Tag Archives: obesity

Evolutionary Aspects of Obesity, Insulin Resistance, and Cardiovascular Risk

paleo diet, Paleolithic diet, hunter-gatherer diet

Huaorani hunter in Ecuador

Spreadbury and Samis have a review-type article in Current Cardiovascular Risk Reports. Here’s the abstract:

Cardiovascular disease (CVD) is still virtually absent in those rare populations with minimal Western dietary influence. To date, exercise, altered fats, fibre, anti-oxidants or Mediterranean diet do not appear to overcome the discrepancy in CVD between hunter-gatherer and Western populations. The CVD risk factors of obesity and diabetes are driven by increased caloric intake, with carbohydrates potentially implicated. Paradoxically, non-Westernized diets vary widely in macronutrients, glycemic and insulinemic indices, yet apparently produce no obesity or CVD regardless, even with abundant food. ‘Ancestral’ grain-free whole-food diet may represent the best lifestyle intervention for obesity and CVD. Such diets are composed of the cells of living organisms, while Western grains, flour and sugar are dense, acellular powders. Bacterial inflammation of the small intestine and vagal afferents appears a crucial step in leptin-resistance and obesity. Therefore it may be important that the Western diet resembles a bacterial growth medium.

You may remember Spreadbury’s name from his theory about acellular carbohydrates causing obesity via alterations in gut microorganisms. Spreadbury is with the Gastrointestinal Diseases Research Unit, Queen’s University, Kingston, Ontario, Canada.

You can read the articles for yourself. The following are a few of the authors points I found interesting or want to remember.

Does physical activity explain differences in CVD between Westernized and non-Westernized Peoples? They say “maybe.”

Throughout the article are references to aboriginals like the Hadza, Kitavans, Ache, Shuar, Australian aborigines, and Inuits. I always take comparisons of them to modern Europeans with a grain of salt, because of potential genetic differences between the populations. Moreover, diet and activity levels are only two of myriad cultural differences.

Australian Aborigine in Swamp Darwin

Australian Aborigine in Swamp Darwin

Can dietary changes reduce the incidence of CVD? They say it’s unclear.

Regarding modern paleo diet trials, “All the studies with ad libitum eating [eat all you want] have reported a spontaneous reduction in caloric intake in the order of 15-30%.” (Three references.) “The reduced food intake appeared driven by a satiety increase that was apparently not explicable by energy density, fiber or macronutrient content.” (One reference.)

“In those eating a Westernized diet, carbohydrates are increasingly recognized as being associated with poor metabolic health.” Evidence? Only one reference cited: Zienczuk’s 2012 article on high arctic Inuits.

“…non-Westernized populations with excellent metabolic and cardiovascular health almost invariably have negligible dietary contribution from grains, as well as refined sugar.” No citations.

“For ‘western-style’ diets and most obesogenic diets tested, gut microbiota appear to play a crucial role in obesity.” That’s a bold statement. References? Only one, a mouse study.

The rest of the article is about Spreadbury’s acellular carb/obesity theory. He suggests that small intestine bacteria play a more prominent role than colonic germs. Bacterial-driven inflammation….

The authors provide an example of a grain-free whole-food diet. It’s unrestricted in fruit, leafy or root vegetables, unprocessed meats, eggs, fish, nuts (except peanuts), mushrooms, herbs and spices. Occasional foods to be eaten in moderation are legumes, rice, yogurt, milk, cheeses, sweet corn, palm oil/lard/olive oil, and salt. Avoid almost all processed foods, breads, cereals, cakes/cookies/donuts etc., refined sugars, dried or processed fruits, vegetable/seed oils, and processed meats. They advise a vitamin D supplement. I’m not sure if they came up with this diet on their own, or it’s S. Lindeberg’s outline.

A final quote:

The macronutrient independence of the health from ancestral diet suggests whole foods are more important to health than their macronutrient or other chemical components, and that good health is associated with unprocessed cellular foods. Flour, sugar and processed foods appear to be important drivers of Western metabolic dysfunction, overweight and inflammation, and may prove to have a profound impact on, or even be the initiators of cardiovascular disease.

I’m sure Spreadbury and Samis would agree we need more basic science and clinical research into these issues, involving human test subjects. Maybe I’m prejudiced, but I’m more interested in Asians, Africans, and Europeans than Shuar people.

Steve Parker, M.D.

Reference: Spreadbury, Ian and Samis, Andrew J.S. Evolutionary aspects of obesity, insulin resistance, and cardiovascular risk. Current Cardiovascular Risk Reports, April 2013, vol. 7, issue 2, pp. 136-146.

Is Dining Out Making Us Fat?

So easy to over-eat!

So easy to over-eat!

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987-88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977-78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977-78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977-78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977-78 to 1,807 calories per person per day in 1987-88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

Update:

Here’s a pie chart I found with more current and detailed information from the U.S. government (h/t Yoni Freedhoff):

feb13_feature_guthrie_fig03

Does Dining Out Cause Obesity?

Home-cooked meal

Home-cooked meal

The U.S. trend of increasing overweight and obesity started about 1970. I wonder if eating away from home is related to the trend. I found a USDA report with pertinent data from 1977 to 1995. It also has interesting info on snacking and total calories consumed. Some quotes:

“We define home and away-from-home foods based on where the foods are obtained, not where they are eaten. Food at home consists of foods purchased at a retail store, such as a grocery store, a convenience store, or a supermarket. Food away from home consists of foods obtained at various places other than retail stores (mainly food-service establishments).”

***

“Over the past two decades, the number of meals consumed has remained fairly stable at 2.6 to 2.7 per day. However, snacking has increased, from less than once a day in 1987-88 to 1.6 times per day in 1995. The increased popularity in dining out is evident as the proportion of meals away from home increased from 16 percent in 1977-78 to 29 percent in 1995, and the proportion of snacks away from home rose from 17 percent in 1977-78 to 22 percent in 1995. Overall, eating occasions (meals and snacks) away from home increased by more than two-thirds over the past two decades, from 16 percent of all eating occasions in 1977-78 to 27 percent in 1995.”

***

“Average caloric intake declined from 1,876 calories per person per day in 1977-78 to 1,807 calories per person per day in 1987-88, then rose steadily to 2,043 calories per person per day in 1995.”

***

“These numbers suggest that, when eating out, people either eat more or eat higher-calorie foods or both.”

Parker here. I’m well aware that these data points don’t prove that increased eating-out, increased snacking,  and increased total calorie consumption have caused our overweight and obesity problem. But they sure make you wonder, don’t they? None of these factors was on a recent list of potential causes of obesity.

If accurate, the increased calories alone could be the cause. Fast-food and other restaurants do all they possibly can to satisfy your cravings and earn your repeat business.

If you struggle with overweight, why not cut down on snacking and eating meals away from home?

Steve Parker, M.D.

The Mellberg Study: Paleo Diet and Obese Postmenopausal Women

Sweden's Flag. Most of the researchers involved with this study are in Sweden

Sweden’s Flag

Swedish researchers compared a Paleolithic-type diet against a lower-fat, higher-carb diet so often recommend in Nordic countries and in the U.S. Test subjects were obese but otherwise healthy older women. The study lasted two years. Dieters could eat as much as they wanted.

They found that the paleo-style dieters lost more weight, lost more abdominal fat, and lowered their trigyceride levels. When measured six months into the study, the paleo dieters had lost 6.5 kg (14 lb) of body fat compared to 2.6 (6 lb) kg in the other group.

Measured at two years out, the paleo dieters had lost 4.6 kg (10 lb) of body fat compared to 2.9 kg (6 lb) in the other group, but this difference wasn’t statistically significant.

The greatest weight loss was clocked at 12 months: Paleo dieters were down 8.7 (19 lb) kg compared to 4.4 kg (10 lb)  in the other group.

But this study was about more than weight loss. The investigators were also interested in cardiometabolic risk factors and overall body composition.

The Set-Up

I don’t know what the researchers told the women to get them interested. Weight loss versus healthier diet versus ?  This could have influenced the type of women who signed up, and their degree of commitment.

A newspaper ad got the attention of 210 women in Sweden; 70 met the inclusion criteria, which included a body mass index 27 or higher and generally good health. Average age was 60. Average BMI was 33. Average weight was 87 kg (192 lb). Average waist circumference was 105 cm (41 inches). The women were randomized into one of two diet groups (N=35 in each): paleolithic-type diet (PD) or Nordic Nutrition Recommendations diet (NNR). There were no limits on total caloric consumption. (Were the women told to “work on weight loss”? I have no idea.)

We don’t know the ethnicity of these women.

Here’s their version of the paleo diet:

  • 30% of energy (calories) from protein
  • 40% of energy from fat
  • 30% of energy from carbohydrate
  • high intake of mono- and polyunsaturated fatty acids
  • based on lean meat, fish, eggs, vegetables, fruits, berries, and nuts
  • additional fat sources were avocado and oils (rapeseed [canola] and olive) used in dressings and food preparation
  • cereals (grains), dairy products, added salt and refined fats and sugar were excluded
  • no mention of legumes, potatoes, or tubers

The NNR diet:

  • 15% of energy from protein
  • 25-30% of energy from fat
  • 55-60% of energy from carbohydrate
  • emphasis on high-fiber products and low-fat dairy products

Over the 24 months of the study, each cohort had 12 group meetings with a dietitian for education and support, including “dietary effects on health, behavioral changes and group discussion.”

Various blood tests and body measurements were made at baseline and periodically. Body measurements were made every six months. Body composition was measured by dual energy x-ray absorptiometry. Diet intake was measured by self-reported periodic four-day food records.

Stockholm Palace

Stockholm Palace

Results

30% of participants (21) eventually dropped out by the end of the study and were lost to follow-up, leaving 27 in the PD group and 22 in the NNR cohort.

Food record analysis indicated the PD group indeed reduced their carb intake while increasing protein and fat over baseline. Baseline macronutrient energy percentages were about the same for both groups: 17% protein, 45% carb, 34% (I guess the percentages don’t add to 100 because of alcohol, which wads not mentioned at all in the article.) Two years out, the PD group’s energy sources were 22% protein, 34% carb, 40% fat. For the NNR group, the energy sources at two years were 17% protein, 43% carb, and 34% fat. As usual, dietary compliance was better at six months compared to 24 months. The PD group failed to reach target amounts of protein energy (30%) at six and 24 months; the NNR group didn’t reach their goal of carbohydrate energy (55-60%). The PD group ate more mono- and poly unsaturated fatty acids than the NNRs.

In contrast to the food record estimates of protein intake, the urine tests for protein indicated poor adherence to the recommended protein consumption in the PD group (30% of energy). Both groups ate the same amount of protein by this metric. (This is an issue mostly ignored by authors, who don’t say which method is usually more accurate.)

“Both groups had statistically significant weight loss during the whole study, with significantly greater weight loos in the PD group at all follow up time points except at 24 months.” Largest weight loss was measured at 12 month: 8.7 kg (19 lb) in the PD group versus 4.4 kg (10 lb) in the NNRs.

The PD group lost 6.5 kg (14 lb) of body fat by six months but the loss was only 4.6 kg (10 lb) measured at 24 months. Corresponding numbers for the NNR group were 2.6 and 2.9 kg (about 6 lb). So both groups decreased their total fat mass to a significant degree. The difference between the groups was significant (P<0.001) only at six months. The greatest weight loss was clocked at 12 months: PD dieters were down 8.7 kg (19 lb) compared to 4.4 kg (10 lb) in the NNRs. Both groups saw a significant decrease in waist circumference during the whole study, with a more pronounce decrease in the PD group at six months: 11 versus 6 cm (4.3 versus 2.4 inches).

Fasting blood sugars, fasting insulin levels, and tissue plasminogen activator activity didn’t change.

Both groups had improvements in blood pressure, heart rate, c-reactive protein, LDL cholesterol, PAI-1 activity, and total cholesterol. The PD group saw a greater drop in triglycerides (by 19% at two years, but levels were normal to start with at 108 mg/dl or 1.22 mmol/l).

Reported daily energy intake fell over time for both groups, without statistically significant differences between them.

paleo diet, Steve Parker MD, diabetic diet

Sweet potato chunks brushed with olive oil, salt, pepper, and rosemary. Ready for the oven.

Discussion

As measured at six months, the paleo dieters lost 10% of their initial body weight, compared to 5% in the NNR group. That’s worth something to many folks. However, the researchers didn’t find much, if any, difference in the groups in terms of cardiometabolic risk factors. They wonder if that reflects the baseline healthiness of these women. Would a sicker study population show more improvement on one of the diets?

I’m surprised the NNR group lost any weight at all. In my experience it’s hard for most folks to lose weight and keep it off while eating as much as they want, unless they’re eating very-low-carb. We’ve seen short-term weight loss with ad libitum paleo diets before (here for example, and here, and here). I bet the women signing up for this study were highly motivated to change. 

Legumes and potatoes are a debatable part of the paleo diet. Most versions exclude legumes. We don’t know if these women ate legumes and potatoes. Other than this oversight, the study paleo diet is reasonable.

The authors noted that the paleo diet group failed to reach their protein intake goal (30% of total calories), and suggested reasons “such as protein-rich foods being more expensive, social influences on women’s food choices or a lower food preference for protein-rich food among women.”

The results of this study may or may not apply to other population subgroups and non-Swedes.

The authors write:

In conclusion, a Palaeolithic-type diet during two years with ad libitum intake of macronutrients, including an increased intake of polyunsaturated fatty acids and monounsaturated fatty acids reduces fat mass and abdominal obesity with significantly better long-term effect on triglyceride levels vs an NNR diet. Adherence to the prescribed protein intake was poor in the PD group suggesting that other component of the PD diet are of greater importance.

Does this study have anything to do with diabetes? Not directly. But it suggests that if an overweight diabetic needs to lose excess body fat without strict calorie control, a lower-carb paleo-style diet may be more effective than a low-fat, higher-carb diet. I would have liked to have seen lower fasting blood sugar and insulin levels in the paleo dieters, but wishing doesn’t make it so.

Steve Parker, M.D.

PS: Carbsane Evelyn has taken a look at this study and blogged about it here and here. I’ve not read those yet, but will now.

Reference: Mellberg, C., et al (including M. Ryberg and T Olsson). Long-term effects of a Palaeolithic-type diet in obese postmenopausal women: a 2-year randomized trial. European Journal of Clinical Nutrition, advance online publication January 29, 2014. doi: 10.1038/ejcn.2013.290

Don’t Kid Yourself: Obesity Still Shortens Life Even If “Metabolically Healthy”

I'll eat my hat if this dude doesn't have metabolic syndrome

I’ll eat my hat if this dude doesn’t have metabolic syndrome

See details at MedPageToday.

Some folks can get away with smoking or drinking too much, but others can’t. They have hell to pay. There’s one sure-fire way to eliminate smoking-related disease risk.

Some studies suggest you can be healthy and long-lived while obese as long as you’re “metabolically healthy.” That is, if you have normal blood pressure, LDL cholesterol, triglycerides, blood sugar, and waist circumference. (You can be obese with a “normal” waist circumference, but it’s not easy.) A new meta-analysis finds the “metabolically healthy” label is a misnomer: you’re still at higher risk for death or cardiovascular events if you’re obese and free of metabolic syndrome features.

“Our results do not support this concept of ‘benign obesity’ and demonstrate that there is no ‘healthy’ pattern of obesity,” Kramer and colleagues wrote. “Even within the same category of metabolic status (healthy or unhealthy) we show that certain cardiovascular risk factors (blood pressure, waist circumference, low high-density lipoprotein cholesterol level, insulin resistance) progressively increase from normal weight to overweight to obese.”

Click for the scientific journal abstract.

This report does not directly address the “fat but fit” concept, whereby you can counteract some of the adverse health effects of obesity by being fit. By fit, I mean regularly exercising and achieving a decent level of capacity and tolerance for physical activity. Fat but fit still holds.

Steve Parker, M.D.

PS: For an opposing view of the study at hand, see comments by psychologist Deb Burgard. (h/t Beth Mazur)

Heresy! Sleep Deprivation NOT Linked to Adult Obesity

Paleobetic diet

I bet she’s faking

It’s currently popular to blame inadequate sleep time for overweight and obesity. I found a study supporting that idea in children, but not adults. Here’s the authors’ conclusion:

While shorter sleep duration consistently predicts subsequent weight gain in children, the relationship is not clear in adults. We discuss possible limitations of the current studies: 1.) the diminishing association between short sleep duration on weight gain over time after transition to short sleep, 2.) lack of inclusion of appropriate confounding, mediating, and moderating variables (i.e. sleep complaints and sedentary behavior), and 3.) measurement issues.

I found another analysis from a different team that is skeptical about the association of sleep deprivation and obesity in adults.

Everybody knows adults are getting less sleep now than we did decades ago, right? Well, not really. From Sleep Duration Across the Lifespan: Implications for Health:

Twelve studies, representing data from 15 countries and a time period of approximately 40 years, attempted to document changes in sleep duration over that time period. They found that, overall, there is no consistent evidence that sleep durations worldwide are declining among adults. Sleep duration decreased in six countries, sleep duration increased in seven countries, and mixed results were detected in two (one of which was the USA). In particular, the data from the USA suggest that although mean sleep duration may have actually increased slightly over the past 40 years, the proportion of short sleepers (six hours per night or less) also seems to have increased over the past several decades.

See, it’s complicated. Don’t believe everything you read. Not even this.

Steve Parker, M.D.

PS: It’s fun being an iconoclast now and then!

Do Environmental Contaminants Cause Type 2 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 month ago I watched part of a documentary called “Plastic Planet” on Current TV (Now Al Jazeera TV). It was alarming. Apparently chemicals are leaking out of plastics into the environment (or into foods contained by plastic), making us diabetic, fat, 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 chemicals I remember being mentioned 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 and often cover microwaved food with Glad Press’n Seal plastic wrap.

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 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 CDC suggests a slight drop in childhood obesity in recent years (2010 data).

“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 decided 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.

Do Warm Houses and Workplaces Contribute to Obesity?

Dr. Stephan Guyenet thinks they might. It’s not so much heat as it is failing to expose our bodies adequately to temperatures around 60° F (15.6° C) or lower on a regular basis. Here’s a human experiment Dr. G wrote about:

The second study went further, using a longer cold exposure protocol to investigate changes in fat mass among people with low brown fat activity at baseline (4).  Researchers exposed volunteers to 63 F (17 C) air for two hours a day over a six-week period; again I assume they were lightly clothed.  As in the previous study, they observed an increase in brown fat activity with cold training, and they found that calorie expenditure was higher when subjects were in the ‘cold’ air.  After six weeks of training, body fat mass had declined by about 5 percent.  This is despite the fact that all subjects were lean to begin with!

Read the rest.

I thought this study tied in with that one showing an inverse relationship between altitude and obesity. Environmental temperature rises roughly 3° F with every 1,000 feet (305 meters). But the altitude study controlled for (accounted for) temperature, meaning that the temperature had nothing to do with the association.

Somebody’s probably already tried to link environmental temperatures—whether inside the house or out—to obesity rates. Let me know if you find it.

—Steve

PS: A few minutes at Pubmed.gov revealed this 2013 abstract:

Objective: Raised ambient temperatures may result in a negative energy balance characterized by decreased food intake and raised energy expenditure. This study tested whether indoor temperatures above the thermoneutral zone for clothed humans (approx. 23 o C) were associated with a reduced body mass index (BMI). Design and Methods: Participants were 100,152 adults (≥ 16 years) drawn from 13 consecutive annual waves of the nationally representative Health Survey for England (1995 – 2007). Results: BMI levels of those residing in air temperatures above 23 o C were lower than those living in an ambient temperature of under 19 o C (b = -.233, SE =.053, p <.001), in analyses that adjusted for participant age, gender, social class, health and the month/year of assessment. Robustness tests showed that high indoor temperatures were associated with reduced BMI levels in winter and non-winter months and early (1995 – 2000) and later (2001 – 2007) survey waves. Including additional demographic, environmental, and health behavior variables did not diminish the link between high indoor temperatures and reduced BMI. Conclusions: Elevated ambient indoor temperatures are associated with low BMI levels. Further research is needed to establish the potential causal nature of this relationship.

PPS: And there’s this abstract, probably from the altitude study I mentioned:

http://www.ncbi.nlm.nih.gov/pubmed/23357956

“There was an approximately parabolic relationship between mean annual temperature and obesity, with maximum prevalence in counties with average temperatures near 18 °C [64.4° F].”

I don’t have the full article, but parabolic, to me in this context, probably means the obesity incidence was highest at 64.4° F, with lower obesity incidence both above and below 64.4°.

Of course, living in a particular environment doesn’t equate to exposing yourself to outdoor temperatures. But it makes sense that someone living in a cold environment will have more cold exposure than someone in a hot climate.

Perhaps 64.4° F is a sweet spot for efficient body temp regulation and energy partitioning. Living at temps significantly above or below that may cost you energy-wise: you expend extra calories maintaining a normal body temperature, tending to result in lower obesity incidence.

Do High Insulin Levels Cause Memory Loss and Dementia?

dementia, memory loss, Mediterranean diet, low-carb diet, glycemic index, dementia memory loss

Don’t wait to take action until it’s too late

Insulin resistance and high blood insulin levels promote age-related degeneration of the brain, leading to memory loss and dementia according to Robert Krikorian, Ph.D. He’s a professor in the Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati Academic Health Center.  He has an article in a recent issue of Current Psychiatry – Online.

Proper insulin signaling in the brain is important for healthy functioning of our brains’ memory centers.  This signaling breaks down in the setting of insulin resistance and the associated high insulin levels.  Dr. Krikorian makes much of the fact that high insulin levels and insulin resistance are closely tied to obesity.  He writes that:

Waist circumference of ≥100 cm (39 inches) is a sensitive, specific, and independent predictor of hyperinsulinemia for men and women and a stronger predictor than body mass index, waist-to-hip ratio, and other measures of body fat.

Take-Home Points

Dr. Krikorian thinks that dietary approaches to the prevention of dementia are effective yet underutilized.  He mentions reduction of insulin levels by restricting calories or a ketogenic diet: they’ve been linked with improved memory in middle-aged and older adults. His theory is also consistent with the commonly seen association of type 2 diabetes with dementia: overweight and obese type 2’s quite often have high insulin levels, at least in the early years.

Dr. K suggests the following measures to prevent dementia and memory loss:

  • eliminate high-glycemic foods like processed carbohydrates and sweets
  • replace high-glycemic foods with fruits and vegetables (the higher polyphenol intake may help by itself)
  • certain polyphenols, such as those found in berries, may be particularly helpful in improving brain metabolic function
  • keep your waist size under 39 inches (99 cm), or aim for that if you’re higher and overweight

Nearly all popular versions of the paleo diet would qualify as being low glycemic index.

I must mention that many dementia experts, probably most, are not as confident  as Dr. Krikorian that these dietary changes are effective.  I think they are, to a degree.

The Mediterranean diet is high in fruits and vegetables and relatively low-glycemic.  It’s usually mentioned by experts as the diet that may prevent dementia and slow its progression.

Read the full article.

I’ve written before about how blood sugars in the upper normal range are linked to brain degeneration.  Dr. Krikorian’s recommendations would tend to keep blood sugar levels in the lower end of the normal range.

Steve Parker, M.D.

PS: Speaking of dementia and ketogenic, have you ever heard of the Ketogenic Mediterranean Diet?  (Free condensed version here.)

Could Acellular Carbohydrates Be the Cause of Obesity?

Ivor Goodbody in a recent tweet reminded me of an interesting nutrition science article.  Ian Spreadbury hypothesizes that carbohydrate density of modern foods may be the cause of obesity.  Refined sugars and grains—types of acellular carbohydrates—are  particularly bad offenders.

Harvesting acellular carbs

These acellular carbs may alter our gut microorganisms, leading to systemic inflammation and leptin resistance, etc.  Our Paleolithic ancestors had little access to acellular carbohydrates.

Read more about it in “Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity,” in Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 2012, vol. 5, pp. 175-189.

To reverse our modern obesity epidemic, we need better understanding of the underlying pathophysiology.

—Steve

PS:  For Spreadbury’s formal definition of acellular carbohydrates, see my long comment below.