re: The Character Asassination Continues
Pissed off scientists who have been quotemined by a popsci writer are nothing new.
Pointing out that Taubes is dishonest is easy when half a dozen scientists have come forward to highlight his dishonesty.
It appears that Reaven's objects not to what he is quoted as saying, which he concedes is accurate...
This is disingenuous, Percy.
Of course a quotemine is "accurate" is some sense of that word.
The point each of these half dozen PIs is making is that he ripped their words out of context and twisted them to fit his agenda.
Their science does not support what he says.
Apparently Taubes' descriptions in his book about the zeal with which some researchers defend their status quo is accurate.
Have you any idea how much this sounds like a creo?
The zeal with which researchers defend their work against its misinterpretation is indeed a thing to behold.
Researchers fight all the time. And the squabbling is part and parcel of advancing science. You know that.
It is rare, tho, that they accuse a colleague of quotemining. For good reason. Were a PI to quotemine a paper that he cited in his work, he would be eviscerated by the community as a whole.
Taubes isn't subject to any such community censure, however.
Which is why the bookshelves groan under the weight of unbelievably bad popsci books.
This reminds me of the deception that the producers of Expelled used with Dawkins and Myers.
When their words were ripped out of context, the shit hit the fan. As it should. Deception, like that used by Taubes and by those that made Expelled, is reprehensible.
I have wasted far too much time already tracking many charges and accusations from Molbiogirl that turn out to be false and without foundation.
You know, I've let this pass one too many times, because I didn't want to sidetrack the discussion.
But, since you have chosen to end the discussion, I see no reason to continue to ignore this nonsense.
You have not shown anything I've said to be (1) wrong (2) false (3) inaccurate or (4) erroneous.
I, on the other hand, have caught you with your pants down around your ankles on several occasions.
The latest of which was your wrong/false/inaccurate/erroneous insistence that Taubes did not claim that VLDL overproduction was the end result of dietary carb intake.
At this point it has become just a case of waiting for the next diatribe instead of discussing actual science.
You said you were no longer interested in discussing "the science".
From 107.
From my point of view, trying to figure out the story from individual research papers is like trying to do a jigsaw puzzle where the pieces are the size of grains of sand ... I'm just telling you up front that that particular approach is not where it's worthwhile for me to spend my time.
I can understand your frustration. You don't have access to the literature, for one thing. I do.
However. It is vital to pick apart his bogus arguments using the available research.
For example. I can make the argument that when one eats sugar, the liver converts the available glucose into ammonia and this lowers blood pH which then interferes with brain function.
How would you go about disproving that nonsense?
By referencing the literature, of course.
I have shown that Taubes simply manufactures nonexistant metabolic pathways. No temporary fat storage, no TAG biosynthesis, no overproduction of VLDL particles in carb metabolism, for instance.
Don't you understand that this undermines his entire argument?
There is NO metabolic pathway that fits his description!
I could do the same with the rest of the bogus "science" in his book. I've done quite a bit of the research already.
Dr. Ornish and Dr. Howard did the same thing on Charlie Rose. Picked his arguments to pieces. Using current research.
But you aren't interested.

This message is a reply to:
 Message 117 by Percy, posted 05-26-2008 7:47 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 120 of 451 (468219)
05-28-2008 1:29 PM
Reply to: Message 117 by Percy
05-26-2008 7:47 PM


Scientists don't want the Nobel
Apparently Taubes' descriptions in his book about the zeal with which some researchers defend their status quo is accurate.
Another thought.
Taubes has offered the scientific community the golden key to curing -- not alleviating, but curing -- 3 of the deadliest diseases in the U.S. today ... heart disease, diabetes, and obesity.
#1 - Diseases of the heart (27.2%)
#3 - Obesity (13.5%)
#5 - Diabetes mellitus (3.1%)
But those goddamn scientists are just too blind, just to wedded to the status quo!
Apparently, hundreds of thousands (millions?) of American scientists are just too stubborn to run with Taubes' brilliant idea and pick up a Nobel for their efforts.
The nerve.

This message is a reply to:
 Message 117 by Percy, posted 05-26-2008 7:47 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 122 of 451 (468270)
05-28-2008 6:49 PM
Reply to: Message 121 by Percy
05-28-2008 5:36 PM


Those darn scientists! It's a vast conspiracy!
Percy, don't even front.
You've been talking "to" me in the third person for a week now.
When you're ready to discuss the science, let me know.
And, yes, this means the nitty gritty biochemical details.
Taubes made up, out of whole cloth, biochemical pathways.
It's up to you, or some other forum member, to provide evidence to the contrary.
It speaks volumes that no one on this board has leapt to your defense.
I'm not too awful worried, tho.
I've reviewed the literature and I know Taubes is wrong.
Here's another question for you, Percy.
Name a scientific theory as earth-shattering as "Carbs and carbs alone cause heart disease, diabetes, obesity" that has no support in the scientific community.
Go on. Name one.
Even string theory has a whole host of scientific reseachers willing to stand up for it.
Where're the carb guys?
Why is it that folks like Dr. Atkins (who NEVER published in the peer reviewed literature), Gary Taubes, and Arthur Agaston are out there on their own?
Oh, lest I forget, alt med gurus Dr. Oz and Dr. Weil, too.
Why is it that no one, absolutely no one, who has published in the peer reviewed literature has published anything in support of this ... "theory"?
Even conspiracy theorists have their supporters!
Look at polywater.
In 1966 the Soviet scientist Boris Valdimirovich Derjaguin lectured in England on a new form of water that he claimed had been discovered by another Soviet scientist, N. N. Fedyakin. Formed by heating water and letting it condense in quartz capillaries, this "anomalous water," as it was originally called, had a density higher than normal water, a viscosity 15 times that of normal water, a boiling point higher than 100 degrees Centigrade, and a freezing point lower than zero degrees.
Over the next several years, hundreds of papers appeared in the scientific literature describing the properties of what soon came to be known as polywater. Theorists developed models, supported by some experimental measurements, in which strong hydrogen bonds were causing water to polymerize. Some even warned that if polywater escaped from the laboratory, it could autocatalytically polymerize all of the world's water.
Then the case for polywater began to crumble. Because polywater could only be formed in minuscule capillaries, very little was available for analysis. When small samples were analyzed, polywater proved to be contaminated with a variety of other substances, from silicon to phospholipids. Electron microscopy revealed that polywater actually consisted of finely divided particulate matter suspended in ordinary water.
Gradually, the scientists who had described the properties of polywater admitted that it did not exist. They had been misled by poorly controlled experiments and problems with experimental procedures. As the problems were resolved and experiments gained better controls, evidence for the existence of polywater disappeared.
http://www.cs.cmu.edu/~dst/ATG/polywater.html
Even bogus shit like polywater can garner scientific support.
Wherefore art thou carb-causes-heart-disease-diabetes-obesity supporters?
FYI.
In his own words.
Carbohydrates cause obesity.
https://www.youtube.com/watch?v=JPyme62niYM
10:51
Carboyhydrates cause heart disease, type II diabetes, cancer, Alzheimers.
http://www.blogtalkradio.com/StopSugarShock/2007/...
5:33
Edited by molbiogirl, : sp
Edited by molbiogirl, : cites
Edited by Adminnemooseus, : Shorten display form of long URL, to restore page width to normal.

This message is a reply to:
 Message 121 by Percy, posted 05-28-2008 5:36 PM Percy has replied

Replies to this message:
 Message 123 by Percy, posted 05-29-2008 8:10 AM molbiogirl has replied

molbiogirl
Member (Idle past 2672 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 135 of 451 (468871)
06-02-2008 1:13 AM
Reply to: Message 123 by Percy
05-29-2008 8:10 AM


Carbs are the sole cause of cancer and Alzheimers
Taubes claims that carbs are the sole cause of cancer and Alzheimer's, along with heart disease, obesity and type II diabetes.
As I've said before, Percy, when you are ready to discuss the science, let me know.

This message is a reply to:
 Message 123 by Percy, posted 05-29-2008 8:10 AM Percy has seen this message but not replied

Replies to this message:
 Message 136 by randman, posted 06-02-2008 1:38 AM molbiogirl has not replied
 Message 140 by AdminNosy, posted 06-02-2008 10:18 AM molbiogirl has replied
 Message 176 by Buzsaw, posted 06-06-2008 11:07 PM molbiogirl has not replied

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