Manifest Destiny is an funny video related to the report of recent stable obesity rate.

This is a good omen. This means that we will see the diabetes prevalence going to reach the platform soon.
_____________________________________________
Obesity rate appears to be stabilizing.

ABC World News (1/13, story 8, 0:20, Stephanopoulos) reported, "New numbers today from the CDC show the rate of obesity stabilizing."
The New York Times (1/14, A20, Belluck) reports that "Americans, at least as a group, may have reached their peak of obesity." The good news is that "the numbers indicate that obesity rates have remained constant for at least five years among men and for closer to 10 years among women and children -- long enough for experts to say the percentage of very overweight people has leveled off." The bad news is that "nearly 34 percent of adults are obese, more than double the percentage 30 years ago," while "the share of obese children tripled during that time, to 17 percent," according to studies published online Jan. 13 in the Journal of the American Medical Association.
The first study "examined height and weight data in a nationally representative sample of 5,555 adult Americans collected in 2007 and 2008," the Los Angeles Times (1/14, Stein) reports. "In the sample, 33.8% of the subjects" were "obese." After comparing "those numbers...to ones collected from 1999 to 2006 in a similar sample," researchers found that "among women, obesity statistics remained fairly flat throughout the period encompassed by the two studies," while "obesity rates among men rose slightly during the decade, but leveled off in the later years."
In the second study of nearly 4,000 children ranging in age from two to 19, the Wall Street Journal (1/14, Dooren) reports, researchers found that 17% of the youngsters met the threshold for obesity and 32% could be deemed to be overweight, a pattern similar to what was seen a decade ago. For both studies, the Journal notes that the CDC researchers based their estimates on data derived from the most recent National Health and Nutrition Examination Surveys.
USA Today (1/14, Hellmich) reports that "William Dietz, director of the CDC's Division of Nutrition, Physical Activity and Obesity, says this may reflect that people are becoming aware of 'the adverse health consequences of obesity' and are adopting healthier habits." Still, when it comes to the impact of obesity on children, Cynthia L. Ogden, PhD, the author of both studies, is concerned, because "obese kids are at a greater risk of weight-related health problems such as high cholesterol, blood pressure, and diabetes, plus they are at a greater risk of becoming obese adults, she says."
Bloomberg News (1/14, Ostrow), the AP (1/14, Tanner), Reuters (1/14, Steenhuysen), Time (1/13, Kluger), HealthDay (1/13, Gordon), &&&WebMD (1/13, DeNoon), and &&&HeartWire (1/13, O'Riordan) also covered the story.

Why Genes Aren't Destiny
 An article from Time

A nice article for understanding the relation of disease and DNA and epigenetic markers

... Biologists offer this analogy as an explanation: if the genome is the hardware, then the epigenome is the software. "I can load Windows, if I want, on my Mac," says Joseph Ecker, a Salk Institute biologist and leading epigenetic scientist. "You're going to have the same chip in there, the same genome, but different software. And the outcome is a different cell type."...

High-Fructose Corn Syrup Linked to Obesity, Diabetes


High-fructose corn syrup (HFCS) is also known as corn syrup, isoglucose and fructose on package labels and has been undergoing scrutiny for the last several years. Back in the '80s, when the low-fat craze started, HFCS began to be added to everything as a relatively easy way to add flavor and moisture to lower-fat products. Seemed like a great idea at the time. Corn is in abundance in the United States, and corn syrup is cheap and easy to add to commercially prepared foods. Little did we know that this type of sugar is digested very differently, and unlike glucose, actually prevents you from feeling full even when you have eaten a lot. Here's how it works: You eat something with HFCS and the sugar goes to your liver for processing. There it gets broken down into smaller components and eventually gets broken down completely. This is how all sugars are managed by the body. The problem is HFCS uses a lot more of the cell's energy to breakdown and leaves the cell with less energy to properly metabolize other foods. In addition, the breakdown products of the process cause an increase in lipid levels and triglycerides in the blood and within the cell itself, causing the fat to fill the cell. HFCS metabolism increases circulating insulin levels significantly and results in insulin resistance (the precursor of adult onset diabetes and metabolic syndrome). Lastly, unlike glucose, HFCS byproducts in the blood send a message to the brain that you are still hungry and need to eat. The more you eat, the more you crave! Most other sugars get stored in the cell, not as fat but as a substance called glycogen that can be easily mobilized for energy when needed, unlike the lipid that is formed from HFCS that is hard to mobilize when needed. HFCS leads to fatty liver, high blood lipids and triglycerides, high blood insulin levels and a continued craving to eat even when the body doesn't need any more calories. This is a recipe for central body obesity, heart disease, diabetes and liver failure from fatty deposits. Interestingly, this is the exact outcome when alcohol is consumed (minus the buzz or drunken feeling). If you drink alcohol too much, you get a "beer belly" (central obesity), fatty liver, heart disease from high triglycerides and lipids, and type 2 diabetes. We wouldn't dream of giving our kids alcohol, but as it turns out, HFCS is metabolized in the exact same way with the same damage done, calorie for calorie. For most adults, some alcohol drinking is OK, but excessive use or abuse can lead to serious long-term physical consequences. The same is true for HFCS. By the way, even though fresh fruit contains fructose, because it is "packaged" with natural fiber, it is digested very differently and doesn't cause these changes. Whole, fresh fruit is healthy, but fruit juices, fruit roll-ups and fruit snacks are devoid of the fiber and therefore no better than candy. I encourage families to spend time reading labels and becoming aware of how ubiquitous this additive is. It is in store-bought bread, crackers, pop, cookies, some lunch meats, fruit juices, packaged chocolate milk, candy, all-natural fruit snacks and many other packaged foods. I am not suggesting you need to completely eliminate it from your life, but I encourage you to decrease the amount your family eats every day.

Dr. Molly O'Shea is a Troy pediatrician. Read Dr. Molly's blog, get answers to your questions and discuss children's health issues at detnews.com/drmolly.

Health News Review - Objective Ratings of Health and Medical Journalism
http://www.healthnewsreview.org/

NHS 2009 Annual Evidence Update on Diabetes and Complication

http://www.library.nhs.uk/Diabetes/ViewResource.aspx?resID=328114

This is the third year of review on diabetes issues.

Colorbrewer: Color Advice for Maps

Colorbrewer: Color Advice for Maps

http://colorbrewer2.org/

Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause

The metabolic abnormalities of type 2 diabetes can be reversed reproducibly by bariatric surgery. By quantifying the major pathophysiological abnormalities in insulin secretion and insulin action after surgery, the sequence of events leading to restoration of normal metabolism can be defined. Liver fat levels fall within days and normal hepatic insulin sensitivity is restored. Simultaneously, plasma glucose levels return towards normal. Insulin sensitivity of muscle remains abnormal, at least over the weeks and months after bariatric surgery. The effect of the surgery is explicable solely in terms of energy restriction. By combining this information with prospective observation of the changes immediately preceding the onset of type 2 diabetes, a clear picture emerges. Insulin resistance in muscle, caused by inherited and environmental factors, facilitates the development of fatty liver during positive energy balance. Once established, the increased insulin secretion required to maintain plasma glucose levels will further increase liver fat deposition. Fatty liver causes resistance to insulin suppression of hepatic glucose output as well as raised plasma triacylglycerol. Exposure of beta cells to increased levels of fatty acids, derived from circulating and locally deposited triacylglycerol, suppresses glucose-mediated insulin secretion. This is reversible initially, but eventually becomes permanent. The essential time sequence of the pathogenesis of type 2 diabetes is now evident. Muscle insulin resistance determines the rate at which fatty liver progresses, and ectopic fat deposition in liver and islet underlies the related dynamic defects of hepatic insulin resistance and beta cell dysfunction. These defects are capable of dramatic reversal under hypoenergetic feeding conditions, completely in early diabetes and to a worthwhile extent in more established disease.

Qian Xuesen, Tsien Hsue-shen

http://zh.wikipedia.org/wiki/%E9%92%B1%E5%AD%A6%E6%A3%AE
http://en.wikipedia.org/wiki/Tsien_Hsue-shen

Association of A1C and Fasting Plasma Glucose Levels With Diabetic Retinopathy Prevalence in the U.S. Population


... CONCLUSIONS The steepest increase in retinopathy prevalence occurs among individuals with A1C ≥5.5% and FPG ≥5.8 mmol/l. A1C discriminates prevalence of retinopathy better than FPG...

Diagnosis of diabetes using the oral glucose tolerance test

The prevalence of type 2 diabetes varies greatly by ethnic group within and across countries. The most reliable data on the prevalence of diabetes are based on two hour plasma glucose values after an oral glucose tolerance test,¹ which is currently the gold standard epidemiological and clinical diagnostic test for diabetes and impaired glucose tolerance. In Newcastle, England, on the basis of clinical evidence and oral glucose tolerance test results, about 20% of British South Asians had diabetes, compared with only 4% of white Europeans, after age adjustment in a sample of 25-74 year olds.² Might such observed differences in prevalence, at least in part, be artefacts of the diagnostic method?

In 1965, the World Health Organization expert committee drew attention to the "lack of suitable epidemiological information about glucose tolerance in various populations of various races and cultures in different countries"³ and highlighted the need for research in different populations. The call was repeated in 1980,¹ with special reference to the oral glucose tolerance test and the dose of glucose, with 75 g being recommended pending further investigations. The International Diabetes Federation in consultation with WHO and the American Diabetes Association (ADA) have raised similar concerns, particularly about the oral glucose tolerance test.^{4 5} With a 75 g dose, a venous plasma glucose value of 11.1 mmol/l or more is indicative of diabetes, as indicated by its association with complications such as retinopathy. A value of 7.8-11.0 mmol/l is indicative of impaired glucose tolerance. Yet these concerns have not been dealt with.
The prevalence of diabetes is increasing worldwide, and accurate testing is more important than ever. The best way to make a diagnosis has been debated for decades,^{1 3 4 5} and more guidance is imminent. In some ethnic groups, comparatively low fasting plasma glucose concentrations are seen in people who have two hour postload glucose values that are diagnostic for diabetes.⁶
In the light of these concerns it is vital to know whether the 75 g carbohydrate load is appropriate for all adults, regardless of ethnicity. Glucose tolerance is influenced by several factors—from genetics, to body build (height and weight), to diet and lifestyle. Differences in body composition and skeletal muscle mass are important determinants of postprandial glucose metabolism, and height measurement partly reflects such differences.
An independent inverse association with two hour plasma glucose after the oral glucose tolerance test has been repeatedly shown for height in diverse populations.^{7 8} In a study of the prevalence of type 2 diabetes in white Europeans, African-Caribbeans, and Pakistanis, height almost completely accounted for ethnic differences in two hour plasma glucose in multiple regression models. Pakistanis, in whom the prevalence was the greatest, were markedly shorter (by 2-5 cm) than people in other ethnic groups.⁷ The implications of these findings are that a uniform oral glucose load may not accurately assess glucose tolerance across populations,¹ and a high two hour plasma glucose after the oral glucose tolerance test may overdiagnose impaired glucose tolerance in some ethnic groups compared with white populations.
Other factors related to body composition that vary by ethnicity may also be important. Varying the glucose load, as is done in children, or adjusting the results according to ethnicity or height (or both), may improve measures of glucose tolerance. These general observations could have wider implications in explaining inequalities. Impaired fasting glucose is more prevalent in men, whereas impaired glucose tolerance is more prevalent in women.⁹ Women are generally shorter than men, so this difference could simply reflect height differences by sex.
Whereas height has been shown to have a marked association with two hour plasma glucose after the oral glucose tolerance test, fasting plasma glucose and glycated haemoglobin measurements vary very little with height or sex.^{8 10} We should consider whether the oral glucose tolerance test can be replaced with other measures, such as glycated haemoglobin, in everyday clinical practice. This was a topic of debate at this year’s ADA annual conference in New Orleans, and work is already under way to standardise the measurement of glycated haemoglobin. However, as with the oral glucose tolerance test, the validity of glycated haemoglobin needs to be shown across ethnic groups before it is accepted and implemented.
WHO’s warnings in 1965 about the validity of the oral glucose tolerance test across various populations were prescient and deserve continuing attention. The uniform size of the oral glucose load used in this test, even though body size and composition vary, may account for some of the variation in the prevalence of diabetes between men and women and different ethnic groups. Nonetheless, the excess of diabetes in South Asians is marked using other criteria, such as those based on fasting glucose used by the ADA.¹¹ The complications of diabetes, such as retinopathy and nephropathy, are also greater in South Asians.¹²
Clinicians must be confident that the key tests for diabetes or impaired glucose tolerance are accurate, because the consequences of these diagnoses are considerable and lifelong. Although a false positive result might lead to good advice about diet and exercise, it could also provoke anxiety and adoption of the sick role. A false negative result is potentially dangerous in view of the high levels of cardiovascular diseases and renal dysfunction in South Asians. We must always establish the validity of diagnostic tests across sexes, age groups, and ethnic groups. This still applies to the oral glucose tolerance test and its likely successor, the measurement of glycated haemoglobin.
Cite this as: BMJ 2009;339:b4354

Open and free courses

Open and free courses
http://oli.web.cmu.edu/openlearning/forstudents/freecourses
Carnegie Mellon’s Open Learning Initiative (OLI) Meets with Bill Gates
Bill Gates, chairman of Microsoft Corp. and co-chair and trustee of the Bill & Melinda Gates Foundation came to Carnegie Mellon University on Tuesday, September 22, for the dedication of the Gates and Hillman Centers at the Pittsburgh campus. As part of his campus visit, Gates, accompanied by Foundation Senior Program Officer Josh Jarrett and Microsoft Corporate Vice President Anoop Gupta, met for nearly 90 minutes with the Open Learning Initiative (OLI) team to discuss the past, present, and future of the project as it moves forward under support from the Bill and Melinda Gates Foundation. CMU personnel in attendance were Provost Mark Kamlet, Vice Provost and CIO Joel Smith, Director of OLI Candace Thille, Director of the Pittsburgh Science of Learning Center Kenneth Koedinger and OLI Senior Software Engineers John Rinderle and Bill Jerome.
A brief presentation by Thille highlighted OLI’s unique approach of applying learning science research results and methods to open course design and then collecting data to continuously improve the learning experience--a combination that has been drawing increasingly positive attention from a variety of sources. Discussion then centered around the possibilities and challenges inherent in the potential for rapid growth of the initiative, with a particular emphasis on possible ways to overcome technical, organizational, and cultural barriers to scale.
“The opportunity to discuss with Bill Gates what we’ve accomplished and get his advice first-hand is truly a privilege and an honor,” said Thille. Later that day, in his keynote address celebrating the opening of the Gates Center for Computer Science and the Hillman Center for Future Generation Technologies, Gates referred to OLI as “an amazing and critical piece of work. . . . The idea of these virtual labs and intelligent tutoring systems, I think, can really revolutionize education. And we need to revolutionize education.”

Online - Diabetes in America, 2nd Edition

Diabetes in America, 2nd Edition, is a 733-page compilation and assessment of epidemiologic, public health, and clinical data on diabetes and its complications in the United States. It was published by the National Diabetes Data Group of the National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. The book contains 36 chapters organized in five areas:
1) the descriptive epidemiology of diabetes in the United States based on national surveys and community-based studies, including prevalence, incidence, sociodemographic and metabolic characteristics, risk factors for developing diabetes, and mortality.
2) the myriad complications that affect patients with diabetes.
3) characteristics of therapy and medical care for diabetes.
4) economic aspects, including health insurance and health care costs.
5) diabetes in special populations, including African Americans, Hispanics, Asian and Pacific Islanders, Native Americans, and pregnant women.
Diabetes in America, 2nd Edition, has been designed to serve as a reliable scientific resource for assessing the scope and impact of diabetes and its complications, determining health policy and priorities in diabetes, and identifying areas of need in research. The intended audience includes health policy makers at the local and Federal levels who need a sound quantitative base of knowledge to use in decision making; clinicians who need to know the probability that their patients will develop diabetes and the prognosis of the disease for complications and premature mortality; persons with diabetes and their families who need sound information on which to make decisions about their life with diabetes; and the research community which needs to identify areas where important scientific knowledge is lacking.

Education Matters for Health

 

Education Matters for Health

Robert Wood Johnson Fdn, September 9, 2009

Education can influence health in many ways. This issue brief, prepared by the Robert Wood Johnson Foundation Commission to Build a Healthier America, examines three major interrelated pathways through which educational attainment is linked with health­health knowledge and behaviors; employment and income; and social and psychological factors, including sense of control, social standing and social support. In addition, this brief explores how educational attainment affects health across generations, examining the links between parents’ education­and the social and economic advantages it represents­and their children’s health and social advantages, including opportunities for educational attainment.

http://www.rwjf.org/pr/product.jsp?id=48252

Report: S, Braveman P, Sadegh-Nobari T, Grossman-Kahn R and Dekker M. Education Matters for Health. Issue Brief 6: Education and Health. Commission to Build a Healthier America. Robert Wood Johnson Foundation. Sep 2009.

http://www.rwjf.org/files/research/commission2009eduhealth.pdf To leave, manage or join list: https://listserv.yorku.ca/cgi-bin/wa?SUBED1=sdoh&A=1

Building a Bayesian Bridge From Evidence to Guidelines: Comment on "Bayesian Classification of Clinical Practice Guidelines", Aug 10/24, 2009, Goodman 169 (15): 1436

Building a Bayesian Bridge From Evidence to Guidelines: Comment on
"Bayesian Classification of Clinical Practice Guidelines"

http://archinte.ama-assn.org/cgi/content/full/169/15/1436?etoc

If interested Bayesian, this is a nice article with some good
references.

ACSM addresses myths about weight loss, exercise

Dear ACSM members and certified professionals, Last Friday, an article appeared in Time magazine making statements that we believe run counter to fact and the public interest. The article claimed that exercise, contrary to the research with which we’re all familiar, is not an effective health tool, particularly as it pertains to weight loss. While an ACSM member and expert was consulted for the story, he agrees that his research and opinions were selectively reported. Among its numerous claims, the story would have us believe that: Losing weight matters more than being aerobically fit in preventing heart disease One can’t lose weight from exercise because exercise makes you hungrier – and willpower can’t conquer the hunger enough to make good food choices Exercising 60 to 90 minutes most days of the week in order to lose weight (a recommendation from an ACSM Position Stand) is unrealistic Leisure-time physical activity – just moving around more during the day – is more effective for weight loss than dedicated exercise Vigorous exercise depletes energy resources so much that it leads to overeating – i.e., weight gain Your assistance is needed in getting the right health message out to the public. These suggested talking points will help you dispel myths and confirm the value of exercise to your patients, clients and colleagues.   Also, we encourage you to adapt this letter to the editor and submit it to your local news outlets, helping readers and viewers get the best evidence-based facts and information.   Thank you for your involvement as we continue to increase awareness of the true benefits and advantages of a regular physical activity program.   Sincerely, The American College of Sports Medicine

401 W. Michigan St., Indianapolis, IN  46202  |  Privacy Policy To unsubscribe from future emails, click here. © 2009 American College of Sports Medicine

 

FW: Three decade change in the prevalence of hearing impairment and its association with diabetes in the United States

Three decade change in the prevalence of hearing impairment and its
association with diabetes in the United States
Yiling J. Cheng, Edward W. Gregg, Jinan B. Saaddine, Giuseppina
Imperatore, Xinzhi Zhang and Ann L. AlbrightAbstract
Objective: to examine the secular change of the prevalence of hearing impairment over three decades in U.S. adults with and without diabetes.Methods: the cross-sectional National Health and Nutrition Examination Surveys (NHANES, the 1971-1973 [NHANES I] and the 1999-2004 [NHANES 1999-2004]) were used. Average pure-tone audiometry thresholds in decibels (dB) at 1, 2, 3, 4 kHz frequencies of the worse ear were used to represent the participants' hearing status. Any hearing impairment was defined as average pure-tone audiometry threshold of the worse ear >25 dB.Results: From 1971 to 2004, among adults without diabetes aged 25 to 69 years, the unadjusted prevalence of hearing impairment decreased from 27.9% to 19.1% (P <0.001), but among adults with diabetes there was no significant change (46.4% to 48.5%). After adjustment for age, sex, race, and education, the prevalence of hearing impairment in the NHANES I and NHANES 1999-2004, respectively, was 24.4% (95% confidence interval
[CI], 22.3-26.6%) and 22.3% (95% CI, 20.4-24.2) for adults without diabetes and 28.5% (95% CI, 20.4-36.6%) and 34.4 (95% CI, 29.1-39.7%) for adults with diabetes. The adjusted prevalence ratios of hearing impairment for persons with diabetes vs. those without diabetes was 1.17 (95% CI, 0.87-1.57) for the NHANES I and 1.53 (95% CI, 1.28-1.83) for NHANES 1999-2004.Conclusions: Persons with diabetes have a higher prevalence of hearing impairment, and they have not achieved the same reductions in hearing impairment over time as have persons without diabetes.

DOMAIN statement of PROC SURVEYLOGISTIC

DOMAIN statement of PROC SURVEYLOGISTIC

In SAS 9.2 there is a DOMAIN statement. Prior to SAS 9.2, there is a
trick to getting the a close approximate analysis might be helpful.

What you can do is to assign a near zero weight to observations that
don't belong to your current domain. The reason that you can not simply
make the weight zero is that the procedure will exclude the observation
with zero weight. For example, if you have a domain gender=male or
female, and if you do

if gender=male then newweight=weight; else newweight=1e-6;

Then you perform the logistic regression using the newweight:

weight newweight;

Do Contaminants Play a Role in Diabetes?

Do Contaminants Play a Role in Diabetes?
A study linking a pesticide in fish to diabetes adds to the growing chorus of studies suggesting that environmental contaminants may play a role in the widespread disease.

By Andrew McGlashen and Environmental Health News, http://www.scientificamerican.com/article.cfm?id=pesticide-and-diabetes&print=true

Eat right and exercise, conventional wisdom has it, if you want to avoid joining the diabetes epidemic.
But a new study adds some muscle to a growing body of research suggesting those steps, though beneficial, might not be enough for people exposed to chemicals in the environment.

The scientists linked diabetes and people’s body burdens of DDE, a chemical produced as the body breaks down the pesticide DDT, banned in the United States more than 35 years ago.

“Even though we haven’t used DDT in decades, its metabolites are still detected in almost everyone in the country,” said lead researcher Mary Turyk, an epidemiologist at the University of Illinois-Chicago’s School of Public Health.

Since the early 1990s, researchers have monitored a group of Great Lakes charter boat captains, recreational fishermen and others to learn about the health effects of eating fish tainted with persistent organic pollutants – chemicals that remain in the environment for decades and grow more concentrated as they move up food chains.

For the new study, blood samples from the Great Lakes group showed “consistent, dose-related associations of DDE” with diabetes, the researchers wrote in the July issue of Environmental Health Perspectives.

Among 471 adults, including 36 with diabetes, there was no link to the disease based on the amount of fish consumed or exposure to other pollutants. But the higher the concentration of DDE in the blood, the more likely they were to develop diabetes.

The study is among the strongest voices in a chorus of research supporting the link between environmental chemicals and diabetes, according to David O. Carpenter, director of the Institute for Health and the Environment at the University of Albany in New York. He was not involved in the study.

“Most people have not thought of diabetes as a disease related to environmental exposure,” he said, “and these studies show that it is. The science has been growing very, very rapidly, and to my mind, it’s one of the most exciting developments in the study of diabetes.”

Diabetics cannot produce or use enough insulin, a hormone that lets glucose – the body’s fuel – enter cells. More than 23 million Americans, or eight percent of the population, are diabetic, and that group swelled by 13.5 percent from 2005 to 2007, according to the American Diabetes Assn.

For the most common type of diabetes, Type 2, obesity and lack of exercise play a key role. The bulk of studies searching for a cause have focused on lifestyle factors, while research on environmental influences hasn’t been prominent in journals devoted to the disease, said Henry Kahn, an epidemiologist with the Centers for Disease Control and Prevention’s Division of Diabetes Translation.

“But maybe it should be. It would be foolish to overlook pollution as a factor,” he said, adding that he and colleagues have lately taken a greater interest in the role of pollutants. “We recognize it’s possibly a very important thing,” he said. “We agree it’s on the list of things worth studying.”

Oliver Jones, a biochemist at the University of Cambridge, wrote in the journal Lancet last year that “if there is indeed a link” between contaminants and diabetes, “the health implications could be tremendous. There has been almost no consideration for the possible influence of environmental factors such as pollution."

Among the reasons to believe that the environment might be involved in diabetes, according to Carpenter, is that its prevalence varies across geographic areas, and people who move to places where it’s more common become more likely to get sick. Kahn, however, said that effect could be due to people migrating to more developed areas, where a richer diet and more sedentary lifestyle are the norm.

Further evidence came from a sweeping study of more than 2,000 adults, conducted by the U.S. Centers for Disease Control and Prevention, that found people with the highest levels of six pollutants were 38 times more likely to have diabetes than those with the lowest exposure. The chemicals, including PCBs, dioxins and DDE, were chosen because they were present in at least 80 percent of participants.

“That’s just mind-boggling,” Carpenter said.
Also, Vietnam veterans exposed to the dioxin-laced defoliant Agent Orange were significantly more likely than average to become diabetic, prompting the government to offer compensation to diabetic veterans.

The way the new Great Lakes study was conducted makes its findings especially convincing, according to the authors and other experts.

Other research has found similar links between diabetes and pollutants, but they were cross-sectional studies, which means “you measure the level of a chemical and ask people if they have diabetes,” Turyk said.

Those studies could easily be skewed, Turyk said, because they don’t indicate whether diabetes developed before a person was exposed to pollutants. But in the new paper, she and colleagues measured participants’ exposure to DDE from blood samples taken in the mid-1990s, then followed up with them for nearly a decade to see who among them became diabetic, thereby ensuring that diabetics were exposed before they were diagnosed.

The paper further bulwarked the claim by discrediting the hypothesis that the link between the two is a statistical fluke. Critics have suggested that pollutants like DDE only appear to be potential causes of the disease because diabetics more slowly break down the chemicals, and therefore carry more of them.

But Turyk, sharing principal research duties with Henry Anderson of the Wisconsin Division of Public Health and Victoria Persky at the University of Illinois-Chicago, quashed that theory by showing no difference in DDE metabolism rates between diabetics and non-diabetics.

“This paper clearly shows that’s not the case,” said Carpenter. “It’s a very important contribution because of that fact.”

The researchers controlled for obesity, age and other risk factors, and still found a link to DDE exposure. The study didn’t distinguish between Type 2 and Type 1, or early-onset diabetes, but most diabetics in the study suffered from Type 2, which is more common in adults.

The authors said the relatively small number of participants and short duration limit the reliability of the findings. In addition, the link to DDE was relatively weak compared with past research.

Like nearly all human health research, it doesn’t directly show that chemicals in the environment cause diabetes.
“With epidemiology, you gather a body of evidence against something,” she said. “You can never really prove something causes something else.”

Scientists still don’t understand the mechanism by which DDE and other chemicals might contribute to diabetes, according to Carpenter, though he said pollution seems to disrupt the way genes produce proteins and “basically change the biochemistry of the cell.”

“It may be that they’re toxic to the pancreas,” which produces insulin Kahn added. “We don’t know.”
For now, common-sense precautions are everyone's best bet, Carpenter said.
“Obese people are usually obese because they eat too many animal fats, and animal fats are where these contaminants are commonly found,” he said.

Turyk added that “people should definitely follow sport fish advisories,” which warn about contaminants in waterways.
This article originally ran at Environmental Health News, a news source published by Environmental Health Sciences, a nonprofit media company.

HOMA2 calculator

HOMA2 calculator

New insights on the simultaneous assessment of insulin sensitivity and beta-cell function with the HOMA2 method