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The answer seems to be no, at least for muslims.

From http://care.diabetesjournals.o...: "The prevalence of diabetes in several countries with large Muslim populations appears to be similar to the rates observed in western countries and increasing by 10% per year as a result of urbanization and socioeconomic development."

I haven't the patience to search for research on other religions. I do know (from Indian colleagues with diabetes) that South-East Asian populations are genetically predisposed towards a greater diabetes incidence.

When humans stop eating meat and switch to whole-food plant based diets, the rates of all leading causes of death (obesity, cancer, heart disease, and pretty diseases of inflammation) drop. To anyone with a scientific mind, modern nutritional-science's data should pretty much indict animal based foods as the direct cause of obesity, along with the consumption of heavily processed foods. It's no wonder that the nations with the highest meat consumption have the highest rates of lifestyle diseases like obesity, diabetes, heart disease, etc.

A tiny sample of the tens of thousands of papers stemming from clinical studies of meat's role in disease
Non-industry funded Research

Meat consumption is associated with obesity and central obesity among US adults
International Journal of Obesity (2009) 33, 621–628; doi:10.1038/ijo.2009.45; published online 24 March 2009
http://www.nature.com/ijo/journal/v33/n6/abs/ijo200945a.html

DIET, OBESITY, AND RISK OF FATAL PROSTATE CANCER
Am. J. Epidemiol. (1984) 120 (2): 244-250. 1.
http://aje.oxfordjournals.org/content/120/2/244.short

Diet and body mass index in 38000 EPIC-Oxford meat-eaters, fish-eaters, vegetarians and vegans
International Journal of Obesity (2003) 27, 728–734. doi:10.1038/sj.ijo.0802300
http://www.nature.com/ijo/journal/v27/n6/abs/0802300a.html

Prevalence of obesity is low in people who do not eat meat.
Key T, Davey G. BMJ: British Medical Journal. 1996;313(7060):816-817.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2352221/

Meat consumption and prospective weight change in participants of the EPIC-PANACEA study.
Vergnaud AC1, Norat T, Romaguera D, Mouw T, May AM, Travier N, Luan J, Wareham N, Slimani N, Rinaldi S, Couto E, Clavel-Chapelon F, Boutron-Ruault MC, Cottet V, Palli D, Agnoli C, Panico S, Tumino R, Vineis P, Agudo A, Rodriguez L, Sanchez MJ, Amiano P, Barricarte A, Huerta JM, Key TJ, Spencer EA, Bueno-de-Mesquita B, Büchner FL, Orfanos P, Naska A, Trichopoulou A, Rohrmann S, Hermann S, Boeing H, Buijsse B, Johansson I, Hellstrom V, Manjer J, Wirfält E, Jakobsen MU, Overvad K, Tjonneland A, Halkjaer J, Lund E, Braaten T, Engeset D, Odysseos A, Riboli E, Peeters PH.
Am J Clin Nutr August 2010. vol. 92 no. 2 398-407
http://ajcn.nutrition.org/content/92/2/398.short

Type of Vegetarian Diet, Body Weight, and Prevalence of Type 2 Diabetes
Serena Tonstad, Terry Butler, Ru Yan, Gary E. Fraser. Diabetes Care May 2009, 32 (5) 791-796; DOI: 10.2337/dc08-1886
http://care.diabetesjournals.org/content/32/5/791.short

There's some indication that your body actually reacts to the taste of sweetness... although I only half-believe that myself, it's still interesting to think about at minimum.

From what I understand artificial sweeteners causes insulin to increase the way that sugar/HFCS does, but since they don't have any calories, you're left feeling more hungry.

From your article:

Serum insulin levels tended to be higher after diet soda, without statistical significance.

This basically means they didn't get enough data to form a solid conclusion.

There's some indication that your body actually reacts to the taste of sweetness... although I only half-believe that myself, it's still interesting to think about at minimum.

From what I understand artificial sweeteners causes insulin to increase the way that sugar/HFCS does, but since they don't have any calories, you're left feeling more hungry.

There is evidence diet sodas may further insulin resistance, http://care.diabetesjournals.o....

The sweet taste also triggers insulin production, when causes hunger when the sugar that the tongue predicted doesn't show up in the stomach.

There is a quite a bit of contrary evidence to that hypothesis. For one thing, the onset of Type II Diabetes, the most glaring result of disturbed insulin response, is associated with decreased rather than increased first-phase insulin response, so if artificial sweeteners are increasing first-phase insulin response it is not clear why that would be a problem.

And if artificial sweeteners cause an overproduction of insulin in the face of no actual glucose, then consuming them in the absence of no accompanying carbohydrate should be expected to trigger hypoglycemia as insulin triggers body tissues to absorb blood glucose. Yet there is no evidence that this actually happens.

That said, if the choice is between artificial sweeteners and no artificial sweeteners, then the safer bet is not to consume them as they have no precedent in our food supply for most of human evolution. However, if the choice is between artificial sweeteners and the equivalent quantity of sugar (which also has no precedent in our food supply in the quantities consumed in modern diets and has far more well-established deleterious effects on metabolism), the risk of artificial sweeteners seems pretty low in comparison based on currently available evidence.

It's not quite "punishing your pancreas", it's that you become insulin resistant. Your pancreas could be putting out MORE insulin and you could still have type 2 diabetes. If the pancreas was "getting worn out", then the mechanism of treating type 2 diabetes with excercise would not work.

(You can also have a pancreas that does not work well, but that is not the mechanism being discussed.)

At a constant height, body fat is added to the cross-section. I guess that's part of the rationale for the ballpark guess that is BMI.

Except the "cross-section" has height too. A 6'8" man with a giant beer belly compared to a 5'0" man with a giant beer belly not only adds cross-sectional area, but also a larger "height" over the stomach area where the excess weight is distributed. It's not like short men have a rounded belly, but taller men have a giant bulging rubber tire around the waist and flat upper abs! The bulge is roughly the same shape in 3-dimensions, excepting of course extreme cases (dwarfism, etc.).

Is there a better obesity metric that is as convenient to measure as BMI?

Sure -- how about using height cubed instead of height squared? Or, more likely, the best exponent probably falls between 2 and 3, since you're somewhat right that mass doesn't quite increase cubically when height does. Maybe it's 2.7 or maybe it's 2.3, and I'm sure epidemiological studies could easily come up with the best figure to correlate to bodyfat. And have two separate scales for men and women, just like doctors do for actual bodyfat measurements.

It still won't take into account things like muscle mass vs. fat and body type, but at least it doesn't have a built-in dimensional problem that skews diagnosis whenever you get more than a few inches off of average.

Aside from improving the BMI formula with a simple exponent change, they could also just use another simple measurement. Lots and lots of recent studies have shown that even taking a waist measurement (or a waist-to-hip ratio) is more accurate at predicting disease than the idiotic BMI formula.

I mean, how screwed up is that? If a formula that can be used with a simple tape measure -- like "if your waist is more than X inches, you're at higher risk," regardless of height, weight, or whatever -- is significantly better than some more complex formula involving squaring numbers and division and accurate scales, why the heck are we still using BMI?!?

P2RX7 was all the hype back in January. Here's a blog entry on it... Or the paper abstract for the more technically inclined (pay-wall for paper)...

If people are interested, I think there is some more info in English concerning the earlier Tampere research here (for free)...

Sometimes it's hard to predict what is going to work in bio-science just by seeing the techno-press response. Although polio is caused by an Enterovirus, so is the common cold (the variety caused by a Rhinovirus). Generally you get Enterovirus infections orally. Some Enteroviruses can eventually enter the bloodstream and infect other organs.

Apparently, the Tampere study looked at the small-bowel mucosal biopsies of 120 patients and did a PCR technique to assess if there was likely a Enterovirus infection. 74% of people with type 1 diabetes tested positive, compared with 29% of the non-diabetic ones. On that basis they conclude that a persistent Enterovirus infection in the small-bowel might eventually spread to the pancreas where the on-going immune response might destroy the insulin producing cells leading to diabetes...

So, I wasn't totally impressed after reading that paper, but you never know...

Enteroviruses have been connected to type 1 diabetes in various studies. The current study evaluates the association between specific enterovirus subtypes and type 1 diabetes by measuring type-specific antibodies against the group B coxsackieviruses (CBV) which has been linked to diabetes in previous surveys. Altogether 249 children with newly diagnosed type 1 diabetes and 249 control children matched according to sampling time, gender, age and country were recruited in Finland, Sweden, England, France and Greece during the years 2001-2005 (mean age 9 years; 55 % boys). Antibodies against CBV1 were more frequent among diabetic children than in control children (OR=1.7, 95%CI=1.0-2.9) while other CBV types did not differ between the groups. CBV1-associated risk was not related to HLA genotype, age or gender. Finnish children had lower frequency of CBV antibodies than children in other countries. The results support previous studies suggesting an association between group B coxsackieviruses and type 1 diabetes, highlighting the possible role of CBV1 as a diabetogenic virus type.

Yes, at least in theory, but you'd have to build it into a pair of glasses.

Depends a lot on the field. There are probably a lot more errors in medicine than in physics.

So, this was my first impression on reading the title. "What the fuck, first we rediscover calculus, and now it's the compass?" Then I actually read the summary, and realized it was kind of a cool idea... I don't think it'll be reliable, yes, but its not trivially a compass.

People with type 2 diabetes are insulin resistant. And yes, obesity can cause insulin resistance, but does not have to. Interestingly, insulin resistance is not solely caused by a large simple carbohydrate intake, but instead by a large quantities of dietary fat. You can look it up yourself here: http://diabetes.diabetesjournals.org/content/40/11/1397.short

Oh yes, another cause is also lack of physical activity:
http://jama.jamanetwork.com/article.aspx?volume=279&issue=9&page=669.

And here you are, preaching that carbohydrates and physical activity are the root of all evil and only fat is good.

It seems to me that our general body of knowledge is growing so large, and economic competition is so fierce, that people are being forced to specialize on particular areas, to the point that they lack even introductory knowledge about other fields of study. Case in point: this paper, where a doctor basically rediscovered calculus.

Then I'd expect this paper to have different results:

          http://care.diabetesjournals.org/content/24/5/838.full

Non-identical twins raised in the same womb and the same dietary environment would experience the same protein exposures, and as children experience similar infections or environmental factors, and have an elevated risk of sharing Type 1 diabetes if one of them has it. They don't.

From where did you hear this theory or see this claim?

"I'm very sorry that a can of Pepsi killed your mother"

My mother does not have type 2 diabetes, but I know many others with it.

And for some that may suggest diet soda, sorry but that also leads to weight gain and diabetes.

http://care.diabetesjournals.org/content/32/4/688
http://www.webmd.com/diet/news/20050613/drink-more-diet-soda-gain-more-weight

"last time I checked no one is marching into people's homes and forcing cola down people's throats."

You underestimate the power that marketing has over people.

Tobacco TV advertisement has been banned for some time because of the power of marketing, but currently soda advertisement has little regulation, so they are free to "march into peoples homes [television]".

http://www.alternet.org/story/45498/

Unlike glucose, fructose is almost entirely metabolized in the liver. "When fructose reaches the liver," says Dr. William J. Whelan, a biochemist at the University of Miami School of Medicine, "the liver goes bananas and stops everything else to metabolize the fructose." Eating fructose as compared to glucose results in lower circulating insulin (pancreatic beta cell insulin release is controlled only by blood glucose levels) and leptin levels, and attenuation in the suppression of ghrelin postprandially.[53] These hormones are implicated in the control of appetite and satiety, and it is suspected that eating large amounts of fructose increases the likelihood of weight gain.[54]

Or you could google it, read, say, this review see, this article in elsevier and see for yourself that it is already pretty well-accepted that HFCS is bad.
As to the link to your post: You assert that GMO haters are unreasonable, or something to that effect, and that there is no reasoning with them, (but that they're wrong; at least, that seemed to me to be your unspoken conclusion/assertion). In response, I suggested that they might be less wrong than you suppose, and further, that it's not entirely unreasonable to be careful when considering how next to mess with human food intake, specifically because, per my assertion, metabolism is ill-understood, and we know very little of what the body actually needs to function properly. And that it's not a priori unreasonable to assume that we have evolved uses for everything we used to eat, and that some of these new functions we were able to develop are now things we can no longer do without without breaking.
I'm really sorry that you were so shocked by my assertion that Americans are somewhat fucked by being forced to eat quite so much junk (just because HFCS is cheaper to produce than other sugars), but it sort of saddens me that you were so shocked that you couldn't even be bothered googling the two relevant terms just to see if there is a suggested link between HFCS and diabetes (and other metabolic diseases) before stating so triumphantly that my post contains "zero science".

"Soft drinks sweetened with High Fructose Corn Syrup are up to 10 times richer in harmful carbonyl compounds, such as methylglyoxal, than a diet soft drink control. Carbonyl compound are elevated in people with diabetes and are blamed for causing diabetic complications such as foot ulcers and eye and nerve damage."
http://en.wikipedia.org/wiki/High_fructose_corn_syrup

Soda Warning? New Study Supports Link Between Diabetes, High-fructose Corn Syrup
http://www.newswise.com/articles/view/532433/

Diabetes fears over corn syrup in soda. New Scientist (04 September 2007)
http://www.newscientist.com/channel/health/mg19526192.800-diabetes-fears-over-corn-syrup-in-soda.html

Theresa Waldron Sugary Sodas High in Diabetes-Linked Compound
http://www.healthfinder.gov/news/newsstory.asp?docID=607536

Bantle, John P.; Susan K. Raatz, William Thomas and Angeliki Georgopoulos (November 2000). "Effects of dietary fructose on plasma lipids in healthy subjects". American Journal of Clinical Nutrition 72 (5): 1128-1134.
http://www.ajcn.org/cgi/content/full/72/5/1128

Whey Protein and Fructose, an Unhealthy Combination. Enerex Botanicals. Retrieved on 2007-1-17.
http://www.enerex.ca/articles/whey_protein_and_fructose.htm

Jurgens, Hella; et al. (2005). "Consuming Fructose-sweetened Beverages Increases Body Adiposity in Mice". Obesity Res 13: 1146-1156.
http://www.obesityresearch.org/cgi/content/abstract/13/7/1146

Faeh D, Minehira K, Schwarz JM, Periasamy R, Park S, Tappy L (July 2005). "Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men". DIABETES 54 (7):1907-1913. PMID 15983189
http://diabetes.diabetesjournals.org/cgi/content/full/54/7/1907

It's NOT chemically identical to sucrose.

Fructose != Sucrose, they're chemically different with different absorbtion pathways in your body.
Fructose is only processed directly by your liver. Sucrose is processed in the gut.
Fructose causes massive insulin spikes and crashes, worse than sucrose does (which is one part fructose
and one part glucose- HFCS is pretty much nothing but Fructose...)

I suggest doing a little reading up on your organic chemistry and biochemistry before making bold
comments like your own. I know I have done my research- and it's not been the organic or health
food industry for this one (The Aspartame one started there, but went to more "reputable" sources...).

And you've not been doing your reading...

http://care.diabetesjournals.org/cgi/content/full/ 25/1/202
http://www.washingtonpost.com/wp-dyn/articles/A294 34-2004Aug24.html
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd= Retrieve&db=PubMed&list_uids=10520226&dopt=Abstrac t
http://www.centre4activeliving.ca/publications/res earch_update/2004/June.htm

Fructose makes you fat. Fructose makes you have vicious insulin spikes because your body
doesn't distinguish glucose from fructose- and you end up with fructose in your blood stream
until the liver can process it. Your liver can run off of either sugar- but it stores only
one day's worth of energy reserve in glucogen inside it's structures and then starts converting
the rest of the fructose and other sugars into FAT.

Combine the two and you end up with Type II Diabetes, heart disease, and so forth.

You see, Two years ago this week, I discovered by accident I was a Type II Diabetic, checking
into the Emergency room with a blood sugar of 607. At that point, I started digging into causes
with my doctor and other people.

Fructose was a major contributing factor. In and of itself, it's natural and you're supposed
to be taking it in. But refined like it is in HFCS, it's more of a poison than Sucrose is.
This is because while Fructose is bound up in the disaccaride Sucrose, it's got to be broken
apart, and there's as little as a third as much fructose, all things being considered, if you
stick with just Sucrose where it really IS a good thing in the mix.

Also worth noting is that there's very little need to be placing sugar of any kind in about 2/3
of the food we eat. The food industry currently does this to increase sales because it "tastes
better" and they know you're inclined to be addicted to the sweet taste.

But hey, keep drinking that damn soda with corn syrup in it. Me, I'm trying to find answers that
don't involve even Splenda if I can help it at all.

the hyperglycemia oxidizes proteins and kills off pancreatic islets, until the pancreas is unable to produce insulin, just as in Type 1.

You are right on the result (pancreas no longer able to produce insulin), but your mechanism (oxidative stress) is at best only part of the picture. If oxidized proteins induced by hyperglycemia were cytotoxic, a lot more cell types in addition to pancreatic islets would be killed off.

The exact mechanism of beta cell burn out in advanced type II diabetes is unclear
http://diabetes.diabetesjournals.org/cgi/content/f ull/54/suppl_2/S108/
however it certainly related to a prolonged an inappropriately high production of insulin (hyperinsulinemia) in response to high levels blood glucose.

In subjects with diabetes, fructose produces a lower postprandial [after eating] response when it replaces sucrose or starch in the diet; however, this benefit is tempered by concern that fructose may adversely effect plasma lipids. Therefore, the use of added fructose as a sweetening agent is not recommended; however, there is no reason to recommend that people with diabetes avoid naturally occurring fructose in fruits, vegetables, and other foods.

I got Type 1 Diabetes five years ago at age 30. I've definitely never skimped on coffee, and it didn't stop me, either. Not too surprising, since while the symptoms of Type 1 and Type 2 are similar (i.e., high blood glucose), the causes are different. Type 1 is caused by an autoimmune attack on the insulin-producing islet cells of the pancreas. Type 2 is a disease of insulin resistance, and is typically correlated with obesity.

As for benefits of caffeine for Type 1 Diabetes, there was a study published in Diabetes Care 23:455-459, 2000 demonstrating improved recognition of hypoglycemia. I've noticed this for myself: When I'm feeling the effects of my morning coffee, I seem to notice low blood sugar earlier than if I haven't had caffeine. Hypoglycemia feels (to me) similar to caffeine jitters, so I can see where caffeine might help that way.

Or maybe it's just that if I skip coffee for a day, I'm too busy with a headache to notice my sugar is going low...