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Author Topic:   Good Calories, Bad Calories, by Gary Taubes
molbiogirl
Member (Idle past 2642 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 91 of 451 (465920)
05-11-2008 5:56 PM
Reply to: Message 90 by Percy
05-11-2008 4:28 PM


You're driving both me and you crazy jumping with a big "Aha!" on every little detail, and you've been mostly wrong with your citations so far and wasting both our time.
The devil is in the details. And they are worthy of an "Aha."
Without specific metabolites and their relationship to the known metabolic pathways, then Taubes is doing nothing more than speculating.
And I have revealed 3 holes in his "carb = CHD/diabetes II disease link" hypothesis so far.
And to suggest that "further study is warranted" is ... beyond silly. This is a hot topic. Has been for over a decade.
And yet, despite literally hundreds of papers re: carb metabolism and its relationship to disease, no one else (reputable researchers, I mean) is jumping the gun and touting carbs as the new evil nutrient.
Taubes doesn't have any metabolic pathways of his own, he's just trying to present the research, and I've just been trying to present what he presents.
He doesn't present the research. He selectively picks only that research which supports his position and ignores the rest. He also quotemines papers to support his ideas.
You know, I didn't mention it previously ... but I stumbled across an example of this quotemining when you posted those 3 cites that I had such a hard time finding.
The first paper had one sentence that referred to carbs and sdLDLs. One, Percy. The rest of the paper had nothing whatsoever to do with Taubes' hypothesis.
Book'll be here Wednesday.

This message is a reply to:
 Message 90 by Percy, posted 05-11-2008 4:28 PM Percy has replied

Replies to this message:
 Message 93 by Percy, posted 05-11-2008 6:22 PM molbiogirl has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 92 of 451 (465921)
05-11-2008 6:20 PM
Reply to: Message 88 by Percy
05-11-2008 9:57 AM


Re: Looking for More Country Obesity Data
I'm back to looking into the origins of the "Other countries have a high intake of carbohydrates and don't get fat" information.
I found this at The Economist saying that French figures on obesity are self-reported:
But it points out that the French figures, unlike British and American ones, are based on polls asking people if they are fat. Unsurprisingly, denial intrudes; self-reporting produces underestimates.
If true, that means the data isn't reliable unless there are other studies of how French self-reporting of obesity correlates with reality so that the figures can be adjusted.
Here's something from the Associated Press:
In Cyprus, the Czech Republic, Finland, Germany, Greece, Malta and Slovakia, a higher percentage of men are obese or overweight than the estimated 67 percent of men in the United States, according to a report from the International Obesity Task Force, a coalition of researchers and institutions.
...
Obesity is especially acute in Mediterranean countries, underscoring concerns that people in the southern region are turning away from the traditional diet of fish, fruits and vegetables to fast food high in fat and refined carbohydrates.
One of the countries you mentioned was Greece, and this AP article says that the men of Greece having a higher obesity rate than the US. It also mentions refined carbohydrates as a possible culprit. Oh, next it says this:
In Greece, for example, 38 percent of women are obese, compared with 34 percent in the United States, the group said.
One would think that if your assertion were true that France, Italy and Greece have low obesity rates coincident with high carbohydrate intake that I would find hints of it somewhere.
The intake levels of refined carbohydrates correlates with obesity, so unless France, Italy and Greece strongly emphasize unrefined carbohydrate varieties (e.g., cereals high in fiber, products made from unrefined flour), if they truly have high intake levels of carbohydrates then they should be fat.
--Percy

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 Message 88 by Percy, posted 05-11-2008 9:57 AM Percy has seen this message but not replied

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 Message 96 by molbiogirl, posted 05-12-2008 11:44 AM Percy has replied

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 93 of 451 (465922)
05-11-2008 6:22 PM
Reply to: Message 91 by molbiogirl
05-11-2008 5:56 PM


Okay, I'm done. You're just making stuff up while patting yourself on the back for your great work. Continue the ad hominem by yourself.
--Percy
Edited by Percy, : .

This message is a reply to:
 Message 91 by molbiogirl, posted 05-11-2008 5:56 PM molbiogirl has replied

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 Message 94 by molbiogirl, posted 05-12-2008 11:15 AM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2642 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 94 of 451 (466004)
05-12-2008 11:15 AM
Reply to: Message 93 by Percy
05-11-2008 6:22 PM


I have a biochem final tomorrow.
But here's a thought.
Taubes thinks carbs are responsible for type II diabetes.
Diabetes is one of the oldest diseases known to science. It is described in ancient Egyptian writings from 5000 bee as a disease with frequent urination as a primary symptom. In 100 ad a Greek physician, Areteus the Cappadocian, described it as a chronic condition, "the melting down of flesh and limbs into urine," and named the condition diabetes after the Greek word for "siphon" or "going through." Mellitus, the Latin for "sweet," was added because the urine of people with diabetes was sweet. Thus, diabetes became known as diabetes mellitus the "sweet water" disease. In fact, until the 1800s, when the first chemical test for measuring sugar in urine was developed, diabetes was diagnosed by tasting the urine for sweetness when someone was suspected of having diabetes mellitus (Canadian Diabetes Association [CDA], 2006).
Do you think Taubes would agree that the Egyptians and the ancient Greeks had a dietary carb problem?

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 Message 93 by Percy, posted 05-11-2008 6:22 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2642 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 95 of 451 (466005)
05-12-2008 11:16 AM
Reply to: Message 92 by Percy
05-11-2008 6:20 PM


Re: Looking for More Country Obesity Data
You're not going to find it on google.
Try "french paradox" on scholar.google.

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 Message 92 by Percy, posted 05-11-2008 6:20 PM Percy has seen this message but not replied

molbiogirl
Member (Idle past 2642 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 96 of 451 (466007)
05-12-2008 11:44 AM
Reply to: Message 92 by Percy
05-11-2008 6:20 PM


Re: Looking for More Country Obesity Data
I said historically.
The French and The Greeks have had their obesity rates double in the past few years.

This message is a reply to:
 Message 92 by Percy, posted 05-11-2008 6:20 PM Percy has replied

Replies to this message:
 Message 98 by Percy, posted 05-12-2008 9:05 PM molbiogirl has replied

molbiogirl
Member (Idle past 2642 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.

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 98 of 451 (466043)
05-12-2008 9:05 PM
Reply to: Message 96 by molbiogirl
05-12-2008 11:44 AM


Re: Looking for More Country Obesity Data
In Message 85 you said:
molbiogirl writes:
The obesity and CHD rates for France, Greece and Italy have historically been extraordinarily low.
All 3 countries eat lots of refined carbs.
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). No wonder I couldn't find it, since I was including carbohydrates and obesity in my search. From the abstract for Wine, alcohol, platelets, and the French paradox for coronary heart disease:
In most countries, high intake of saturated fat is positively related to high mortality from coronary heart disease (CHD). However, the situation in France is paradoxical in that there is high intake of saturated fat but low mortality from CHD.
This is from Recent national French food and nutrient intake data:
In comparison with international recommended daily allowances, the food pattern in France seems to be low in carbohydrates and rich in fatty acids, especially in saturated fats as in other developed countries.
The falsity of your claim that carbohydrates are somehow associated with the French paradox is consistent with many of your other claims.
--Percy

This message is a reply to:
 Message 96 by molbiogirl, posted 05-12-2008 11:44 AM molbiogirl has replied

Replies to this message:
 Message 99 by molbiogirl, posted 05-15-2008 2:36 PM Percy has replied

molbiogirl
Member (Idle past 2642 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 2642 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.

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 101 of 451 (466559)
05-15-2008 2:55 PM
Reply to: Message 99 by molbiogirl
05-15-2008 2:36 PM


Re: Looking for More Country Obesity Data
Well, you certainly have an interesting way of making your case, but it doesn't seem to me one that many will find convincing.
--Percy

This message is a reply to:
 Message 99 by molbiogirl, posted 05-15-2008 2:36 PM molbiogirl has replied

Replies to this message:
 Message 102 by molbiogirl, posted 05-16-2008 1:35 AM Percy has replied

molbiogirl
Member (Idle past 2642 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.

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 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

Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 103 of 451 (466664)
05-16-2008 8:44 AM
Reply to: Message 102 by molbiogirl
05-16-2008 1:35 AM


Taubes doesn't say that the insulin response to carbohydrate intake increases VLDL production.
What Taubes does say is that J. W. Gofman's research from the 1950s showed that increased carbohydrate intake correlated with increased VLDL levels. Gofman's technique was to use an ultracentrifuge to separate out the various lipoproteins from blood plasma. Details are sketchy without having the paper in hand (Diet in the prevention and treatment of myocardial infarction is not available on-line), but there's no hint from Taubes that Gofman was analyzing internal metabolic pathways involving insulin or anything else.
Poking around on Google Scholar, I did find a paper concerning a study on rats from 1984 that also indicated a correlation between carbohydrate intake and VLDL levels: Short term essential fatty acid deficiency in rats. Influence of dietary carbohydrates. This article does not mention insulin, but it does mention the correlation between carbohydrate intake and VLDL levels. This is from the abstract:
...whereas the sucrose induced an increase in very low density lipoprotein (VLDL) triglycerides.
Here's what might be a very significant paper by Krauss et. al. (Krauss appears in Taubes book, I think beginning in the chapter you're reading now) titled Effects of a low-fat, high-carbohydrate diet on VLDL-triglyceride assembly, production, and clearance. In the abstract it says:
(a) whole-food LF/HC diets reduce VLDL-TG clearance and do not increase VLDL-TG secretion or de novo lipogenesis;
For any audience we might have, LF/HC is "low-fat/high-carbohydrate". 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.
Here's another Krauss paper that makes a similar point in passing: Metabolic origins and clinical significance of LDL heterogeneity. About carbohydrates it says:
Dietary intervention studies have shown that variation in dietary fat and carbohydrate can strongly influence expression of the small LDL phenotype (152, 153), and contribute to variations in LDL particle size distribution that are observed among individuals and population groups (154). It has been demonstrated in offspring genetically predisposed to phenotype B that a very low fat, high carbohydrate diet can induce expression of this phenotype (155, 156).
Again for the audience, phenotype B means a tendency to obesity and high blood pressure. Anyway, what this passage is saying is that a high carbohydrate diet increases expression of phenotype B, i.e., increases obesity and blood pressure, and also increases the levels of small, dense LDLs. More detail is available by following the references (that's what those number are) whose links conveniently appear in the paper.
I'm distressed that even after you have the book in hand that you continue to criticize Taubes for claims he does not make, and that you even attempt to discredit his book for one of its outstanding qualities, tracing the research all the way back to the late 1800s and providing references every stop along the way.
The urgency you obviously feel to dispatch Taubes' claims is forcing you into many simple errors. This is wasting my time and yours, and it certainly brings you no credit. You claim that the insulin response to carbohydrate intake is to inhibit VLDL production, and whether true or not, no one is disputing this or saying anything to contradict this. Taubes is not saying anything about the cause of the elevated VLDL levels, only the correlation with carbohydrate intake. If what you say is true that it's impossible for it to be produced while insulin levels are elevated, then obviously that's not a factor in the increased VLDL levels. But nobody claimed that it was.
--Percy

This message is a reply to:
 Message 102 by molbiogirl, posted 05-16-2008 1:35 AM molbiogirl has replied

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 Message 104 by molbiogirl, posted 05-16-2008 1:49 PM Percy has replied

molbiogirl
Member (Idle past 2642 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 2642 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.

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