Culture War, Obesity and the New Puritans

I almost forgot I’m a blogger. Nah, not really, but it’s been difficult to keep up lately. I write longer posts, and want to take care to do the homework, so that I’m not producing something that’s misleading. For example, take this recent post by Paul Campos over at Lawyers, Guns and Money. Paul objects to the idea that public health measures involving promoting changes in lifestyle, specifically with what we eat or drink, might help reduce health care costs, or as he says it:

[i]n any case the notion we can cut health care costs significantly by getting people to drink less soda and eat fewer Doritos is unsupported by any evidence.

Riffing off of a post by Matthew Yglesias, Campos also makes lifestyle intervention – public health matters an outpost in the culture war, putting those of us who are interested in the social benefits of exercise and healthy eating into the bin of “cultural Puritanism. We’ll put aside for a moment the point that equating “puritan” with someone who disapproves of pleasure is a bit of historical misdirection. You can even find some evidence for his point that long-term health care costs are driven by old age and not lifestyle choices.

Last year, RIVM published a study modeling lifetime health care costs for cohorts of obese people, smokers and “healthy living” folks, defined as non-smokers with BMIs between 18.5 and 25. The results were that annual health care costs were highest for obese people earlier in life, until age 56, and were highest for smokers in later years. However, the overall highest lifetime health care costs were for the healthy-living folks. Life expectancy from age 20 is reduced by 5 years in obese people and 7 years in smokers. Healthy-living people live on to incur greater medical expenses, more than compensating for the expenditures related to smoking or obesity.

So, I should start smoking again and eat like this to do my part to control health care costs. However, before you shout “gotcha”, take a look at the commentary traveling along with this article. Compare a lean and obese population with the same age and sex distribution, and the latter will have greater health-care costs throughout life. So during the productive adult years of your life, when you should be spending money on other things, such as books, vacations and family, your're spending it on health care. There are other costs associated with obesity such as absences from work and lost productivity, in addition to health care costs. In the UK, these extra costs are estimated to be about four times as great in obese than in lean people.

The problem in the health care debate that no-one seems to want to talk about is that people want to live forever, and it in those years at the end where the health care costs are highest. However, living longer shouldn’t be the goal, rather maximizing the number of years free of disease burden. For me at least, I’d rather not be clomping around on knee or hip replacements, being treated for diabetes or putting up with erectile dysfunction.

Holding ED at bay. . . ok, now we’re getting to why I really pay attention to exercise and what I eat. I’m so transparent. See you in the gym.

Losing the War on Obesity

There’s little doubt that obesity is bad for your health, and that it is an environmental health problem. And, the news just came out the other day that we as a nation are steadily becoming fatter (under the fatuous title that we need a national strategy to combat obesity). As if on cue, someone is coming out with preliminary research findings that sugary drinks made with high fructose corn syrup (HFCS) contain reactive carbonyls, which may have a role in the progression of diabetes as well as other diseases.

After reading this though, I can see what’s coming next:

Adding a beneficial antioxidant compound found in tea called "epigallocatechin gallate," or EGCG, to drinks that contain HFCS appears to lower reactive carbonyl levels, Ho said. That could mean that drinking beverages that contain both tea extracts and HFCS may not be as harmful as drinking HCFS-sweetened sodas, he said. However, further research is needed to prove that.

Set your watches, folks, and let’s see how long it takes before “healthy” sweetened beverages spiked with green tea extract start showing up on the shelves. Some strategy.

Soft Drinks: and You Worry About the Benzene?

Consumption of sugar-sweetened beverages, and in particular, carbonated soft drinks may be a key contributor to the current epidemic of overweight and obesity. High-fructose corn syrup, a principal ingredient in these beverages has been suggested as a cause of the increased incidences of obesity and metabolic syndrome in the US. sugar-sweetened soft drinks contribute more than 7 percent of Americans’ calories, making them the largest single source of calories in the US diet. They contribute to the erosion of tooth enamal and dental caries. Consumption of caffeine and phosphoric acid in colas may have an adverse effect on bone mineral density in older women. Consumption of sugar-sweetened foods, including sweetened beverages and soft drinks, are being investigated as risk factors in pancreatic cancer. As if that isn't enough, Coca-Cola has been studied as a possible animal carcinogen.

With all of that, what is it that people worry about? Trace levels of benzene formed from the reaction of sodium benzoate and ascorbic acid. While I'm pleased that action is being taken to get a carcinogen out of the food supply (though the term "food" applies very loosely to sugar-sweetened beverages and soft drinks), I question the wisdom of being concerned about the benzene at all; there's more than enough evidence to persuade a reasonable person that drinking sugar-sweetened beverages, and particularly carbonated soft drinks is a really bad idea for your health. If you sat down and did the math, you might find that the cancer risks from the benzene exposure are probably trivial by comparison.

Memo to Ezra Klein: How Not to Cite a Health Study

Question for Ezra Klein. Why are you getting your health data from the Cato Institute? It was headache-making for me to read the progression from a rather limited study. . .

Rational decision-makers will take into account forecasts of longevity and quality of life in making their work and savings decisions. Public policy must account for this as well. Every additional year of life after age 65 is associated with about $15,000 of social security and medical care spending, and years spent disabled result in substantially greater medical spending than years spent without disability. . . .

. . . to one sweeping generalization . . .

Americans are getting healthier in spite of a little extra flab.

. . . to another. . .

Americans are actually becoming substantially healthier, even as our waistlines expand.

Let’s first review the quantitative results from the Cutler, Glaeser and Rosen study, and then look at where the authors might have overstated their conclusions a bit based on those findings. First, the results (from the summary):

For the population aged 25-74, the 10 year probability of death fell from 9.8 percent in 1971-75 to 8.4 percent in 1999-2002. Among the population aged 55-74, the 10 year risk of death fell from 25.7 percent to 21.7 percent. The largest contributors to these changes were the reduction in smoking and better control of blood pressure.

So, there’s a reduction in overall mortality, and it might be related to people smoking less and better blood pressure medication (I’m fairly sure people aren’t controlling their blood pressure better using exercise and diet. . . ). However, the authors don’t make clear how this translates to:

Examining these factors as a whole, we show significant improvements in the health risk profile of the U.S. population between the early 1970s and the early 2000s. Reduced smoking, better control of medical risk factors such as hypertension and cholesterol, and better education among the older population have been more important for mortality than the substantial increase in obesity.

Reduction in mortality doesn’t translate directly to “significant improvement in the health risk profile”. For example, the authors didn’t go into why they feel we’re getting healthier if the overall prevalence of diabetes is increasing over time, and if we’re spending more to treat it. I have to wonder if Ezra and the Cato Institute are implying that we’re getting healthier because we spend more money to keep at bay a lifestyle-related chronic degenerative disease. Shades of Mad Hatter economics. . . .

While the underlying purpose for the study isn’t mentioned in the paper, it is interesting to note that it was funded by the Social Security Administration. I have to wonder if it’s intended to figure out how much of an impact there’s going to be to the Fund from the reduced mortality. For example, the Centers for Disease Control have reported:

At least 80% of seniors have at least one chronic condition, and 50% have at least two. These conditions can cause years of pain, disability, and loss of function. About 12 million seniors living at home report that chronic conditions limit their activities. Three million older adults say they cannot perform basic activities of daily living, such as bathing, shopping, dressing, or eating. Their quality of life suffers as a result, and demands on family and caregivers can be challenging.

And, the introduction of the Cutler, Glaeser and Rosen study does state:

Every additional year of life after age 65 is associated with about $15,000 of social security and medical care spending, and years spent disabled result in substantially greater medical spending than years spent without disability.

So, is the Cutler, Glaeser and Rosen study is one piece of information about the impact of increased longevity on social security and medical spending? The study doesn’t really say that, but it’s not an unreasonable inference. But it is a broad overstatement to say the Cutler, Glaeser and Rosen paper is evidence that we’re getting healthier even as we get fatter.

It’s no surprise to me that the Cato Institute would go there. However, I am surprised that Ezra Klein would fall for it.

Phthalates and Obesity

Awhile back, the news cycle was all atwitter about this paper published in the International Journal of Obesity. I had posted about it over on Daily Kos last year, to a lukewarm response (political blogs aren’t really in to environmental health, I guess).

The investigators begin by observing that the relationship between obesity and The Big Two, their term for inactivity and inbalanced diet is based on presumed mechanisms and "ecological studies". An ecological study is a type of epidemiological study that examines broad trends in environmental factors and disease; it is not designed to examine specific relationships between exposure and disease, and is considered more useful for generating rather than testing scientific hypotheses. Food industry apologists use this fact to cast doubt on the relationship between diet, exercise and obesity. The investigators argue this doesn't disprove that relationship, but points to the need to look for other factors to help explain the obesity epidemic.

One of the arguments they explored is the relationship between exposure to endocrine disruptors and increased adiposity. The relationship between endocrine disruptor exposure and obesity is an active area of environmental health research. Last year, I posted about a paper exploring the relationship between exposure to the plasticizer bisphenol-A and insulin resistance in mice, occurring at fairly low levels. More recently, a paper has been published describing the relationship between phthalate exposure, girth in males and insulin resistance.

A bit about insulin resistance. Insulin is a hormone that is released from the pancreas after eating. It signals insulin-sensitive tissues, principally muscle, to absorb glucose, which correspondingly reduces blood glucose levels. In an insulin-resistant individual, the normal levels of insulin secreted do not signal cells to absorb glucose. Years of hyperglycemia, from excess carbohydrates in the diet, are thought to disrupt the release of insulin, resulting in glucose intolerance and subsequently Type-2 diabetes. The mechanism for this phenomenon is not entirely clear, and it has not been fully resolved If this loss of pancreatic function results primarily from excessive secretion of insulin (exhaustion of beta-cells in the pancreas) or toxicity to beta-cells (hyperglycemia or other causes). More recent research seems to point to the latter.

Insulin resistance is part of the metabolic syndrome that includes central obesity, elevated insulin secretion, and elevated fatty acids in the bloodstream. Central (visceral) obesity elevates levels of free fatty acids in serum, which might provoke insulin resistance and disrupt lipid metabolism. Testosterone can reduce body fat and increase insulin sensitivity in men, which is where phthalates come in to the picture. Phthalates have been shown to be antiandrogenic agents in male laboratory animals, disrupting testicular steroid hormone synthesis and reproductive function. Some observations suggest that anti-androgenic effects also occur in humans. These investigators were evaluating the hypothesis that increased phthalate exposure would be associated with increased abdominal obesity and insulin resistance, which correspondingly could be precursors to Type-2 diabetes and cardiovascular disease.

The short answer from the study was that concentrations of several prevalent phthalate metabolites showed statistically significant correlations with abdominal obesity and insulin resistance. The authors caution that phthalate exposure only explains some of the variability in measurements of girth and insulin resistance, which they chalk up to obesity being a complex, multi-factorial syndrome (critics may conclude this means there’s no meaningful relationship between phthalate exposure and obesity. . . ). The authors also caution this is a snapshot in time (i.e. a cross-sectional study), and that longitudinal studies (which follow trends over time) are needed to better understand the possible relationship between phthalates and insulin resistance. Other factors to consider in judging the significance of phthalate exposure in metabolic diseases such as diabetes include cumulative exposures to multiple phthalates and exposures to other common contaminants including bisphenol-A, PCBs, dioxins and organochlorine pesticides.

The Washington Post has a reasonably carefully worded article about this issue. Sadly, most other newspapers are mangling what is actually a fairly carefully worded study.

Phthalate exposure isn’t going away any time soon (that’s a story for another day), so what do you do about this? Well, we still have control over the Big Two – diet and activity level.