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Category Archives: Diabetes
It sounds like Jerome Ruzzin is convinced it does. I put some thought into it last August and was skeptical—still am, but I’m keeping an open mind. Mr. Ruzzin has a review article published in 2012 at BMC Public Health (“Public health concern behind the exposure to persistent organic pollutants and the risk of metabolic diseases”). Here’s his summary:
The global prevalence of metabolic diseases like obesity and type 2 diabetes, and its colossal economic and social costs represent a major public health issue for our societies. There is now solid evidence demonstrating the contribution of POPs [persistent organic pollutants], at environmental levels, to metabolic disorders. Thus, human exposure to POPs might have, for decades, been sufficient and enough to participate to the epidemics of obesity and type 2 diabetes. Based on recent studies, the fundaments of current risk assessment of POPs, like “concept of additive effects” or “dioxins and dl-PCBs induced similar biological effects through AhR”, appear unlikely to predict the risk of metabolic diseases. Furthermore, POP regulation in food products should be harmonized and re-evaluated to better protect consumers. Neglecting the novel and emerging knowledge about the link between POPs and metabolic diseases will have significant health impacts for the general population and the next generations.
The cold-water fatty fish I so often recommend to my patients could be hurting them. They are major reservoirs of food-based POPs.
There are ways of slowing or reversing losses in cognitive function. The most effective discovered so far is physical exercise, which protects the brain by protecting the body’s cardiovascular health. Mental exercise, often called brain training, is widely promoted, but it boosts only the particular skill that is practised – its narrow impact mirroring that of educational interventions at other ages. Various drugs are being investigated for their value in staving off normal cognitive decline, but for now preventive maintenance is still the best bet – avoid smoking, drinking to excess, head injuries and the like.
Don’t forget regular exercise. Also, I think the Mediterranean diet helps preserve brain function, but it’s difficult to prove.
That quotes from an Instant Expert paper on intelligence. It’s full of interesting facts such as the typical difference in IQ between strangers is 17 points. It answers the question whether an enriched school or home environment can increase intelligence.
The article mentions overload of patients’ brains when medical care is too complicated:
Given the complexity of self-care regimes, it is hardly surprising that some people make dangerous errors or fail to comply. The effective management of diabetes, for example, requires a person to keep blood sugar levels within a healthy range, which means coordinating diet, exercise and medication throughout the day, which in turn requires planning for contingencies, recognising when blood sugar is veering too high or low, knowing how to regain control and conceptualising the imperceptible but cumulative damage caused by failing to maintain control. There is no set recipe for people with diabetes to follow – their bodies and circumstances differ. Moreover, they get little training, virtually no supervision and no days off. Effectively managing your diabetes is a cognitively complex job and poor performance has serious consequences, including emergency room visits, lost limbs or eyesight, and even death. The lower the diabetic person’s IQ, the greater the risks.
You’ll also learn about the Flynn effect and possible explanations for it:
Over the past century, each successive generation has answered more IQ test items correctly than the last, the rise being equivalent to around 3 IQ points per decade in developed nations. This is dubbed the “Flynn effect” after the political scientist James Flynn, who most thoroughly documented it. Are humans getting smarter, and if so, why?
I’m more inclined to think Idiocracy describes our future.
h/t James Fulford
Book Review: The Heart Healthy Lifestyle – The Prevention and Treatment of Type 2 Diabetes, by Sean Preuss
I recently finished an ebook, The Heart Healthy Lifestyle: The Prevention and Treatment of Type 2 Diabetes by Sean Preuss, published in 2013. Per Amazon.com’s rating system, I give it five stars (I love it).
♦ ♦ ♦
This is an invaluable resource for 1) anyone recently diagnosed with type 2 diabetes or prediabetes, 2) those who aren’t responding well to their current therapeutic regimen, and 3) type 2 diabetics who want to reduce their drug use.
Mr. Preuss is a fitness trainer who has worked with many type 2 diabetics. He demonstrates great familiarity with the issues diabetics face on a daily basis. His science-based recommendations are familiar to me since I reviewed many of his references at on of my other blogs, Diabetic Mediterranean Diet.
Like me, Mr. Preuss recognizes the primacy of lifestyle modification over drug therapy for type 2 diabetes, as long as drugs can safely be avoided or postponed. The main lifestyle factors are diet and exercise. Too many physicians don’t spend enough time on these, preferring instead to whip out the prescription pad and say, “Here ya go. I’ll see you in three months.”
I have gradually come to realize that most of my sedentary type 2 diabetes patients need to start a work-out program in a gym where they can get some personal attention. That’s Mr. Preuss’s opinion, too. The clearly explained strength training program he recommends utilizes machines most commonly found in a gym, although some home gyms will have them also. His regimen is easily done in 15-20 minute sessions two or three times a week.
He also recommends aerobic activity, such as walking at least several days a week. He recommends a minimum of 113 minutes a week of low intensity aerobic work, citing evidence that it’s more effective than higher intensity effort for improving insulin sensitivity.
I don’t recall specific mention of High Intensity Interval Training. HIIT holds great promise for delivering the benefits of aerobic exercise in only a quarter of the time devoted to lower intensity aerobics. It may be that it just hasn’t been studied in type 2 diabetics yet.
I was glad to see all of Mr. Preuss’s scientific references involved humans, particularly those with type 2 diabetes. No mouse studies here!
Another strength of the book is that Sean tells you how to use psychological tricks to make the necessary lifestyle changes.
The author notes that vinegar can help control blood sugars. He suggests, if you can tolerate it, drinking straight (undiluted) red wine vinegar or apple cider vinegar – 2 tbsp at bedtime or before carbohydrate consumption. I’ve heard rumors that this could be harmful to teeth, so I’d do some research or ask my dentist before drinking straight vinegar regularly. For all I know, it could be perfectly harmless. If you have a definitive answer, please share in the comments section below.
I read a pertinent vinegar study out of the University of Arizona from 2010 and reviewed it at one of my blogs. The most effective dose of vinegar was 10 g (about two teaspoons or 10 ml) of 5% acetic acid vinegar (either Heinz apple cider vinegar or Star Fine Foods raspberry vinegar). This equates to two tablespoons of vinaigrette dressing (two parts oil/1 part vinegar) as might be used on a salad. The study authors also say that “…two teaspoons of vinegar could be consumed palatably in hot tea with lemon at mealtime.”
The diet advice herein focuses on replacement of a portion of carbohydrates with proteins, healthy oils, and vegetables.
I highly recommend this book. And sign up for Mr. Preuss’s related tweets at @HeartHealthyTw.
Disclosure: Mr. Preuss gave me a free copy of the book, otherwise I have received no monetary compensation for this review. I met him once, about two years ago.
The findings suggest that eliminating or strictly limiting high glycemic load foods such as those high in refined sugars and grains and following the largely plant-based Mediterranean diet, which emphasizes vegetables, fruits, nuts and legumes, can have a significant impact on diabetes risk, La Vecchia said.
“The impact of the diets was synergistic,” he told MedPage Today. “The message is that eating a largely Mediterranean diet that is also low in glycemic load is particularly favorable for preventing diabetes.”
On the heels of a report finding no association between Alzheimer’s disease and abnormal blood sugar metabolism, MedPageToday features an new study linking high blood sugars to future development of dementia. And diabetics with sugar levels higher than other diabetics were more prone to develop dementia.
Some of you have already noted that not all cases of dementia are Alzheimer’s dementia. But Alzheimer’s accounts for a solid majority of dementia cases.
Some quotes from MedPageToday:
During a median follow-up of 6.8 years, 524 participants [of the 2000 total] developed dementia, consisting of 74 with diabetes and 450 without. Patients without diabetes and who developed dementia had significantly higher average glucose levels in the 5 years before diagnosis of dementia (P=0.01). The difference translated into a hazard ratio of 1.18 (95% CI 1.04-1.33).
Among the patients with diabetes, glucose levels averaged 190 mg/dL in those who developed dementia versus 160 mg/dL in those who did not. The difference represented a 40% increase in the hazard for dementia (HR 1.40, 95% CI 1.12-1.76).
Reminder: Conquer Diabetes and Prediabetes is now available on Kindle.
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].”
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. 2008; Melzer 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.
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.
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).
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:
- 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.
- Consistency: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.
- 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.
- 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).
- 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.
- Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).
- 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”.
- Experiment: “Occasionally it is possible to appeal to experimental evidence”.
- Analogy: The effect of similar factors may be considered.
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.
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
…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.”
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.
…according to a new report in Diabetes Care. As if that weren’t bad enough, brain functioning was also adversely affected! The next question is: Would prevention or reversal of insulin resistance preserve the brain? Stay tuned, because nobody knows yet.
Only a few of the study participants had diabetes. The study at hand supports others that suggest diabetes predisposes to dementia.
What Can I Do About It Now?
You could have your doctor order some expensive blood tests to see if you’re insulin resistant. (Insurance may not pay for them, either.) Or you can measure your waist size. If your waist circumference is over 39 inches (99 cm) and you’re overweight or obese, odds are good that you have some insulin resistance.
A couple ways to improve your insulin sensitivity (reduce insulin resistance) are:
- lose your excess fat weight
- start a regular exercise program