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Is portion size to blame for obesity?

I've often seen presentations where the authors show the size of an average hamburger or soda in the 1960s, 70s, 80s, and 90s as a way of making the point that portion sizes have increased, and thus contributes to the rise in obesity.  Changes in portion size probably have played some role, but at least according to this experiment published in the journal Obesity, it may play less of a role than first meets the eye. The researchers recruited over 233 people working in a large medical complex and randomly assigned them to treatments that differed according to the size of the free lunch they were given (one control group was given no free lunch at all).  Here's what they found:

Adults (n = 233) were randomly assigned to one of three lunch size groups (400 kcal, 800 kcal, and 1,600 kcal) or to a no-free lunch control group for 6 months. . . .

Body weight change at 6 months did not significantly differ at the 5% level by experimental group (1,600 kcal group: +1.1 kg (SD = 0.44); 800 kcal group: −0.1 kg (SD = 0.42); 400 kcal group: −0.1 kg (SD = 0.43); control group: 1.1 (SD = 0.42); P = 0.07). Weight gain over time was significant in the 1,600 kcal box lunch group (P < 0.05).

A remarkable increase in portion size from 400 kcal to 1600 kcal for lunch over a 6 month time period resulted in no statistically significant differences in weight across groups at the end of the period.  If you compare the pre- and post-weight of the people in the 1600 kcal group, there was a slight increase (0.19kcal/month) in weight for people in that group but not for people in the 400 kcal group or the 800 kcal group.  Curiously, those in the control treatment, which included people who were not given a free lunch, gained a statistically significant 0.24 kcal/month - more than those in the 1600kcal free lunch group! 

The trouble with many "interventions" such as this (similar to those that happen at school lunches) is that people can substitute across time.  If I eat a big lunch, I'm likely to eat less for dinner. And vice versa.  If I eat a 400 kcal lunch, I'm more likely to grab a snack in the afternoon than if I eat a 1,600 kcal lunch.  

Apply this thinking to related policy ideas.  Ban sodas or transfats. What will people drink and eat instead?  Tax restaurants.  What will people eat at home?  Add more veggies to the plate at school.  What will happen to veggie consumption at home?  I'm not saying that such policies might not have some effect on weight, only that because of substitutes and compensating behavior, they will often have less effect than is expected.

Interview on Economics of GMOs

I was recently interviewed by the website The Daily Meal on GMOs.  Here is what I had to say:

“The world is facing many challenges,” says Lusk. “(They include) a growing world population, climate change, and droughts in many areas of the U.S., just to name a few.  Biotechnology and genetic engineering do not hold all the answers, but all tools should be on the table to sustainably address these societal challenges."

On a domestic level, proponents of GM products see the opportunity to develop strain-resistant crops that cost less to manufacture. These lower food costs would benefit the farmers, and in turn would reduce the cost of foods for the retail consumer.

"In the U.S., about 90% of all corn and soybean acres are planted with GE varieties,” says Lusk. “These were decisions made by real-life, flesh and blood farmers. No one was (or is) holding a gun to their head. The fact that farmers willingly adopted GE varieties at such a fast clip (even while paying a premium price for them) reveals their belief that it is in their best interest to do so.  The scientific evidence shows that adopters of GE corn, soy, and cotton have enjoyed slightly higher levels of profitability.”

The support from that last claim, incidentally, comes from numerous peer-reviewed studies.  For a summary of the early research on the topic, see this USDA report, which shows that profitability tends to be either similar or higher among GMO adopters.  Even in cases where measured profitability is similar for GMO adopters, these simple measures often do not take into consideration the value of risk reduction or value of time saved by the farm operator.  We ultimately have to look at the decisions farmers made, and it seems quite clear corn and soybean farmers believe themselves better off adoption GE varieties.

The article goes on to interview Jeffrey Smith, a long time anti-biotechnology crusader.  The article seems to give the impression that we couldn't profitably produce corn or soy without government subsidies.  I am aware of no good research that would support that assertion.  

Then, Smith is quoted as saying the following:

“Independent research confirms that average farmer profit does not increase with GMOs,” Smith writes.  “And numerous examples of closed markets and suppressed prices have followed the introduction of genetically modified crops worldwide. In Hawaii; for example, GM papaya was blocked by Japan. Prices dropped from $1.29 per kilo to about $.80, and in spite of increased papaya consumption in United States, papaya production in Hawaii dropped by 40 percent.”

I wonder which "independent research" he is referring to?  As I indicated above, you can find some studies indicating no profit gains from biotech adoption.  But, what does the cumulative evidence in the peer reviewed journals suggest?  Not what Smith claims.  And, why are 90% of corn/soy farmers so dumb as to adopt a more expensive technology that isn't making them better off?

Also, to suggest that adoption of GM papaya in Hawaii hurt that industry because the Japanese blocked imports is just silly.  Hawaiian producers adopted a genetically engineered papaya that is resistant to a virus that was devastating that industry.  Yes, Hawaiian papaya growers would have been more profitable had Japan not reacted the way they purportedly did.  But, how profitable to you think Hawaiian growers would be if they had no papayas to sell at all?

 

More on Atrazine

About a week ago, I posted on a New Yorker article about Atrazine - a widely used herbicide in agriculture.  After reading the article, I was a bit dismayed about the ability of science to resolve the controversy, writing:

More disconcerting still is what this says for the ability of science to resolve disputes about knowledge.  Whether atrazine causes abnormalities in a particular type of frog at a certain dosage should be one of those questions science can answer.  Either atrazine causes these effects or it doesn't.  This isn't one of the mysteries of the cosmos.  This isn't macroeconomics.  Yet, there are apparently findings on both sides of the issue (Note: I have't personally delved into the scientific literature on this particular matter in any detail). 

Well, I spent a bit more time digging into the issue, and the science on frog abnormalities seems much more settled than the New Yorker article let on.

It seems the defining study on the issue is the so-called Kloas study.  Here is what the New Yorker said about it:

The Kloas study was the most comprehensive of its kind: its researchers had been scrutinized by an outside auditor, and their raw data turned over to the E.P.A. But the scientists wrote that one set of studies on a single species was “not a sufficient edifice on which to build a regulary assessment.” Citing a paper by Hayes, who had done an analysis of sixteen atrazine studies, they wrote that “the single best predictor of whether or not the herbicide atrazine had a significant effect in a study was the funding source.”

While saying the Kloas study was the "most comprehensive", the article immediately  cites skepticism and immediately brings up the issue of industry funding. It seems to me an attempt to downplay the significance of this particular study and it's findings.

From what I can gather, the Kloas study (a long white paper about it is on the EPA web site) is by far the largest and most careful study on the issue (some additional background on it can be found in this article in the journal Environmental Science and Technology).  The study was mandated by the EPA because it felt that there were too many flaws in previous studies to make a definitive judgement.  Syngenta (the maker of atrazine) funded the study (because the EPA mandated they do so), but it was carried out by two independent laboratories, one in Maryland and one in Germany (under the supervision of the scientist Werner Kloas, which is where the study gets its name).  The study followed protocol set up by the EPA scientific advisory panel.  Data collection was audited and overseen by the EPA; the data was analyzed by a third party, which did not know the particular identify of each treatment, and the data itself is available to other researchers via the EPA.

The study employed over 1,000 frogs in each location.  There were five treatment groups, which varied the level of Atrazine from 0.01 to 100 parts per billion.  There was also a conventional control (with no Atrazine).  Interestingly, there was also a "positive" control - one group of frogs was given 17β-estradiol - a compound known to cause sexual abnormalities in frogs.  The idea with this "positive" control was to determine whether the conditions were such that abnormalities could develop (or were not being prevented via some other choice of the experiment environment).

Here are the results:  The "positive control" using the compound known to cause abnormalities, indeed caused a statistically significant rise in abnormalities.  However, there was no consistent statistically significant evidence that Atrazine caused abnormalities - either it's presence or in a dose-response fashion.  The EPA concluded (see page 115):

Because of the experimental design protocols and quality control of the [Kloas] studies, the data are sufficiently robust to outweigh previous efforts to study the potential effects of atrazine on amphibian gonadal development.

Based on the negative results of these studies, the Agency concludes that it is reasonable to reject the hypothesis formulated in the 2003 SAP that atrazine exposure can affect amphibian gonadal development. The Agency believes at this time, there is no compelling reason to pursue additional testing with regard to the potential effects of atrazine on amphibian gonadal development.

What about the previous studies showing effects?  Typically, such studies: 1) used a smaller sample size, 2) did not study whether there was a dose-response relationship, 3) did not utilize a proper control group (or "positive" control like the one described above), and/or 4) have not made their data available to other researchers.  In several places, the EPA has commented on these weaknesses, and on the inability to get specific data from researchers claiming ill effects.

One of the things that bothered me about the New Yorker article was the sense that science could not settle such an issue. I wrote:

But, I also fear this is part of an attempt to undermine the ability of scientific inquiry to settle empirical disputes. . . I hold out hope that science can, indeed, provide knowledge for those willing to follow the evidence where it leads.  Otherwise, every issue is simply a PR battle.

I have no idea whether Atrazine might cause other deleterious effects, and I cannot condone Sygenta's alleged actions against Hayes.  Nor can I condone his alleged actions against employees of Synenta. But, it seem to me the science has provided us a reasonably good answer to the question of whether Atrazine causes frog abnormalities at levels below 100ppb.  It is a shame that the New Yorker let telling a good story get in the way of this fundamental fact.   

How problematic are food deserts?

Not very according to this piece in Slate:

Unfortunately, more fresh food closer to home likely does nothing for folks at the bottom of the socioeconomic ladder. Obesity levels don’t drop when low-income city neighborhoods have or get grocery stores. A 2011 study published in the Archives of Internal Medicine showed no connection between access to grocery stores and more healthful diets using 15 years’ worth of data from more than 5,000 people in five cities. One 2012 study showed that the local food environment did not influence the diet of middle-school children in California. Another 2012 study, published inSocial Science and Medicine, used national data on store availability and a multiyear study of grade-schoolers to show no connection between food environment and diet. And this month, a study in Health Affairs examined one of the Philadelphia grocery stores that opened with help from the Fresh Food Financing Initiative. The authors found that the store had no significant impact on reducing obesity or increasing daily fruit and vegetable consumption in the four years since it opened.

and

Earlier research suggesting that better fresh-food access improves diet and would therefore improve the health of people living in poverty was drawn from small samples or looked at store availability in narrow geographical slices—often without information about how or where the people who lived there shopped. “They never link the neighborhood characteristics to actual individuals,” explains Helen Lee, author of the Social Science and Medicine study. “Without that, all you have is speculation.”

Lee also notes in her study that, on closer inspection, food deserts don’t actually exist in the U.S., at least not as a national problem—on average, poor neighborhoods have more grocery stores than wealthier neighborhoods.

The writer concludes on a note which which I agree.  The real issue here probably isn't access to fruits and veggies.  These are simply symptoms of a larger problem.  Poverty.  Alas, solving the problem of poverty is no easier or no less complex than solving the problem of obesity.  But, if you could made headway on poverty, I'd argue people would have a greater incentive to consider their own future health outcomes.  

Big Food = Big Tobacco?

From Politico:

Lawyers are pitching state attorneys general in 16 states with a radical idea: make the food industry pay for soaring obesity-related health care costs.

It’s a move straight from the playbook of the Big Tobacco takedown of the 1990s, which ended in a $246 billion settlement with 46 states, a ban on cigarette marketing to young people and the Food and Drug Administration stepping in to regulate.

Who is behind the action?

McDonald’s [not be be confused with the food company by the same name] law firm has allied with a number of well-known obesity and diabetes researchers, including Barry Popkin at the University of North Carolina Chapel Hill, Robert Lustig at the University of California San Francisco and economist Frank Chaloupka at the University of Illinois at Chicago, to help hash out the strategy. . . . “We need policy to change,” said Lustig, who recently got a law degree and launched a nonprofit to continue his advocacy. “I think we’re going to have to battle [the food industry] like we battled tobacco.”

Some are skeptical:

James Tierney, director of the National State Attorneys General Program at Columbia Law School and former attorney general of Maine, laughed when asked about the proposal.

“It’s just not going to happen,” said Tierney, who noted that tobacco companies lied about the health effects of their products for decades. “The food industry doesn’t deny that eating lots of food causes obesity.”

Others are cynical:

The proposal drew ire, in part, because it would rely on a contingency fee agreement, which allows a private firm to do legal work for attorneys general offices in exchange for a cut of the settlement. It’s an increasingly common practice because it allows cash-strapped AG offices to tackle expensive litigation without taking as much risk.

“Pay-to-play relationships between [plaintiff’s attorneys and attorneys general] that exchange campaign contributions for lucrative government lawsuit contracts mean the food industry has a big target on its back,” said Lisa Rickard, president of the U.S. Chamber Institute for Legal Reform