Tag Archives: overweight

Do Environmental Pollutants Cause Diabetes or Obesity?

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

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

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

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

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

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

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

What Does the Science Tell Us?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

You need a break. Enjoy.

You need a break. Enjoy.

My Conclusions

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

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

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

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

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

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

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

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

Steve Parker, M.D.

Additional Resources:

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

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

From Wikipedia:

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

The list of the criteria is as follows:

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

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

Why Aren’t South Koreans Fat Like Us?

Based on a trip there, Ned Kock has some ideas:

In our meal, the way in which at least one of the carbohydrate-rich items was prepared possibly decreased its digestible carbohydrate content, and thus its calorie content, in a significant way. I am referring to the rice, which had been boiled, cooled and stored, way before it was re-heated and served. This likely turned some of its starch content, maybe a lot of it, into resistant starch. Resistant starch is essentially treated by our digestive system as fiber. 

This was one of several traditional Korean meals I had, and all of them followed a similar pattern in terms of the order in which the food items were consumed, and the way in which the carbohydrate-rich items were prepared. The order in which you eat foods affects your calorie intake because if you eat high nutrient-to-calorie ratio foods before, and leave the low nutrient-to-calorie ones for later, my experience is that you will eat less of the latter. 

Another possible hidden reason for the low rate of obesity in South Korea is what seems to be a cultural resistance to industrialized foods, particularly among older generations; a sort of protective cultural inertia, if you will. Those foods are slowly being adopted – my visit left me with that impression – by not as quickly as in other countries. And there is overwhelming evidence that consumption of highly industrialized foods, especially those rich in refined carbohydrates and sugars, is a major cause obesity and a host of other problems.

Read the rest.

Low-Carb Ketogenic Diet Appears Safe and Effective for Children and Adolescents

A ketogenic diet was safe and effective for weight loss in children and adolescents, according to a small study in the Journal of Pediatric Endocrinology and Metabolism.  Fifty-six children were placed on either a ketogenic diet or a calorie-restricted diet.  The investigators judged the low-carb ketogenic diet more effective.

I don’t treat children, so I don’t normally follow the pediatric scientific literature.  Thanks to Diet Doctor Andreas Eenfeldt for bringlng this to my attention.  I’ve not read the full research report.

In 2010 I reported on research showing a low-carb, high-protein diet was safe and effective for severely obese adolescents.

Is Fructose the Cause of Our Obesity Epidemic?

Mainly because of its low cost, HFCS [high fructose corn syrup] consumption replaced approximately one-third of the total sugar consumption in the USA between 1970 and 2000, paralleling to some extent the increasing prevalence of obesity during this period. Consequently, HFCS has been a particular focus of possible blame for the obesity epidemic. However, HFCS consumption has remained very low in other parts of the world where obesity has also increased, and the most commonly used form of HFCS contains about 55% fructose, 42% glucose, and 3% other sugars, and hence is associated with similar total fructose and glucose intakes as with sugar. Furthermore, sucrose is hydrolyzed in the gut and absorbed into the blood as free glucose and fructose, so one would expect HFCS and sucrose to have the same metabolic consequences. In short, there is currently no evidence to support the hypothesis that HFCS makes a significant contribution to metabolic disease independently of the rise in total fructose consumption.

Given the substantial consumption of fructose in our diet, mainly from sweetened beverages, sweet snacks, and cereal products with added sugar, and the fact that fructose is an entirely dispensable nutrient, it appears sound to limit consumption of sugar as part of any weight loss program and in individuals at high risk of developing metabolic diseases. There is no evidence, however, that fructose is the sole, or even the main factor in the development of these diseases…

— Luc Tappy in BMC Biology, May 21, 2012 (the article is a review of fructose metabolism and potential adverse effects of high consumption)

PS: Luc Tappy believes that excessive calorie consumption is an important cause of overweight and obesity.

Steve Parker, M.D.

For Weight Loss, What’s More Important: Exercise or Food?

This is NOT diet food

What you eat, and how much, are more important than your physical activity.  By far.

  • Your genetics largely determines your response to an exercise program
  • Physical activity isn’t a great way to lose weight
  • School-based or other programs to increase childhood physical activity probably won’t reverse childhood obesity statistics
  • Disregarding weight loss, exercise has other worthwhile metabolic advantages
  • Highly advanced societies shouldn’t blame our overweight problem on decreased levels of physical activity

Skyler Tanner slaughters some sacred cows in his blog post June 4, 2012. I pulled these bullet points from his post. Click on his embedded links for details.

Steve Parker, M.D.

Which Diet Is Better for Weight Loss: Low-Carb or Low-Fat?

I’ve written about a 2009 New England Journal of Medicine article comparing weight-loss diets of various macronutrient (fat, protein, carbohydrate) composition. Its conclusion: Cut back on calories and you will lose weight, regardless of macrontrient percentages.

A blurry low-carb high-fat breakfast

A blog reader, Matt, brought up some interesting comments and questions. What follows will make little sense unless you read that prior post.

Matt writes:

Dr. Parker,

If the study folks didn’t do the real low carb diet because they “knew” that ketosis wouldn’t occur, couldn’t they at least have tried it, since what they were trying to prove was a calorie is a calorie?

Looking at the menus, the diet that they are purporting as low carb is really nothing close to a real low carb diet. It is a slightly lower carb diet, and not high enough in fat to prove anything. 35% carb is not Atkins phase anything. For a participant consuming 1600 calories, that’s 140g carb — too high for anyone attempting to restrict carbohydrates for health.

Please comment on the fact that the highest carb diet provided the worst lipid improvement.

Following up a little more, there really is no inference whatsoever that can be made with regard to a low carb diet with this study. Did you read the sample menu? No low carb diet phase would have any of the following as a typical meal. You can tell by looking at the menus that they had to be really PC about a “high fat” diet as well. I mean skim milk on a low carb / high fat diet? Note my level of surprise by the ? and ! in the parens with each “typical meal” option:


1 poached egg

1/2 bagel (??)

4 oz apple juice (????!!!!)

skim (????) milk


1/2 cup spaghetti (??!!)

1/2 cup squash

1/2 cup peppers

1/2 cup mushrooms

1.5 T Olive Oil

1 small banana (????)


2 oz beef

1 small potato (????!!!!)

3/4 mixed veggies/legumes corn/carrots/lima/peas/green beans (???? since these are among the higher carb veggie choices)

1/2 cup cabbage

1 mini box raisins (??)

1 small apple (?????)

4 t Olive Oil

7 walnut halves


Skim (???) Milk

1 Graham cracker sheet (??????)

If you want a LC diet with what LC would consider a higher level of carbs (~60g) you need to do this:


2-4 poached eggs

2 T olive oil


1 cup whole milk


1/2 cup squash

1/2 cup peppers

1/2 cup mushrooms

2 T Olive Oil

4-6 oz fish


4-6 oz beef

3/4 mixed lower carb (cruciferous/leafy) veggies such as broccoli, collards or other greens,

1/2 cup cabbage

2 T Olive Oil

20 walnut halves

1/2 cup low carb fruit such as cantaloupe


1/2 cup strawberries

1 cup whole milk yogurt ot cottage cheese


My response:

Thanks for your thoughtful comments/questions, Matt.

You’re right: The “low-carb” diet they studied indeed was not very low-carb, as succinctly illustrated by the sample menu you provided. (I didn’t read the supplementary appendix myself.)

You mention that the “highest carb diet provided the worst lipid improvement.” It’s not that clear-cut.

(Lipid changes are on pages 865-7 of the article, for anyone following along. Conventional wisdom is that better cardiovascular health is associated, generally, with lower total cholesterols, higher HDL chol, lower total LDL chol, and lower triglycerides.)

The study had two low-fat diets, with either 55 or 65% of total calories derived from carbohydrates. The two high fat diets had either 35 or 45% of total calories from carbohydrates.

Total cholesterol levels dropped by about 3 mg/dl in the low-fat diets compared to “no change” in the high-fat diets (2-year values). Measured at 6 months, total chol levels were down by about 5.5 mg/dl in the low-fat groups, and about 3 mg/dl in the high-fat groups. Baseline total chol levels for the whole group averaged 202 mg/dl.

The authors on page 865 write:

All the diets reduced risk factors for cardiovascular disease and diabetes at 6 months and 2 years. At 2 years, the two low-fat diets and the highest-carbohydrate diet decreased low-density lipoprotein [LDL] cholesterol levels more than did the high-fat diets or lowest-carbohydrate diet.

The lowest-carb diet increased HDL chol more than the highest carb diet, but we’re only talking about a 2 mg/dl difference measured at 2 years. HDL rose in all groups. Average baseline HDL level for the entire study group was 49 mg/dl.

All diets decreased triglycerides similarly, by 12-17%.

The magnitude of these changes is not great, and I question whether clinically important. The take-home point for me is that low-carb eating may not be (and probably isn’t) as atherogenic as warned by the medical community 15-20 years ago, judging purely from lipid changes. Other studies found similar numbers. But we’ve already agreed the this was not a serious trial of low-carb dieting.

The study authors write that HDL chol is a biomarker for carbohydrate intake: reducing dietary carbs tends to increase HDL chol levels, and vice versa.

If I understand “Nutrient Intake per Day” in Table 2 correctly, the participants who were told to increase their percentage of calories from fat really didn’t do it: they reduced it by 3.5% (!?). The low-fat cohorts had more success with compliance.

Clearly, it’s quite difficult to get free-living people to change their macronutrient intake and sustain the change for even six months, much less two years. Would compliance have been better if subjects had been allowed to choose a diet according to their natural inclinations? Maybe.

A recent study suggests that eating low-carb helps with prevention of weight regain because it burns an extra 300 calories a day compared to those eating low-fat.  Dr. Barbara Berkeley took a close look at this research on June 30.

Steve Parker, M.D.

Are We Fat Because We Eat Too Much, Or Lack Physical Activity?

Are we fat because we eat too much, or lack physical activity?

Most people would say, “It’s both.” Most people would be wrong, at least in terms of populations rather than individuals.

Obesity results from a protracted imbalance between energy intake (calories we eat) and energy expenditure (physical activity and resting metabolism).

Overweight and obesity have increased significantly over the last 25 years in most of the developed world. Is it because we started eating more, or that we have so many energy-saving devices that we now expend less energy on physical activity? If we are less active due to technologic advances, yet keep eating as much as in the past, we will gain weight as the excess calories are stored as fat.

Technologic advances over the last 150 years have allowed us to transform from a labor-intensive agrarian economy to one based on services and information. Computers, in particular, have made it much less labor-intensive to get our jobs done. For example, when I was a hospital intern 30 years ago, I made multiple daily trips from the patient care floors downstairs to Radiology to look at x-ray films. Now, the “films” are at my fingertips on computers close to the bedside.

Have trends in technology over the last 25 years continued to reduced the energy expenditure needed to get through our days? Alternatively, are we exercising less? Either explanation would lead to weight gain if caloric intake remained the same.

Researchers in 2008 studied populations in Europe and North America, examining trends in physical activity energy expenditure over time, since the 1980s. Energy expenditure was evaluated with a highly accurate method called “doubly labelled water.” They found that physical activity energy expenditure actually increased over time, although not by much. They conclude that the ballooning waistlines in the study populations are likely to reflect excessive intake of calories.

(All I have is the abstract of the article. I’ll try to get the full article and report back here if anything additional is interesting.)

So according to Westerterp and Speakman, the problem has not been lack of physical activity. We’re simply eating too much.

On the other hand, a 2011 study found that daily work-related energy expenditure decreased by over 100 calories in the U.S. over the last 50 years.  That could certainly contribute to our expanding waistlines.

Steve Parker, M.D.

Reference: Westerterp, K.R., and Speakman, J.R. Physical activity energy expenditure has not declined since the 1980s and matches energy expenditures of wild mammals. International Journal of Obesity, 32 (2008): 1256-1263. Published online May 27, 2008. doi: 10.1038/ijo2008.74

Prostate Cancer Deaths Linked to Overweight and High Insulin Levels

Lancet Oncology in 2008 published a report associating worse prostate cancer outcomes—death, that is—with overweight, obesity, and hyperinsulinemia.

Grapes are an iconic Mediterranean fruit

Researchers looked at data from the respected Physicians’ Health Study, finding 2,546 men who developed prostate cancer during many years of observation. Of these men, 38.8% were overweight (body mass index 25–30) and 3.4% were obese (BMI over 30).

(For definitions of overweight and obesity, and to calculate your body mass index, click here.)

Compared with normal-weight men (BMI under 25) who developed prostate cancer, overweight men with prostate cancer were one-and-a-half times more likely to die from the cancer. Obese men with prostate cancer were two-and-a-half times more likely to die.

A blood test called C-peptide is a marker of insulin resistance and hyperinsulinemia. Obesity is often accompanied by high insulin levels and insulin resistance. Overweight, not so much. Eight hundred twenty-seven of the men with prostate cancer had C-peptide levels drawn at baseline, before diagnosed with cancer. Men with the highest C-peptide levels were almost two-and-a-half times more likely to die of prostate cancer than men with the lowest C-peptide levels.

Study participants having both excess body weight and high C-peptide levels had the worst outcome.

Prostate cancer is the most common invasive cancer in U.S. men, with about 185,000 cases diagnosed every year. It is one of the cancers that can be prevented by following the traditional Mediterranean diet for years. The other prevented cancers are breast, uterus, and colorectal. Obesity predisposes men to cancer of the prostate, colon, rectum, kidney, and esophagus.

The study at hand suggests that if you are overweight or obese and then develop prostate cancer, you have a greater risk of dying from the cancer compared with healthy-weight men. Given that prostate cancer is so common, why not cut your risk of getting it and dying from it by controlling your weight with a Mediterranean-style diet?

Steve Parker, M.D.

Reference: Ma, Jing, et al. Prediagnostic body mass index, plasma C-peptide concentration, and prostate cancer-specific mortality in men with prostate cancer: a long-term survival analysis. Lancet Oncology, online publication October 6, 2008. DOI: 10.1016/S1470-2045(08)70235-3

Are We Fat Because We’re Less Active Now?

Less active

Much of the globe 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.  Considering both these trends together, how could we not be fat?

Steve Parker, M.D. 

Fat Cell Turnover: Implications for Weight Loss

The number of fat cells in our bodies is constant throughout adult life for both lean and overweight people. When adults gain fat weight, it’s because our individual fat cells store more fat, thereby enlarging. We don’t gain more fat cells. Conversely, when we lose weight, the fat cells shrink.

Our number of fat cells is set during childhood and adolescence. Lean individuals generally have fewer fat cells than overweight people.

In many living tissues, individual cells gradually die off and are replaced by new cells. For example, we shed dead skin cells all the time, but they are replaced just as quickly by new skin cells. A red blood cell lives three months then dies and is replaced. The percentage of cells that die and are replaced over a period of time is called “turnover.”

Researchers in Stockholm recently studied the turnover of fat cells in humans. They measured turnover by analysing the incorporation of carbon-14 derived from nuclear bomb tests in genomic DNA. They found that 10% of fat cells die off and are renewed yearly at all adult ages in both skinny and overweight people.

So what?

Well, if 10% of your fat cells die every year, what if you could prevent them from being replaced with new ones? You would lose weight, as long as your remaining fat cells didn’t swell with more stored fat. Next year, another 10% of your fat cells die, and so on.

How can we prevent dead fat cells from being replaced by new ones? Nobody knows . . . yet. You can bet that pharmaceutical companies are thinking about this.

But I wouldn’t hold my breath. Pharmaceutical intervention will not be available for at least eight to 10 years, if ever.

We already have available, in 2009, a tried and true method for reducing fat mass: Eat Less, Move More.

Steve Parker, M.D.

Reference: Spalding, K.L., et al. Dynamics of fat cell turnover in humans. Nature, 453 (2008): 783-787. Epub May 4, 2008. PMID: 18454136.