Category Archives: Overweight

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.

David Mendosa On Weight Loss and Long-Term Management

Maybe his method works only for him, but I doubt it. David has diabetes, by the way. See his 2012 article at HealthCentral for details. Here’s a bit:

One cornerstone of this new way to lose weight and maintain weight loss is a twist on a standard dieting recommendation. But instead of weighing myself once a week, I weigh myself every morning.

Supposedly people get discouraged from daily weigh-ins because our weight seems to fluctuate up or down a couple of pounds every day for no good reason, or for at least for no reason that we can figure out. The fluctuations are certainly true in my experience. But, of course, the same fluctuations happen when we make our weigh-ins once a week, and that would be even more misleading.

Then, when the scales tell me that my weight is up that morning from the previous morning, I make an immediate course correction, which we know is easier in the long run than to wait until things get totally out of hand. My immediate course correction is simple. I skip dinner that day.

Note well, however, that skipping dinner could lead to major hypoglycemia if you’re taking certain diabetes drugs. Work with your personal healthcare provider on drug dose adjustments.

Steve Parker, M.D.

Do Vegetables and Fruits Prevent Disease?

Switching to the paleo diet often leads to increased vegetable and fruit consumption

Switching to the paleo diet often leads to increased vegetable and fruit consumption

Potential answers are in the American Journal of Clinical Nutrition (2012).  I quote:

For hypertension, coronary heart disease, and stroke, there is convincing evidence that increasing the consumption of vegetables and fruit reduces the risk of disease. There is probable evidence that the risk of cancer in general is inversely associated with the consumption of vegetables and fruit. In addition, there is possible evidence that an increased consumption of vegetables and fruit may prevent body weight gain. As overweight is the most important risk factor for type 2 diabetes mellitus, an increased consumption of vegetables and fruit therefore might indirectly reduces the incidence of type 2 diabetes mellitus. Independent of overweight, there is probable evidence that there is no influence of increased consumption on the risk of type 2 diabetes mellitus. There is possible evidence that increasing the consumption of vegetables and fruit lowers the risk of certain eye diseases, dementia and the risk of osteoporosis. Likewise, current data on asthma, chronic obstructive pulmonary disease, and rheumatoid arthritis indicate that an increase in vegetable and fruit consumption may contribute to the prevention of these diseases. For inflammatory bowel disease, glaucoma, and diabetic retinopathy, there was insufficient evidence regarding an association with the consumption of vegetables and fruit.

It bothers me that vegetables and fruits are lumped together: they’re not the same.

The paleo diet is unfairly characterized as meat-centric. It can certainly provide beaucoup vegetables and fruits. Diabetics should be careful which ones they choose, to avoid spikes in blood sugar.

Steve Parker, M.D.

Ancestral Diet May Improve Diabetes in Pima Indians

Saguaro cactus fruit is edible

I ran across a 1991 New York Times article by Jane Brody discussing the benefits to Pima Indians of returning to their ancestral diet.  The Pima have major problems with obesity and diabetes.  (I frequently treat Pima Indians in the hospital.)  Some quotes:

Studies strongly indicate that people who evolved in these arid lands are metabolically best suited to the feast-and-famine cycles of their forebears who survived on the desert’s unpredictable bounty, both wild and cultivated.

By contrast, the modern North American diet is making them sick. With rich food perpetually available, weights in the high 200’s and 300’s are not uncommon among these once-lean people. As many as half the Pima and Tohono O’odham (formerly Papago) Indians now develop diabetes by the age of 35, an incidence 15 times higher than for Americans as a whole. Yet before World War II, diabetes was rare in this population.

Pima Indians traditionally ate a diet of tepary beans, mesquite seeds, corn, grains, greens, and other high-fiber/low-fat foods.  The switch to a diet high in sugar, refined grains, and other highly processed convenience foods may well be responsible for the current high rates of obesity and diabetes.  Australian aborigines have the same problem.

Steve Parker, M.D.

Are We Fat Because We’re Less Active?

Less active

Much of the world has seen a significant decline in populaton-wide physical activity over the last few decades, according to Nike-sponsored research reported in Obesity Reviews.

Countries involved with the study are the U.S., U.K., Brazil, China, and India.  How did they measure activity levels?

Using detailed historical data on time allocation, occupational distributions, energy expenditures data by activity, and time-varying measures of metabolic equivalents of task (MET) for activities when available, we measure historical and current MET by four major PA domains (occupation, home production, travel and active leisure) and sedentary time among adults (>18 years).

The authors note the work of Church, et al, who found decreased work-related activity in the U.S. over the last half of the 20th century.

Inexplicably, they don’t mention the work of Westerterp and colleagues who found no decrease in energy expenditure in North American and European populations since the 1980s.

More active

My gut feeling is that advanced populations around the globe probably are burning fewer calories by physical activity over the last 50 years, if not longer, thanks to technologic advances.  We in the U.S. are also eating more calories lately.  Since the 1970s, average daily consumption by women is up by 150 calories, and up 300 by men.  I’m surprised we’re not fatter than we are.

Steve Parker, M.D. 

Prediabetes and Diabetes on the March in U.S. Adolescents

The June, 2012, issue of Pediatrics has an article stating that the incidence of diabetes and prediabetes in U.S. adolescents increased from 9% in 1999 to 23% in 2008.  The finding is based on the NHANES survey of 12 to 19-year-olds, which included a single fasting blood sugar determination.

The investigators offered no solution to the problem.  I’m no pediatrician, but my educated guess is that the following measures would help prevent adolescent type 2 diabetes and prediabetes:

  • more exercise
  • eat less refined starches and sugar
  • maintain body weight in the healthy range
I’m sure many of the adolescent type 2 diabetics and prediabetics are overweight or obese.  A 2010 study out of Colorado found a low-carbohydrate, high-protein diet safe and effective for adolescents.  Fortunately, the decades-long ascent of the adolescent obesity rate in the U.S. seems to have peaked for now.
The paleo diet would restrict consumption of concentrated sugars and refined starches, but it’s hard to get adolescents to skip those items.

Steve Parker, M.D.

PS: I scanned the article quickly and don’t remember if the researchers broke down the diabetes cases by type 1 and type 2.  I’d be shocked if type 1 diabetes rose this much over the last decade.

Are Dense Acellular Carbohydrates the Primary Cause of Obesity?

That’s a proposal in a recent scientific article, from which I quote:

The present hypothesis suggests that in parallel with the bacterial effects of sugars on dental and periodontal health, acellular flours, sugars, and processed foods produce an inflammatory microbiota via the upper gastrointestinal tract, with fat able to effect a “double hit” by increasing systemic absorption of lipopolysaccharide. This model is consistent with a broad spectrum of reported dietary phenomena. A diet of grain-free whole foods with carbohydrate from cellular tubers, leaves, and fruits may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of non-Westernized populations, and the apparent efficacy of the modern “Paleolithic” diet on satiety and metabolism.

You can read the whole shebang free online.

Steve Parker, M.D.

Bacteria in Petri dish

Reference:  Spreadbury, Ian.  Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity.Diabetes Metab Syndr Obes. 2012; 5: 175–189. Published online 2012 July 6. doi:  10.2147/DMSO.S33473 PMCID: PMC3402009

 

We’re Fat Because We Eat Too Much

At least one group of hunter-gatherers doesn’t burn any more calories in physical activity than Western cultures.  So much for blaming our fatness on low activity levels and labor-saving technology.

Cliff Notes version from the BBC.

—Steve

h/t Colby Vorland at nutsci.org