Readers Respond to "How to Fix the Obesity Crisis" and Other Articles

Letters to the editor from the February 2011 issue of Scientific American

In “How to Fix the Obesity Crisis,” David H. Freedman proposed behavior modification as a solution, but it cannot be applied to 200 million overweight people. Freedman also seems to support subsidies for fruits and vegetables and other government-sponsored programs. But where is the money going to come from?

For decades now the U.S. government has subsidized corn production. Corn is used as inexpensive feed to fatten cows in feedlots and to make a cheap sweetener called high-fructose corn syrup. Fat cows and high-fructose corn syrup are key ingredients in most fast food, including hamburgers and sugary soft drinks—the foods that Freedman correctly acknowledges contribute greatly to the obesity epidemic. By subsidizing corn, the U.S. is making fast food cheaper than healthy food. What if we transferred the subsidies from corn to healthy, sustainable crops? 

Now schools would have to choose healthier food because it would be cheaper than junk food, and it would be a simpler decision for the poor to choose the healthier food. Although the full solution to obesity would undoubtedly involve a change to our entire culture, an easy first step would be to stop subsidizing the food that is helping to make us so overweight.
Gunnar Newquist
Cell and Molecular Biology graduate program
University of Nevada, Reno

It was disappointing that your cover article on obesity did not include any mention of recombinant bovine growth hormone, or rBGH, which is banned in virtually every developed country on earth but not in the U.S. The corporate lobbies that control our legislature have done an excellent job of sweeping all controversy about these artificial hormones under the rug—especially because rates of obesity in countries that ban rBGH are much lower than the rates here in the U.S.
Charles Carignan
Windham, N.H.

As an expert on the psychology of eating and weight and a four-book author on the subject, I thoroughly applaud Freedman’s covering the wide range of biological and social factors involved. But one major factor was left out: the underlying, often unconscious, intrapsychic conflicts eaters have about eating healthfully, losing weight, being thin or giving up food as comfort. In more than 30 years of working with troubled eaters, I have rarely met one who does not have unresolved, mixed feelings about substantially changing their eating or their weight. Psychotherapy works to identify and resolve these conflicts so that people stop sabotaging their progress and instead form a healthy relationship with food and their body.
Karen R. Koenig
Sarasota, Fla.

I’m wondering how chromatin, the thick fiber formed from DNA folding on itself, knows where to become loose or tight to enable DNA transcription, as Tom Misteli describes in “The Inner Life of the Genome.” I imagine that some signal goes out from the activated gene, along the chain of histones [“spools” around which DNA twists], to loosen ties between the histones. After transcription is completed, another signal would need to follow from said gene to retighten the chain. Maybe chromatin-remodeling complexes simply carry and execute these signals?
Matthew Morycinski
Vancouver, B.C.

MISTELI REPLIES: The chromatin fiber opens and closes continuously because of the stochastic action of chromatin-remodeling complexes that roam the cell nucleus. Once a chromatin region is open, it will stay open for a certain period. If during that time an activating transcription factor binds, we might see gene activation; if no factor binds, the chromatin will “close” again. In response to signals such as hormones, transcription factors often become modified so that they have higher affinity to bind to their target sites. This leads to increased and prolonged binding at their gene targets, thus sustaining the transcriptional response. When the signal abates, the transcription factors fall off the target gene, thus reducing its activity. An incoming factor may also be a histone modifier protein that more permanently marks a region to be open or closed.

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