the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or from new versions of deprivation diets, which rarely lead to permanent weight loss. the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or from new versions of deprivation diets, which rarely lead to permanent weight loss. the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or from new versions of deprivation diets, which rarely lead to permanent weight loss. When I was a child I thought my grandfather and Jackie Gleason were two of the fattest men in the world. Last year I happened on a rerun of The Honeymooners and was taken aback by Mr. Gleason’s modest girth. And an old movie of my grandfather shows, at most, a size 40 waist – practically svelte these days. What’s happened to us? We’ve become accustomed to widespread obesity in men, women and children. Is this one of the prices we pay for our market-driven, entertainment-loving culture? Look at all the factors conspiring to load the scales: escalating inactivity, a vast snack and soft drink industry, supersizing, frenetic lives, fast food restaurants, the demise of the family-centered, home-cooked meal and its replacement with eating anywhere and everywhere, all the time. There is blame aplenty to go around, but this is a medical column, so we’ll stick to the role of science. Why pick on the medical science? Because we need to know how the expert advice we rely on plays out over time and if well-intentioned advances lead us astray.
Taking fat out of the diet
In the 1950s, medical researchers took on the epidemic of heart disease that had begun around 1900. Fatty streaks in the aortas of young soldiers dead in the Korean War made pathologists think that heart disease actually began early in life. They created an animal model for study, feeding rabbits cholesterol dissolved in vegetable oil instead of lettuce and carrots. When fat showed up in the rabbit arteries, the dietary theory of heart disease came to life. Some scientists quibbled, claiming that the problem was more complex, that other dietary factors like sugar might be equally to blame, but they lost the debate. Dietary cholesterol became the enemy, and over the next half-century the public learned to view the egg as a toxic substance, despite its near perfect protein and yolk full of valuable vitamins.
Along came the observation that Mediterranean populations had little heart disease compared to Americans. They also walked more, ate regular meals in family settings, didn’t snack, doused all but breakfast in olive oil, and scoffed at tasteless, pre-packaged food. But what we saw was lots of pasta, with not an ounce of cholesterol in it. Pasta was the ideal candidate to replace fat. We embraced the carbohydrate age, and turned a blind eye to the fact that, for years, we had managed to turn cattle fat by feeding them carbohydrates.
The national waistline ballooned, but can we at least say that the dietary agenda paid off in terms of heart disease? The answer is murky, because there were other, simultaneous prongs of attack: a fruitful campaign against tobacco use; drug treatment of high blood pressure; drugs that keep the body from absorbing or making cholesterol and drugs that calm the heart. Galloping technological advances allowed doctors to ream out plugged coronary arteries, prop them open with metal struts, or bypass them altogether. Nevertheless, cardiovascular disease remains our leading cause of death and the total number of patients with the disease has increased. Only the death rate from heart attacks has fallen and that statistic is attributable to the interventions and drugs and declines in smoking. The effect of the officially sanctioned diet on the epidemiology of heart disease, if any, is hard to discern. Now we face even more cardiovascular disease as epidemic abdominal obesity brings with it more diabetes, high blood pressure, and inhibition of physical activity.
A contribution from chemistry: artificial sweeteners
Science contributes to the obesity epidemic in other, more subtle ways. Through chemistry, we possess the magic of intense sweetness without a caloric price. An enormous rise in artificial sweetener use parallels the obesity epidemic. Well, is that a surprise? Everyone’s trying to lose weight. But what if, in addition to failing to stem the tide of weight gain, non-nutritive sweeteners are contributing to it? A few studies raise this unsettling possibility, and no study shows any significant effect of these chemicals on the process of weight loss, unless they are used in conjunction with a disciplined program of eating and exercise.
How could something with no caloric value contribute to obesity? Perhaps by raising levels of insulin, hormone which promotes fat storage. At least one artificial sugar (Xylitol) stimulates enough insulin release in dogs (who ate the stuff accidentally) to cause profound hypoglycemia and death. Do “non-nutritive” sweeteners cause release of insulin in people as well? This hasn’t been studied well. Artificial sweeteners were developed for Type I diabetics, who lack insulin altogether, so there wasn’t any point in measuring the hormone. But there is an insulin burst from the pancreas within thirty seconds of sweetness arriving in the mouth (the cephalic insulin response), and most people who use non-nutritive sweeteners do make insulin, which efficiently converts any extra calories in the meal accompanying the drink to fat. Some studies do suggest that insulin levels are higher in regular artificial sweetener users than non-users.
Tipping the scales while fixing the mood?
Chemistry also gives us the drugs that make people happy – or at least less unhappy. Over the last 30 years, antidepressant use for life’s inevitable miseries has skyrocketed. We are engaged in the very new practice of using these drugs in children. One side effect, perhaps more common than advertised, is difficulty withdrawing from the drugs. Another is weight gain. Some depression requires drugs, and antidepressants or antipsychotic agents don’t always cause weight gain. But the drugs are in such widespread use that you probably know someone who has packed on 20 pounds in the course of a divorce or other life stress that prompted antidepressant use and someone else who accepts the weight gains because they can’t stop the drugs.
Will science solve the obesity epidemic?
Should we look to medical science or to the mega-million dollar diet industry to reverse our big obesity problem? To the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or new versions of deprivation diets (which rarely lead to permanent weight loss)? I think not. And who knows what unexpected consequences might come along for the ride. For a significant statistical improvement in the obesity problem, the answers will have to come from all of us and from our choices about how we act and what we value – from the culture, not from science. For too long we have treated food as an enemy, taking the joy and taste out of eating, without much to show for our efforts. Heart disease is still the number one killer, obesity is epidemic, and diabetes is hot on its heels. Extra weight comes off for good in the same slow, sneaky way it crept on – a few hundred calories a day out of balance with caloric needs. That’s just one dessert, or a beverage or two. Or a brisk walk instead of an hour of television. Every day we make the choices that determine our energy balance – elevator or stairs? TV or a walk? Coke or water? Vote for the guy who wants to put PE back in school or the one who doesn’t care? Yes, extra weight takes a very long time to lose, but next year will come around before you know it, no matter what you do. The choices will have added up, one way or the other. Every choice counts. In an epidemic, every person counts.