by Kenneth W. Krause.
Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer. Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well. He may be contacted at email@example.com.
We’ve tried almost everything: low-fat, all-liquid, and no-carb diets; allegedly total gyms that fold like aluminum lawn chairs before sliding neatly under the bed; and shelves full of butt-busting, ab-crunching, and cardio-crazy videos performed by disturbingly cheerful fitness models.
Doctors tell us that 30 minutes of moderate exercise three times per week will do the trick, but we know it won’t. Apologists for the “big-boned” crowd claim it’s all in our genes, or perhaps the collective fault of all the micro-organisms living in our guts. Consumer advocates, celebrities, and politicians (or their spouses) blame fast food chains, television ads, school lunch programs, and even corner grocers for their failure to assume responsibility for other people’s children.
So what are we missing? Well, any number of things probably. But if we seriously want to confront this new “epidemic,” as it’s now called, maybe we need to dig a little deeper. Unless we try to “understand the how and why of human obesity,” say biomedical researchers Michael Power and Jay Schulkin, and to regard it as “less the focus and more the example” of how human biology and modern environments interact, all attempts to treat obesity “will be problematic, if not doomed to failure.”
In The Evolution of Obesity (Johns Hopkins, 2009), Power and Schulkin acknowledge the problem’s incalculable complexity—perhaps much to the dismay of less motivated readers. Indeed, most biological systems shaped by natural selection consist of systems so interdependent on the one hand, and multifunctional on the other, so as to completely defy cursory or clear-cut explanations.
Literally dozens of ancient information molecules link, regulate, or coordinate metabolism between cells or cells and end-organ systems. Peptides and steroid hormones, for example, connect the brain and the gut to regulate appetite and satiety in an attempt to synchronize behavior with digestion.
And somewhat surprisingly, scientists’ perception of fat has changed dramatically in recent years. Once conceived as a passive product of positive energy balance, adipose tissue is actually an endocrine organ that produces peptides, steroids, and immune-function molecules to actively regulate physiology and metabolism. “Many of the health consequences of obesity,” the authors instruct, “are due to the metabolic effects of this endocrine and immunological organ becoming ‘oversized.’”
Why an epidemic? More than one billion people worldwide are now overweight or obese. In some countries, up to a third of the population is now considered obese, and in the United States—the current leader among developed nations—the condition’s prevalence is three times what it was just fifty years ago. As of 2002, U.S. adults had become roughly one percent taller but 15 percent heavier since 1961, resulting in a mean body mass index (BMI) increase of 11 percent.
We’ve long known that obesity is associated with diabetes, hypertension, cardiovascular disease, and osteoarthritis. But recent research has revealed a connection to certain cancers as well. High BMI is associated with increased job absenteeism, and U.S. citizens dole out an estimated $61 billion per year for obesity related health care. In the end, severely obese people are 1.5 to 2 times as likely to die as those with normal BMIs.
So given the stakes, one would assume we would zealously protect at least the most vulnerable among us. But U.S. children ate 43 percent fewer vegetables in 2002 than in 1978, almost half of which consisted of fried potatoes. Bread, in fact, has become the leading source of carbohydrates for young people, followed by soft drinks. During the same 25-year period, kids ate 425 percent more pizza and drank 70 percent more soda and 38 percent less milk. For both children and adults, processed and alarmingly fatty meats have become the norm.
By themselves, these facts and figures seem unthinkable—almost as if they’ve taken on a life and an agenda of their own. That’s where evolution enters the picture. According to Power and Schulkin, the obesity epidemic results from an unfortunate mismatch between our contemporary, largely synthetic environment and biological adaptations naturally selected thousands and even millions of years ago.
The authors tender a novel perspective on the problem—one based on the facts of natural history—that they believe will lead to more effective personal, clinical, and public health strategies. “To understand our feeding behavior,” they argue, “an understanding of our evolutionary past is critical.” Modern developed societies supply us with an over-abundance of easily digested and highly palatable (though not always nutritious) food. In return, however, our world requires very little from us in terms of energy expenditure. Contrastingly, the environments for which our bodies and minds actually evolved provided our ancestors with uncertain, variable, and often less appetizing cuisine in exchange for intense and sustained physical effort.
Once rare achievements indeed, positive energy balances are now common among U.S. citizens especially. The ability in humans to accumulate fat served a critically important evolutionary purpose. Our defining trait as a species, of course, is an enormous brain. About one-third lipid, the brain is clearly a high-fat organ, and its growth in all mammals is associated with increased assimilation of long-chain polyunsaturated fatty acids, primarily into the cortex. Animal flesh, of course, is a bountiful source of these substances. Similarly, the increased consumption of dietary fat has been linked to the evolution of vastly bigger brains in early Homo (especially between 700,000 and 250,000 years ago), relative to their australopithecine predecessors.
Many experts hypothesize an evolutionary feedback loop in which the acquisition of protein- and fat-packed animal flesh both required and allowed radically enhanced cognitive abilities. On the one hand, meat’s extraordinary caloric and nutritional density, especially when cooked, was necessary to fuel the evolution of larger brains. On the other, the special skill sets and strategies helpful in the attainment of meat served as intense selective pressures for superior intelligence.
Importantly, our ancestors’ bodies grew significantly larger at about the same time, perhaps also in response to their new preference for animal flesh. Because meat was a very rare commodity, the ability to store energy in the form of adipose tissue would have been highly favored. The bigger the body—at least to a certain point—the more space for storage. Thus, largely due to increased body size and encephalization, early Homo gradually transitioned in two ways. First, they shifted from a predominantly herbivorous grazer and forager of often difficult, low-quality food to a more omnivorous scavenger and hunter of easily digested, energy-dense flesh. Second, they developed excess storage capacity. All of which worked pretty well, apparently, at least until the agricultural revolution beginning about 12,000 years ago.
The rest, of course, is familiar history that unfolded in a flash of evolutionary time. Within a few short centuries, humans settled down, domesticated and bred seed crops and animals, specialized into occupations, gained leisure time, accumulated surpluses, and eventually found themselves surrounded by high-energy foods steeped in fat and loaded with starch and simple sugars—super-sweet fructose, most notoriously.
But for Westerners especially, human biology had precious little time to keep pace with racing technologies and occasionally tragic cultural obsessions. Though perhaps unwittingly, we bear witness to the effects of these profound mismatches every day. In only the last few decades, for example, overweight has become the new normal.
How and why? Because “we have created an obesogenic environment,” argue Power and Schulkin. “We evolved on the savannahs of Africa; we now live in Candyland.” And yes, obesity is fast becoming a disease of the poor. While poverty in underdeveloped nations is associated with being underweight and malnourished, poverty in rich and developing countries is linked to an increased risk of obesity (which, given the low quality of some high-calorie food, does not rule out malnutrition). In such areas, quick explanations should be met with sharp skepticism. But as the authors point out, residents of poor neighborhoods do have more difficulty obtaining quality produce, for instance, and access to recreational facilities.
But what about free will? If we can see what’s happening to us, why don’t we just say no to bad food and yes to vigorous exercise? While certain sequences in the human genome have been associated with an increased risk of obesity, our species’ uniquely commanding neocortex enables us to inhibit inappropriate behavior induced by other regions of the brain. The limbic system, for example, provides potent emotional and motivational cues, and the brain stem is responsible for involuntary actions and the delivery of signals to and from the forebrain. Nevertheless, in the context of any complicated set of behaviors, the desire to partition the human brain into strict regions is naïve at best.
The implied hierarchy is anything but absolute, and the relationships between regions are best described as circuits with intricate connections and feedback loops. “The simple model of bottom-up signaling and top-down control,” the authors caution, “does not describe feeding behavior.” On the other hand, they add, although hunger is a singularly powerful motivator, people in fact can choose when and what to eat and whether and how briskly to exercise. So should we stop looking for quick and easy fixes? Certainly not, so long as proposed remedies are founded primarily on solid science and not on self-deception or laziness. But even then, given the considerable forces that natural history has amassed against us, we shouldn’t be surprised when our most clever designs and fondest hopes are proven haplessly inadequate to the task.
Consider the case of “leptin,” for example, which derives from leptos, the Greek word for thin. Discovered and named in the 1990s, leptin is a peptide synthesized and released by adipose tissue into the bloodstream. Its receptor B is highly expressed in the hypothalamus where it likely plays a significant role in appetite control. Mouse experiments later revealed that obesity was associated with defective leptin receptors and that leptin deficient mice lost weight when the peptide was restored. Central infusions of leptin also reduced food intake. Some suggested that leptin influenced the hedonic perception of food, and that, as a lipostat, it was part of a natural system that attempts to maintain total body adiposity within a stable range.
The popular press seized on the notion and ran with it, portraying leptin as the scientific community’s prescription for rapid weight loss and its miracle cure for human obesity. But, as Power and Schulkin observe, biology is seldom that simple. As it turned out, animals given doses of leptin did not reliably experience reduced appetite and weight loss unless they were already leptin deficient. But again the data make perfect sense when approached from an evolutionary perspective. Leptin’s adaptive function probably had nothing to do with excessive fat, which of course would have been very rare at the time of the peptide’s evolution. More likely, its purpose was to signal low energy stores, and thus to cue strategies related to increased food acquisition or energy conservation.
No competent biologist would ever attempt to reduce a problem as multifaceted and convoluted as obesity to an exclusively evolutionary paradigm. And clearly Power and Schulkin have gone to great lengths to meticulously document and discuss the epidemic’s biological and behavioral complexity. But common sense dictates that doctors and their patients could very well benefit from a more lucid understanding of obesity’s true scientific bedrock.
Although we can’t (and shouldn’t want to) live as our late Pleistocene ancestors once did, we can, if armed with a more sophisticated comprehension of human biology and how it might interact with different environmental milieus, make drastically more informed personal decisions about diet and exercise in particular. And as a society, we might benefit as well by developing the historical wisdom necessary to direct the evolution of a more enjoyable, satisfying, and sustainable culture.