Tag Archives: type 2 diabetes

Do Environmental Pollutants Cause Diabetes or Obesity?

"Today we're going to learn about odds ratios and relative risk."

“Today we’re going to learn about odds ratios and relative risk.”

A week ago I watched part of a documentary called “Plastic Planet” on Current or Al Jazeera TV. It was alarming. Apparently chemicals are leaking out of plastics into the environment (or into foods contained by plastic), making us fat, diabetic, impairing our fertility, and God knows what else. The narrator talked like it was a sure thing. I had to go to work before it was over. A couple mentioned chemicals I remember are bisphenol A (BPA) and phthalates. I sorta freaked my wife out when I mentioned it to her. I always take my lunch to work in plastic containers.

A few days later I saw a report of sperm counts being half of what they were just half a century ago. (It’s debatable.) Environmental contaminants were mentioned as a potential cause.

So I spent a couple hours trying to figure out if chemical contamination really is causing obesity and type 2 diabetes. In the U.S., childhood obesity has tripled since 1980, to a current rate of 17%. Even preschool obesity (age 2-5) doubled from 5 to 10% over that span. In industrial societies, even our pets, lab animals (rodents and primates), and feral rats are getting fatter! The ongoing epidemics of obesity and type 2 diabetes, and our lack of progress in preventing and reversing them, testify that we may not have them figured out and should keep looking at root causes to see if we’re missing anything.

Straightaway, I’ll tell you it’s not easy looking into this issue. The experts are divided. The studies are often contradictory or inconsistent. One way to determine the cause of a condition or illness is to apply Bradford Hill criteria (see bottom of page for those). We could reach a conclusion faster if we did controlled exposure experiments on humans, but we don’t. We look at epidemiological studies and animal studies that don’t necessarily apply to humans.

Regarding type 1 diabetes and chemical contamination, we have very little data. I’ll not mention type 1 again.

What Does the Science Tell Us?

For this post I read a couple pertinent scientific reviews published in 2012, not restricting myself to plastics as a source of chemical contaminants.

The first was REVIEW OF THE SCIENCE LINKING CHEMICAL EXPOSURES TO THE HUMAN RISK OF OBESITY AND DIABETES from non-profit CHEM Trust, written by a couple M.D., Ph.D.s. I’ll share some quotes and my comments. My clarifying comments within a quote are in [brackets].

“It should be noted that diabetes itself has not been caused in animals exposed to these chemicals [a long list] in laboratory studies, but metabolic disruption closely related to the pathogenesis of Type 2 diabetes has been reported for many chemicals.”

“In 2002, Paula Baillie-Hamilton proposed a hypothesis linking exposure to chemicals with obesity, and this is now gaining credence. Exposure to low concentrations of some chemicals leads to weight gain in adult animals, while exposure to high concentrations causes weight loss.”

“The obesogen hypothesis essentially proposes that exposure to chemicals foreign to the body disrupts adipogenesis [fat tissue growth] and the homeostasis and metabolism of lipids (i.e., their normal regulation), ultimately resulting in obesity. Obesogens can be functionally defined as chemicals that alter homeostatic metabolic set-points, disrupt appetite controls, perturb lipid homeostasis to promote adipocyte hypertrophy [fat cells swelling with fat], stimulate adipogenic pathways that enhance adipocyte hyperplasia [increased numbers of fat cells] or otherwise alter adipocyte differentiation during development. These proposed pathways include inappropriate modulation of nuclear receptor function; therefore, the chemicals can be termed EDCs [endocrine disrupting chemicals].”

Don't assume mouse physiology is the same as human's

Don’t assume mouse physiology is the same as human’s

Literature like this talks about POPs: persistent organic pollutants, sometimes called organohalides. The POPs and other chemical contaminants that are currently suspicious for causing obesity and type 2 diabetes include BPA, arsenic, pesticides, phthalates, metals (e.g., cadmium, mercury, organotins), brominated flame retardants, DDE (dichloro-diphenyldichloroethylene), PCBs (polychlorinated biphenyls), trans-nonachlor, dioxins.

Another term you’ll see in this literature is EDCs: endocrine disrupting chemicals. These chemicals mess with hormonal pathways. EDCs that mimic estrogen are linked to obesity and related metabolic dysfunction. Some of the chemicals in the list above are EDCs.

The fear—and some evidence—is that contaminants, whether or not EDCs, are particularly harmful to embryos, fetuses, and infants. For instance, it’s pretty well established that mothers who smoked while pregnant predispose their offspring to obesity in adulthood. (Epigenetics, anyone?) Furthermore, at the right time in the life cycle, it may only take small amounts of contaminants to alter gene expression for the remainder of life. For instance, the number of fat cells we have is mostly determined some time in childhood (or earlier?). As we get fat, those cells simply swell with fat. When we lose weight, those cells shrink, but the total cell number is unchanged. What if contaminant exposure in childhood increases fat cell number irrevocably? Does that predispose to obesity later in life?

The authors note that chemical contaminants are more strongly linked to diabetes than obesity. They do a lot of hemming and hawing, using “maybe,” “might,” “could,” etc. They don’t have a lot of firm conclusions other than “Hey, people, we better wake up and look into this further, and based on the precautionary principle, we better cut back on environmental chemical contamination stat!” [Not a direct quote.] It’s clear they are very concerned about chemical contaminants as a public health issue.

Here’s the second article I read: Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review. About 50 experts were empaneled. Some quotes and my comments:

“Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes. There was also support for the “developmental obesogen” hypothesis, which suggests that chemical exposures may increase the risk of obesity by altering the differentiation of adipocytes [maturation and development of fat cells] or the development of neural circuits that regulate feeding behavior. The effects may be most apparent when the developmental [early life] exposure is combined with consumption of a high-calorie, high-carbohydrate, or high-fat diet later in life.”

“The strongest conclusion from the workshop was that nicotine likely acts as a developmental obesogen in humans. This conclusion was based on the very consistent pattern of overweight/obesity observed in epidemiology studies of children of mothers who smoked during pregnancy (Figure 1) and was supported by findings from laboratory animals exposed to nicotine during prenatal [before birth] development.”

I found some data that don’t support that conclusion, however. Here’s a graph of U.S. smoking rates over the years since 1944. Note that the smoking rate has fallen by almost half since 1983, while obesity rates, including those of children, are going the opposite direction. If in utero cigarette smoke exposure were a major cause of U.S. childhood obesity, we’d be seeing less, not more, childhood obesity. I suppose we could still see a fall-off in adult obesity rates over the next 20 years, reflecting lower smoking rates.  But I doubt that will happen.

“The group concluded that there is evidence for a positive association of diabetes with certain organochlorine POPs [persistent organic pollutants]. Initial data mining indicated the strongest associations of diabetes with trans-nonachlor, DDT (dichloro-diphenyltrichloroethane)/DDE (dichloro-diphenyldichloroethylene)/DDD (dichloro-chlorophenylethane), and dioxins/dioxin-like chemicals, including polychlorinated biphenyl (PCBs). In no case was the body of data considered sufficient to establish causality [emphasis added].”

“Overall, this breakout group concluded that the existing data, primarily based on animal and in vitro studies [no live animals involved], are suggestive of an effect of BPA on glucose homeostasis, insulin release, cellular signaling in pancreatic β cells, and adipogenesis. The existing human data on BPA and diabetes (Lang et al. 2008Melzer et al. 2010) available at the time of the workshop were considered too limited to draw meaningful conclusions. Similarly, data were insufficient to evaluate BPA as a potential risk factor for childhood obesity.”

“It was not possible to reach clear conclusions about BPA and obesity from the existing animal data. Although several studies report body weight gain after developmental exposure, the overall pattern across studies is inconsistent.”

“The pesticide breakout group concluded the epidemiological, animal, and mechanistic data support the biological plausibility that exposure to multiple classes of pesticides may affect risk factors for diabetes and obesity, although many significant data gaps remain.”

“Recently, the focus of investigations has shifted toward studies designed to understand the consequences of developmental exposure to lower doses of organophosphates [insecticides], and the long-term effects of these exposures on metabolic dysfunction, diabetes, and obesity later in life. [All or nearly all the studies cited here were rodent studies, not human.] The general findings are that early-life exposure to otherwise subtoxic levels of organophosphates results in pre-diabetes, abnormalities of lipid metabolism, and promotion of obesity in response to increased dietary fat.”

In case it’s not obvious, remember that “association is not the same as causation.” For example, in the Northern hemisphere, higher swimsuit purchases are associated with summer. Swimsuit sales and summer are linked (associated), but one doesn’t cause the other. Swimsuit purchases are caused by the desire to go swimming, and that’s linked to warm weather.

In at least one of these two review articles, I looked carefully at the odds ratios of various chemicals linked to adverse outcomes. One way this is done is too measure the blood or tissue levels of a contaminant in a population, then compare the adverse outcome rates in animals with the highest and lowest levels of contamination. For instance, if those with the highest contamination have twice the incidence of diabetes as the least contaminated, the odds ratio is 2. You could also call it the relative risk. Many of the potentially harmful chemicals we’re considering have a relative risk ratio of 1.5 to 3. Contrast those numbers with the relative risk of death from lung cancer in smokers versus nonsmokers: the relative risk is 10. Smokers are 10 times more likely to die of lung cancer. That’s a much stronger association and a main reason we think smoking causes lung cancer. Odds ratios under two are not very strong evidence when considering causality; we’d like to have more pieces of the puzzle.

These guys flat-out said arsenic is not a cause of diabetes in the U.S.

Overall, the authors of the second article I read were clearly less alarmed than those of the first. Could the less-alarmed panelists have been paid off by the chemical industry to produce a less scary report, so as not to jeopardize their profits? I don’t have the resources to investigate that possibility. The workshop was organized (and paid for, I assume) by the U.S. government, but that’s no guarantee of pure motivation by any means.

You need a break. Enjoy.

You need a break. Enjoy.

My Conclusions

For sure, if I were a momma rat contemplating pregnancy, I’d avoid all those chemicals like the plague!

It’s premature to say that these chemical contaminants are significant causes of obesity and type 2 diabetes in humans. That’s certainly possible, however. We’ll have to depend on unbiased scientists to do more definitive research for answers, which certainly seems a worthwhile endeavor. Something tells me the chemical producers won’t be paying for it. Universities or governments will have to do it.

You should keep your eyes and ears open for new evidence.

There’s more evidence for chemical contaminants as a potential cause of type 2 diabetes than for obesity. Fetal and childhood exposure may be more harmful than later in life.

If I were 89-years-old, I wouldn’t worry about these chemicals causing obesity or diabetes. For those quite a bit younger, taking action to avoid these environmental contaminants is optional. As for me, I’m drinking less water out of plastic bottles and more tap water out of glass or metal containers. Yet I’m not sure which water has fewer contaminants.

Humans, particularly those anticipating pregnancy and child-rearing, might be well advised to minimize exposure to the aforementioned chemicals. For now, I’ll leave you to your own devices to figure out how to do that. Good luck.

Why not read the two review articles I did and form your own opinion?

Unless the chemical industry is involved in fraud, bribery, obfuscation, or other malfeasance, the Plastic Planet documentary gets ahead of the science. I’m less afraid of my plastic containers now.

Steve Parker, M.D.

Additional Resources:

Sarah Howard at Diabetes and the Environment (focus on type 1 but much on type 2 also).

Jenny Ruhl, who thinks chemical contaminants are a significant cause of type 2 diabetes (search her site).

From Wikipedia:

The Bradford Hill criteria, otherwise known as Hill’s criteria for causation, are a group of minimal conditions necessary to provide adequate evidence of a causal relationship between an incidence and a consequence, established by the English epidemiologist Sir Austin Bradford Hill (1897–1991) in 1965.

The list of the criteria is as follows:

  1. Strength: A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.
  2. Consistency: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.
  3. Specificity: Causation is likely if a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.
  4. Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).
  5. Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.
  6. Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).
  7. Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that “… lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations”.
  8. Experiment: “Occasionally it is possible to appeal to experimental evidence”.
  9. Analogy: The effect of similar factors may be considered.

Science-Based Medicine blog has more on Hill’s criteria.

Sugar Linked To Diabetes: 175 countries studied

Sugar cane

Sugar cane

Robert Lustig and associates looked at sugar consumption and diabetes rates in 175 countries and found a strong link between sugar and type 2 diabetes.  It’s not proof of causation, just suggestive.  From the abstract:

Duration and degree of sugar exposure correlated significantly with diabetes prevalence in a dose-dependent manner, while declines in sugar exposure correlated with significant subsequent declines in diabetes rates independently of other socioeconomic, dietary and obesity prevalence changes. Differences in sugar availability statistically explain variations in diabetes prevalence rates at a population level that are not explained by physical activity, overweight or obesity.

Read the rest.

Steve Parker, M.D.

Reminder: Conquer Diabetes and Prediabetes is now available on Kindle. Also, the Advanced Mediterranean Diet is naturally quite low in sugar.

Reference: Basu S, Yoffe P, Hills N, Lustig RH (2013) The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data. PLoS ONE 8(2): e57873. doi:10.1371/journal.pone.0057873

Mediterranean Diet Among The Best For Type 2 Diabetes

…announces an article at Reuters.  An excerpt:

Ajala and her colleagues reviewed the results of 20 studies comparing the effect of seven popular diets on adults with type 2 diabetes. Mediterranean diets, low-carb diets, high-protein diets and low glycemic index diets – which rank foods by how quickly their carbs turn into glucose – all lowered participants’ blood sugar.

After following the diet for at least six months, the people on a Mediterranean eating plan also lost an average of 4 pounds. No other diet had a significant impact on weight, according to the findings published in the American Journal of Clinical Nutrition.

“We were quite surprised by the Mediterranean diet in particular,” Ajala said. “I would have thought that low-carb would have been the best for losing weight, but Mediterranean seems to be better.”

Beautiful woman smiling as she is wine tasting on a summer day.Here’s the traditional healthy Mediterranean diet.

The researchers also found that HDL cholesterol (“good cholesterol) and triglycerides improved on the Mediterranean diet, low-carb diets, and low glycemic index diets.  Those moves tend to protect against heart disease.

Steve Parker, M.D.

Prevention of Type 2 Diabetes Depends on the Cause

(moonlights as a clown)

The U.S. Centers for Disease Control predicts that one of every three Americans born in 2000 will develop diabetes, mostly type 2.

You can lower your risk of type 2 diabetes significantly by avoiding overweight and obesity, by exercising regularly, and by choosing the right parents.  These provide clues as to the causes of diabetes.

UpToDate.com offers a deceptively simple explanation of what causes type 2 diabetes:

Type 2 diabetes mellitus is caused by a combination of varying degrees of insulin resistance and relative insulin deficiency. [Insulin is the pancreas hormone that lowers blood sugar.] Its occurrence most likely represents a complex interaction among many genes and environmental factors, which are different among different populations and individuals.

So what causes the insulin resistance and relative insulin deficiency?

Understanding the pathogenesis [cause] of type 2 diabetes is complicated by several factors. Patients present with a combination of varying degrees of insulin resistance and relative insulin deficiency, and it is likely that both contribute to type 2 diabetes. Furthermore, each of the clinical features can arise through genetic or environmental influences, making it difficult to determine the exact cause in an individual patient. Moreover, hyperglycemia itself can impair pancreatic beta cell function and exacerbate insulin resistance, leading to a vicious cycle of hyperglycemia causing a worsening metabolic state.

The UpToDate article then drones on for a couple thousand words discussing mouse studies, various genes, free fatty acids, adiponectin, leptin, amylin, insulin secretion, insulin resistance, impaired insulin processing, insulin action, body fat distribution, inflammation, various inflammatory markers, low birth weight, high birth rate, prematurity, etc.  More excerpts:

Increased free fatty acid levels, inflammatory cytokines from fat, and oxidative factors, have all been implicated in the pathogenesis of metabolic syndrome, type 2 diabetes, and their cardiovascular complications.

Insulin resistance may, at least in part, be related to substances secreted by adipocytes [fat cells] (“adipokines” including leptin adiponectin, tumor necrosis factor alpha, and resistin).

Type 2 diabetes most likely represents a complex interaction among many genes and environmental factors.

While it’s too late to pick your parents, you can modify environmental factors that affect your risk of diabetes.  See the second paragraph above.  The Mediterranean diet also prevents diabetes.

Steve Parker, M.D.

Reference: “The Pathogensis of Type 2 Diabetes Mellitus”  by David K McCulloch, MD, and R Paul Robertson, MD, at UpToDate.com, updated June 2012, and accessed November 19, 2012.

Small Study Shows Improved Diabetes and Prediabetes With Biggest Loser Plan

“One more rep then I’m outa here!”

Do you wonder how much exercise it takes to lose a lot of weight quickly?  Read on.

TV’s “The Biggest Loser” weight-loss program works great for overweight diabetics and prediabetics, according to an article May 30, 2012, in MedPage Today.  Some quotes:

For example, one man with a hemoglobin A1c (HbA1c) of 9.1 [poor control of diabetes], a body mass index (BMI) of 51 [very fat], and who needed six insulin injections a day as well as other multiple prescriptions was off all medication by week 3, said Robert Huizenga, MD, the medical advisor for the TV show.

In addition, the mean percentage of weight loss of the 35 contestants in the study was 3.7% at week 1, 14.3% at week 5, and 31.9% at week 24…

The exercise regimen for those appearing on “The Biggest Loser” comprised about 4 hours of daily exercise: 1 hour of intense resistance training, 1 hour of intense aerobics, and 2 hours of moderate aerobics.

Caloric intake was at least 70% of the estimated resting daily energy expenditure, Huizenga said.

At the end of the program, participants are told to exercise for 90 minutes a day for the rest of their lives. Huizenga said he is often told by those listening to him that a daily 90-minute exercise regimen is impossible because everyone has such busy lives.

“I have a job and I work out from 90 to 100 minutes per day,” he said. “It’s about setting priorities. Time is not the issue; priorities are the issue.”

Of the 35 participants in this study, six had diabetes and 12 had prediabetes.  This is a small pilot study, then.  I bet the results would be reproducible on a larger scale IF all conditions of the TV program are in place.  Of course, that’s not very realistic.  A chance to win $250,000 (USD) is strong motivation for lifestyle change.  Can you see yourself exercising for four hours a day?

Steve Parker, M.D.

PS: Although not mentioned in the article, these must have been type 2 diabetics, not type 1.

U.S. Diabetes Prevalence From 1935 to 1979 and Beyond

From 1935 to 1996, the prevalence of diagnosed type 2 diabetes [in the U.S.] climbed nearly 765%.

This shocking statistic is from the Centers for Disease Control and Prevention as cited in Increased Consumption of Refined Carbohydrates and the Epidemic of Type 2 Diabetes in the United States: an Ecologic Assessment, American Journal of Clinical Nutrition, 2004, vol. 79, no.5, pp: 774-779.

I thought 765% might be a misprint, so I did some digging.  A similar figure is in DHHS Publication No. (PHS) 82-1232 published in 1981:

  • Diabetes prevalence rose from 0.4% of the population in 1935,  to 2.4% in 1979.

This is a six-fold increase.  The major part of the upward trend started in 1960.  Interestingly, that’s when corn syrup started working its way into our food supply.  Coincidence?  The authors of the Department of Human Services paper write:

Preliminary evaluation of these trends suggests that the change in the prevalence of known diabetes has resulted from improvements both in detection of diabetes among high-risk groups and in survivorship among persons with diabetes.

Like type 1 diabetics, many type 2’s need insulin shots

To me, it sounds like they weren’t considering an true increase in the number of new diabetes cases (incidence), but better detection of existing cases and improved longevity of existing patients (prevalence).  Incidence and prevalence are often confusing.  Wikipedia has a clarifying article.  These days, both incidence and prevalence of type 2 diabetes are greatly increased over 1935 levels.

In January of 2011, the U.S. Centers for Disease Control and Prevention released the latest estimates for prevalence of diabetes and prediabetes.

  • 8.3% of the total U.S. population has either diagnosed or undiagnosed diabetes (earlier percentages in this post were for diagnosed cases only)
  • 6% of the U.S. adult population has diagnosed diabetes (My calculation: Population in 2011 was 311 million; with 18.8 million diagnosed cases of diabetes, 7 million undiagnosed)
  • Nearly 27% of American adults age 65 or older have diabetes (overwhelmingly type 2)
  • Half of Americans 65 and older have prediabetes
  • 11% of U.S. adults (nearly 26 million) have diabetes (overwhelmingly type 2)
  • 35% of adults (79 million) have prediabetes, and most of those affected don’t know it

Even if type 2 diabetes runs in your family, you may well be able to avoid it.  Here’s a post about prevention of type 2 diabetes.

Steve Parker, M.D.

Mediterranean Diet Cuts Risk of Type 2 Diabetes

The traditional Mediterranean diet has long been associated with lower risk of developing cardiovascular disease, cancer, and dementia.  The diet is rich in olive oil, fruits, nuts, cereals, vegetables, and fish but relatively low in dairy products and meat.  Several studies suggest the Mediterranean diet may also help prevent type 2 diabetes.

Researchers at the University of Navarra in Spain followed 13,380 non-diabetic university graduates, many of them health professionals, over the course of 4.4 years.  Average age was 38.  I assume most of the study participants lived in Spain, if not elsewhere in Europe (the article doesn’t say).  Dietary habits were assessed at the start of the study with a food frequency questionnaire.  Food intake for each participant was scored by adherence to the traditional Mediterranean diet.  Participants were labelled as either low, moderate, or high in adherence.  Over an average follow-up of 4.4 years, 33 of the study participants developed type 2 diabetes.  Compared to the participants who scored low on adherence to the Mediterranean diet, those in the high adherence category had an 83% lower risk of developing diabetes.  The moderate adherence group also had diminished risk, 59% less.

How could the Mediterranean diet protect against diabetes?  The authors note several potential mechanisms: high intake of fiber, low amounts of trans fats, moderate alcohol intake, high vegetable fat  intake, and high intake of monounsaturated fats relative to saturated fats.  Olive oil, loaded with monounsaturated fats, is the predominant fat in the Mediterranean diet.  In summary from the authors:

Diets rich in monounsaturated fatty acids improve lipid profiles and glycaemic control in people with diabetes, suggesting that a high intake improves insulin sensitivity.  Together these associations suggest the hypothesis that following an overall pattern of Mediterranean diet can protect against diabetes.  In addition to having a long tradition of use without evidence of harm, a Mediterranean diet is highly palatable, and people are likely to comply with it.

Please give serious consideration to the Mediterranean diet, especially if you are at risk for developing type 2 diabetes.  Major risk factors include sedentary lifestyle, overweight, and family history of diabetes.

Steve Parker, M.D.

Reference: Martinez-Gonzalez, M.A., et al.  Adherence to Mediterranean diet and risk of developing diabetes: prospective cohort study.  British Medical Journal, BMJ,doi:10.1136/bmj.39561.501007.BE (published online May 29, 2008).

Does White Rice Cause Type 2 Diabetes?

Rice was first domesticated in the Yangtze River Valley in China

The following article at Yahoo News suggests it does.

http://ca.news.yahoo.com/white-rice-seen-type-2-diabetes-says-study-233837784.html

Background

Rice was first domesticated 8 or 9000 thousand years ago in China.

Among populations that eat rice as a staple food, white rice is the primary contributor to glycemic load.

Diabetes is characterized by elevated blood sugars.  Glycemic index (GI) is an indicator of how high a carbohydrate source tends to increase blood sugar.  The higher the GI, the higher the blood sugar.  The average glycemic index for white rice is 64; for brown rice it’s 55, and for whole wheat it’s 41. 

Study Method

Boston-based researchers looked for well-designed research that focused on development of diabetes over time, while measuring white rice consumption in the study population.  They found and combined four studies involving populations in China, Japan, the U.S., and Australia.  Out of a total of 352,328 participants, 13,284 developed type 2 diabetes over the course of four to 22 years.

Findings

Comparing the highest white rice consumers (over 450 g/day) with the lowest consumers (under 300 g/day, roughly), the risk of diabetes was 55% higher in the heavy consumers.  This applied only to the Asian populations.  The more rice servings per day, the higher the risk.

The Asian populations ate an average of 3 or 4 servings of white rice daily.  The Western populations ate quite a bit less: 1 or 2 servings weekly.

So What?

Western populations don’t eat nearly as much rice as Asians.  If they did, would they show a similar dose-response to white rice consumption and development of diabetes?  Nobody knows for sure, but I suspect so. 

Glycemic load has already been linked to development of type 2 diabetes in Western populations, at least in women.  To the extent that heavy white rice consumption is a glycemic load, reducing intake may lower risk of diabetes.

Chinese and Japanese at risk for type 2 diabetes should consider cutting back on white rice if they’re at the very high end of consumption.  That’s probably good advice for Westerner’s, too. 

Steve Parker, M.D.

Reference: Hu, Emily, et al.  White rice consumption and risk of type 2 diabetes: Meta-analysis and systemic reviewBritish Medical Journal, 2012:e1454.   doi: 10.1136/bmj.e1454

Type 2 Diabetes CAN Be Prevented

Not Paula Deen

Paula Deen’s recent announcement of her type 2 diabetes got me thinking about diabetes prevention again. If you’re at high risk of developing diabetes you can reduce your risk of full-blown type 2 diabetes by 58% with intensive lifestyle modification. Here’s how it was done in a 2002 study:

The goals for the participants assigned to the intensive lifestyle intervention were to achieve and maintain a weight reduction of at least 7 percent of initial body weight through a healthy low-calorie, low-fat diet and to engage in physical activity of moderate intensity, such as brisk walking, for at least 150 minutes per week. A 16-lesson curriculum covering diet, exercise, and behavior modification was designed to help the participants achieve these goals. The curriculum, taught by case managers on a one-to-one basis during the first 24 weeks after enrollment, was flexible, culturally sensitive, and individualized. Subsequent individual sessions (usually monthly) and group sessions with the case managers were designed to reinforce the behavioral changes.

Although the Diabetes Prevention Program encouraged a low-fat diet, another study from 2008 showed that a low-fat diet did nothing to prevent diabetes in postmenopausal women.

I don’t know Paula Deen. I’ve never watched one of her cooking shows. She looks overweight and I’d be surprised if she’s had a good exercise routine over the last decade. I’m sorry she’s part of the diabetes epidemic we have in the U.S. I wish her well. Amy Tenderich posted the transcript of her brief interview with Paula, who calculates her sweet tea habit gave her one-and-a-half cups of sugar daily).

  • Nearly 27% of American adults age 65 or older have diabetes (overwhelmingly type 2)
  • Half of Americans 65 and older have prediabetes
  • 11% of U.S. adults (nearly 26 million) have diabetes (overwhelmingly type 2)
  • 35% of adults (79 million) have prediabetes, and most of those affected don’t know it

I think excessive consumption of concentrated sugars and refined carbohydrates contribute to the diabetes epidemic. Probably more important are overweight, obesity, and physical inactivity.

The Mediterranean diet has also been linked to lower rates of diabetes (and here). Preliminary studies suggest the Paleo diet may also be preventative (and here).

Greatly reduce your risk of type 2 diabetes by eating right, keeping your weight reasonable, and exercising.

Steve Parker, M.D.

PS: Paula, if you’d like a copy of Conquer Diabetes and Prediabetes: The Low-Carb Mediterranean Diet, have your people contact my people.

Reference: Diabetes Prevention Program Research Group. Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin. New England Journal of Medicine, 346 (2002): 393-403.