Obesity in America has set off all the traditional alarms – it’s an urgent epidemic with catastrophic implications. But to date, the discussion about obesity lacks context. Apparently, the war on obesity is to be waged on old battlegrounds, and the solutions being offered are more adaptive than prescriptive.

In 2003, there were more than 103,000 gastric bypass surgeries for morbid obesity in the United States. The complication rate was 7 percent. If I were morbidly obese, with my quantity and quality of life slipping away, I’ve no doubt I would grasp on to the last straw of gastric bypass, too. But what an admission of failure for our health care system, where intervention continues to trump prevention, diseases are siloed as if unlinked by physiologic and pathophysiologic processes, and disease burden segregates by gender and race.

If you don’t believe gastric bypass surgery at least in part signals the acceptance of the inevitability of obesity, let’s consider other measures. Take, for instance, the Puget Sound ferry seats, which were recently widened from 18 inches to 20 inches. Or the Colorado ambulances that are now equipped with a hydraulic winch capable of lifting a 1,000-pound human. Or Indiana’s new super-sized casket – it’s 38 inches rather then 24 inches wide.

How should we be thinking about obesity? First, the science of obesity is complex and in its infancy. The hormone leptin, which is produced by fat cells and provides the chemical message to the brain that helps control excessive caloric intake, was first discovered at Rockefeller University just 10 years ago in 1994. With that discovery, researchers and social scientists took a fresh look at obesity. Was it simply a reflection of greed and weak will, or something more? Dr. Michael Schwartz of the University of Washington defined scientists’ new way of thinking when he said, “We like to think that eating is a voluntary act. But the amount you eat is controlled in part by how much fat you have.”

The fat cell is a veritable endocrine factory. In addition to leptin, it makes adiponectin, which enhances insulin’s effect and reduces inflammation; resistin, which dampens insulin’s effect and encourages inflammation; angiotensinogen, which leads to vascular constriction; IL-6 and TNF-Alfa, which both contribute to chronic inflammation; cortisol, which comes from the adrenal glands but converts to active form in the fat cell; and stored triglycerides, which are broken down to fatty acids and, when released in large amounts, can clog liver, heart, and muscle cells.

The logical question: why is there so much activity in the fat cell? Part of the answer is that fat cells, like the brain, stomach, liver, pancreas, and thyroid, are continually absorbing or releasing substances in response to the body’s energy needs.5 But these systems evolved millions of years ago, so it seems that fat cells are better adapted to preserving calories than shedding them. That appears to have been their historic mission.

The fat cell’s work begins early in life, and that helps explain why obesity is an increasingly common early childhood condition. Over the past three decades, the percentage of U.S. children between six and 11 years old with obesity has risen from 4 percent to 13 percent, and the rate in 12 to 19 year olds has increased from 5 percent to 14 percent. Children who are obese at age six have a 50 percent chance of being obese for life, and those who are obese at age 13 have a 75 percent likelihood of life-long obesity. Blacks and Mexican Americans, age six to 19, are 50 percent more likely to be obese than their white counterparts.

Obesity loves inequity. Those with a body mass index of greater than 25 are defined as overweight; those over 30 are obese; those over 40 are morbidly obese. Blacks and Mexican Americans are generally more at risk than whites, and women are more at risk than men. The numbers of obese Black women and obese Mexican American women, as well as Black morbidly obese women, are especially high.9 Socioeconomics appear to have a tie in, as does level of education. In fact, incidence of obesity and diabetes steadily climbs as number of years of schooling drops.

Being obese doesn’t mean you’re a bad person, but it virtually guarantees bad health. Obese individuals have a higher-than-normal rate of hypertension, type 2 diabetes, high lipids, cardiovascular disease, gallbladder disease, osteoarthritis, strokes, respiratory disease and some types of cancers. As the fat cell executes its evolutionary mission, in a land of plenty it does so with little knowledge of or feedback on the havoc it is creating. As Dr. Bruce Spiegelman of Harvard Medical School has stated, “For most of evolution, getting enough to eat was a driving force for survival. How many individuals were lost to morbid obesity?”

But times have changed. Today, there are as many over-nourished people as undernourished around the world. For obesity to be properly addressed we need to target the individual less, and target the molecule, the cell, and the population more. On the chemical level, Dr. Gökhan Hotamisligil of the Harvard School of Public Health, thinks strategically: “In the human body, as in the world, if you control fuel resources, you influence a lot of other things as well.” According to researchers, fat is not a by-product of individual greed and guilt but rather an active organ in its own right, worthy of a significant scientific effort to uncover its complex chemical and biological mysteries that will allow its evolutionary mission to adjust to 21st century realities.5

On a population level, increased prosperity has meant increased calories. Compared to 1971, U.S. women now consume an additional 335 calories per day, and men consume an added 168 calories per day. Advances in technology mean less exertion, and more indoor entertainment options have brought more sedentary behavior. Finally, the marketing of poor food in large quantities has added fuel to the fire.