At a recent research symposium on Addictive and Health Behaviors Research, I heard an informative talk by Kelly Brownell, co-founder and director of the Rudd Center for Food Policy and Obesity at Yale University.
Brownell’s talk was titled “A New and Important Frontier: Food and Addiction.” A key topic of his talk was whether “food addiction” is a real phenomenon for some individuals or a bad analogy drawn with addiction to a variety of mind-altering substances. He concluded that, at least for some, food addiction probably is a real clinical phenomenon, drawing on several bodies of evidence: foods high in sugar or fat have been shown to cause dopamine production in a way similar to that of many drugs (i.e. the experience of pleasure from such foods is not just in the taste buds); there’s evidence of addictive behavior around such foods in some lab animals; the narratives and descriptions of favorite foods by “food addicts” mirrors that of drug addicts.
In the process of laying out his arguments about food addiction, Brownell gave an overview of the obesity epidemic in the U.S. over the past few decades. Much of what he covered was generally available knowledge, though his comprehensive synthesis of a vast amount of material was impressive.
These were by no means the only factors he addressed (see the Rudd Center’s website that I linked above for a fairly comprehensive overview of obesity research), but I was particularly struck by his comments on economics and human evolution.
Economics and Obesity
Brownell addressed economics and obesity in several ways.
Agricultural Economics and Obesity
As many are aware, industrial agriculture is heavily subsidized in the U.S. and many other developed countries. In the U.S., corn (maize) agricultural interests are particularly well set up with regard to subsidization of the industry. In its current form, such heavy subsidization dates back to the Nixon era, intended as a way to combat food price inflation.
An effect of this was the tremendous growth of corn and other agribusiness, and the development of a number of at the time unanticipated corn products (greater availability of corn oil and development of high fructose corn syrup), all kept artificially cheap by agricultural subsidies. A result of this is that processed foods high in fats and sugars are often quite cheap, especially when compared to prices of healthier foods, in particular the relatively high cost of fresh produce. So, for example, even while some fast food chains commendably offer healthy salad options, the healthy options tend to be quite expensive compared to the price of a meal of corn-fed-beef patties, potatoes fried in corn oil, and high-fructose-corn-syrup-laden beverages in giant portions.
Junk Food as a Caloric Bargain
High fat and/or high sugar foods tend to nowadays be available cheaply, at least in the U.S. and other developed countries – and increasingly this seems to be true elsewhere as well. Brownell made another interesting point here, though. If we look at food economics not just in terms of monetary cost but calories, junk food is a tremendous bargain. By weight, junk food is typically already cheaper than healthier food, but calorie for calorie, junk food is tremendously cheaper.
Poverty and Obesity
On top of the basic economics of food in the U.S. today, in impoverished communities, high fat and/or high sugar foods tend to be easily available relatively cheaply (even if not as cheaply as the same foods in other areas because of the lower incidence of full service grocery stores), while things like fresh produce are often hardly available at all and at higher prices, contributing to the problem of obesity in poor communities.
Human Evolution and Obesity
I was happy to see Brownell address a topic often left out of debates about obesity: human evolution. There’s strong evidence that humans generally take great pleasure in fatty or sweet foods (those dopamines mentioned above). This is something we share in common with other mammals, and is almost certainly something selected for in our evolutionary history.
This makes perfect sense – foods high in fats and sugars are caloric bargains, but are not particularly common in many natural environments. Animals who take pleasure in eating these foods would tend to seek them out more often and would tend to have an evolutionary advantage over those who didn’t.
But take this evolutionary heritage and add it to an economic environment unlike any our hominid or earlier primate ancestors ever adapted to, with an over-abundance of sugars and fats, and you get the obesity epidemic.
Genetics and Obesity
Both during his talk and during the question session, Brownell spoke of genetics as a factor in order to dismiss it as significant. I had been similarly dismissive of genetics as a significant factor in producing patterns of obesity before hearing this talk, and generally agree with his perspective here, particularly at the level of populations and gene pools: gene pools haven’t changed in the past 20-30 years in any significant way; the food environment has changed in multiple significant and obvious ways; therefore, genetics is not a serious consideration.
Interestingly, as I listened to Brownell present a position similar to that I have tended to take, I began to see the possibility for a change in genetic predispositions as a factor in obesity at the individual level. With increases in rates of obesity, we’re talking about a change to phenotype. Phenotype is always the product of genotype in interaction with environment. In this case, genotypes haven’t changed; it’s a variety of environmental factors that have changed; but that doesn’t mean that changing phenotype is solely the product of the changing environment necessarily, for phenotype is, again, always the product of that relationship between genotype and environment. A genotype that didn’t contribute to increased predisposition to obesity in one context might in another.
Still, I agree with a point that Brownell made during the Q and A session. Regardless of any potential genetic predisposition to obesity that some individuals may have, from a prevention or intervention stand point, it’s essentially irrelevant. At the population level, environmental factors are clearly the directly relevant ones and genetic predispositions aren’t something that can be particularly addressed at that level anyway. But even for individuals, for a person attempting to lose weight, the trick is to expend more calories than are taken in, irrespective of genotype.