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.
Since the 1940s, the concept of “energy balance” (EB) has governed obesity research worldwide. Springing intuitively from the laws of thermodynamics, this model proposes that excess adiposity results whenever energy intake overtakes energy expenditure. Thus, the behaviors of overeating and failure to exercise, i.e., “gluttony” and “sloth,” have been emphasized over complex metabolic processes and the unique effects certain foods might have on those processes.
The conventional wisdom of EB continues to dominate public policy today. According to the U.S. Centers for Disease Control, “Weight management is all about balance—balancing the number of calories you consume with the number of calories your body uses,” and the World Health Organization, “The fundamental cause of obesity … is an energy imbalance between calories consumed on one hand, and calories expended on the other.”
So instead of testing more sophisticated strategies, dieters are encouraged to count their calories—whether derived from steak, spinach, potatoes, Wonder bread, or Mountain Dew—as if they were all created equal. Unsurprisingly, the relevant popular science literature also tends to reflect this paradigm. As American nutrition scientists Marion Nestle and Malden Nesheim reiterate in their new book, Why Calories Count, the ingestion of too much energy is “arguably the most important cause of public health nutrition problems in the world today.”
Nevertheless, some scientists, physicians, and science journalists have recently challenged the EB equation. In its place, they propose models highlighting the roles of hormones like insulin, leptin, cortisol, and estrogen—even to the absolute exclusion of personal control and responsibility. Here, assorted nutrients—or foods that should be distinguished for their lack of nutrients—are treated very differently because of the chains of metabolic events they are thought to initiate.
For example, Jonathan Wells and Mario Siervo—nutrition researchers from the UK and Italy, respectively—contend that EB fails to explain, among other things, why people continue to gain weight, rather than plateau, after the point when their gains reestablish energy equilibrium (Wells and Siervo 2011). They also remind us that, despite the theoretical logic of EB, neither behavioral prevention nor behavioral treatment has generally proven successful.
“The relationship between energy balance and weight gain,” the Europeans argue, “is a truism, not an explanation, hence no direction of causation can be inferred”. Indeed, the conventional wisdom of EB might have the “logic” entirely backwards. Reversing the direction of causation, Wells and Siervo propose, does not contradict the laws of thermodynamics, or even the EB equation per se. But it does permit us to reconsider the associations between behavior, metabolism, and weight change.
We’ve long understood that hormones regulate weight gain—in growing children and pregnant women, for example. And since the 1930s, European clinicians have used insulin—a hormone released from the pancreas in response to elevated blood glucose levels—to fatten underweight patients. Is it just a coincidence that both obesity rates and the consumption of sweeteners and refined carbohydrates have skyrocketed in recent decades?
The obesity problem is surely a complex and multifaceted one. But testing multiple hypotheses of potential merit is better than testing only one, or none at all. By any reasonable standard, our current strategy has proven largely ineffective. “A more skeptical approach,” Wells and Siervo expect, “is likely to bring valuable returns.”
Pediatric endocrinologist Robert Lustig agrees that adiposity is a hormonal predicament. In his new book, Fat Chance, the child obesity expert indicts simple, super-sweet sugars as the chief culprits, arguing that sucrose and high-fructose corn syrup corrupt our biochemistry and render us hungry and lethargic in ways fat and protein do not. In other words, Lustig insists that sugar-induced hormonal imbalances cause self-destructive behaviors, not the other way around.
What EB proponents fail to consider, Lustig vies, is the overwhelming and far-reaching metabolic influence of insulin. In the body it causes energy to be stored as fat; in the hypothalamus it can cause “brain starvation,” or resistance to leptin, the satiety protein hormone released from adipose tissue. Excess insulin, or hyperinsulinemia, thus causes our hypothalami to increase energy storage (gluttony) and decrease energy consumption (sloth). Add to this process an increasingly insulin-resistant liver (which drives blood insulin levels even higher), a little cortisol (the adrenal stress hormone), and sugar dependence (or at least habituation), and dieters, Lustig concludes, hardly stand a chance.
Lustig labels fructose a “toxin” because he believes it drives these events, along with a cluster of maladies and diseases referred to as “metabolic syndrome.” Although the glucose that always accompanies fructose will stimulate an insulin response directly, fructose itself will not. It will, however, cause liver insulin resistance which, in turn, stimulates the pancreas to release even more insulin. Again, leptin resistance may follow. Notable as well is that fructose, unlike other foods, will not decrease the flow of ghrelin—the hunger signaling peptide hormone—from the stomach to the brain.
Thus, Lustig deems the EB model of weight gain a dangerous and unscientific myth. First, sugar alone proves that all foods are not beneficial nutrients and, thus, that a calorie is not a calorie. Second, he contends, generally eating less and exercising more is a strategy doomed to failure given the profound and wide-ranging metabolic processes and effects that certain foods tend to generate.
But the most outspoken and persistent critic of EB might be veteran science journalist and co-founder of the Nutrition Science Initiative (NuSI), Gary Taubes. In a recent Nature editorial, Taubes blamed the current obesity pandemic on both the research community, for failure to fully comprehend the disease, and the food industry, for exploiting that failure (Taubes 2012). He picks up the theoretical mantle where Lustig leaves it, implicating insulin and condemning fructose, but he expands the list of “nutritional” villains considerably to include all easily digestible carbohydrates that quickly raise glycemic indices.
As Taubes points out, the “hormonal/regulatory defect” hypothesis (H/RD) of obesity is actually nothing new. A German internist, Gustav von Bergmann, proposed it in the early 1900s and it gained general acceptance throughout Europe prior to the Second World War. But, of course, much changed after the conflict ended. Germans and Austrians struggled to redefine themselves, for example, and the lingua franca of science shifted somewhat abruptly from German to English.
Medical practitioners quickly abandoned H/RD for a different idea articulated in the 1920s by University of Michigan physician Louis Newburgh. “All obese persons are alike in one fundamental respect,” the American had argued. “They literally overeat.” In attributing excessive weight gain to either a “perverted appetite” or a “lessened outflow of energy,” Newburgh laid an enduring foundation, Taubes contends, for a failed and yet insufficiently tested hypothesis.
Taubes scoured the relevant literature from 1944 onward and isolated nearly100 experiments (results at nusi.org). In his estimation, however, each study was critically flawed. All free-living trials, of course, lack control over subjects’ actual consumption. On the other hand, the more well-controlled experiments lost statistical power due to small sample sizes and short durations.
Some studies severely restricted caloric intake in carbohydrate-limited diets, thus undermining the investigators’ ability to determine whether carbohydrate content can influence weight gain independent of total caloric content. Others severely restricted control diets, thereby limiting carbohydrate content as well. Finally, some trials failed to either evaluate low-carbohydrate diets at all, distinguish between macronutrient content, or eliminate habitually lean subjects.
Through NuSI, Taubes (and co-founding physician Peter Attia) plan to fund and facilitate more appropriate studies performed by “independent, skeptical researchers” who are also leaders in the field. Designed to rigorously test competing hypotheses, experimental diets would consist of vastly different macronutrient composition and, they hope, demonstrate that fat can be lost or gained while total caloric intake remains fixed.
Subjects would be ward-restricted and randomized into two groups. One would receive a balanced diet, rich in carbohydrates; the second would be severely carbohydrate restricted—ideally to less than sixty grams per day. Both cohorts would be fed an isocaloric diet matching daily intake to pre-experiment daily expenditure. Studies would last for at least two months, and energy expenditure, insulin levels, and body composition would be measured at appropriate stages.
Although she admires Taubes’ commitment, Marion Nestle believes that such experiments will be exceedingly expensive and tough to manage and interpret. Familiar with his and Lustig’s arguments, she maintains that a calorie is still a calorie in the limited context of weight gain. Like many others, she characterizes the H/RD view of obesity as “reductionist,” or lacking in nuance, because it fails to consider, among other things, the role of behavior. “Committed, intelligent people,” she told me, “must find ways to deal with a food environment that encourages frequent eating of large portions.”
Of course some of Lustig’s and Taubes’ ideas have been widely accepted for some time—the most direct effects of insulin and leptin, for instance. The U.S. Department of Agriculture, for example, has recently supplanted its carbohydrate-ridden food “pyramid” with a “plate” relatively lacking in simple sugars and starches. And even daytime network television doctors now advise audiences to avoid such cuisine.
But these writers’ contention that personal control and responsibility have no practical place in the discussion remains highly controversial. The evidence is clear—most (but not all) people who attempt to lose weight—and keep it off—will fail. Less obvious are the reasons why. Has biology stacked the deck against the overweight and obese to the point of utter hopelessness? Or is it merely a fact of life that, in any context, the vast majority always fails to overcome exceptionally challenging obstacles?
Overweight or not, we all have a substantial interest in settling these debates. Obesity rates have doubled in the U.S. and tripled in the UK since the 1980s. Health authorities have drawn persuasive connections between obesity—or the metabolic dysfunction for which obesity is a marker—and a plethora of horrifying diseases, including cancer.
Indeed, recent studies have advised us that obesity is directly responsible for twenty-one percent of all U.S. healthcare costs (Cawley and Meyerhoefer 2012), more than even smoking (Moriarty, et. al. 2012). A genuine medical crisis of this magnitude, I would argue, deserves not so much more attention as it does higher scrutiny. As Taubes urges, Americans in particular can hardly afford not to make the necessary investments.
Cawley, J. and Meyerhofer, C. 2012. The medical costs of obesity: an instrumental variables approach. J. Health Econ. 31(1): 219-30.
Lustig, R. 2012. Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease. NY: Hudson Street Press.
Moriarty, J.P., et. al. 2012. The effects of incremental costs of smoking and obesity on health care costs among adults. J. Occup. Environ. Med. 54(3): 286-91.
Nestle, M. and Nesheim, M. 2012. Why Calories Count: From Science to Politics. Berkeley: University of California Press.
Wells, J.C.K. and Siervo, M. 2011. Obesity and energy balance: is the tail wagging the dog? Eur. J. Clin. Nutr. 65(11): 1173-89.
Taubes, G. 2011. Why We Get Fat and What to Do About It. NY: Knopf.
Taubes, G. 2012. Treat obesity as physiology, not physics. Nature 492: 155.