(This is the fourth installment in a five-part series about fat acceptance.)

To be sure, the idea that weight loss is simply a function of calories eaten versus calories burned is an oversimplification of the complex interrelationships between biochemistry, genetics, physiology and motivation. But while it's unquestionably true that some people - some with clinical endocrine disorders, many others without - have a more difficult time keeping off excess pounds than do others, a glance at the data comparing 1960 weights with those of today shows that eating behavior has clearly played the greatest role in the rapid and continued bloating of America, with the food and restaurant industries - which, like any other businesses, exist not to serve public-health concerns or encourage people to make careful lifestyle choices, but to turn a buck - being the chief broker in this ongoing transaction. Indeed, that fat advocates all but omit from their list of enemies the offerings of a food industry with a clear, insistent and successful aim of encouraging Americans to ramp up their food consumption is glaring in light of the repercussions.

In terms of self-monitoring food intake in the context of the ever-increasing availability of high-calorie foods, health professionals feel that this is one area in which overweight people - and not only overweight people - encounter difficulty. "Do most overweight people under-report their food intake? Absolutely, invariably, unequivocally, irrefutably yes," says Albright. "But this isn't confined to overweight diet diaries; in my experience, we all under-report food intake and over-report the amount of exercise we get."

Interestingly, fat advocates - who might be expected to most adamantly assign blame for a swelling America to the increasing availability of high-calorie foods - are among the most vocal dissidents when it comes to labels like "junk food." This, it seems, is partially the result of their stance that food intake, size and health are largely independent, but primarily because of the stereotype that overweight people are fat because they make poorer choices than others, which could seemingly only be true if people who were lean as children and young adults remained that way. But many don't, and are increasingly obeserved carrying extra heft later in life alongside those who have spent their whole lives being overweight.

It is perhaps this same stereotype that sometimes leads fat advocates to also condemn the food industry itself, not its products; however, when others do this on fat people's behalf - regardless of their intentions - the media stereotype that junk purveyors successfully target fat people on a selective basis is potentially reinforced. And like most everyone, fat advocates balk at the thought of government regulations or taxations on the sale of foods deemed particularly unhealthful.

Fat advocates also oppose encouraging overweight youngsters to shed pounds, believing that this practice merely perpetuates a low-self-esteem cycle and preferring that emphasis avoid the limitation of food choices and focus on the encouragement of physical activity and, moreover, active self-acceptance regardless of size.

So what of "the" physiological etiology of obesity? Some scientists have long touted the concept of a "metabolic set point" that varies from person to person and serves as a sort of internal "fat-o-stat" that acts to keep its owner at a particular size. Experiments performed on rats over a half-century ago demonstrated that lesions in a certain part of the brain resulted in overeating, metabolic changes and profound weight gain, suggesting that a chemical signal might normally be at work in instructing the brain to increase or decrease appetite in accordance with the amount of the signal present. The 1994 discovery of leptin, a substance produced in fat cells, by Dr. Jeffrey Friedman at Rockefeller University seemed to support the set-point idea: a given amount of circulating leptin appeared to signal intact rat brains to decrease appetite, while weight loss - and hence a decrease in leptin - would trigger a drive to eat. The rats with brain lesions were unable to respond to leptin regardless of how much of it their fat cells produced, presumably explaining their marked weight gain. Importantly, it was also observed that naturally fatter mice produced less leptin than lean ones, suggesting that "leptin deficiency" might be a cause of overweight in humans.

However, problems arose when it was found that obese humans produced more leptin, not less, than lean people. Set-point theory also fails to explain migration studies demonstrating that, for example, leaner immigrants tend to gain weight once settled in the U.S., and also doesn't account for the rapid worldwide rise in overweight and obesity developed countries over the past 50 years. Furthermore, set-point theory is not supported by socio-economic trends wherein richer, educated populations include more thin women than do poorer ones. As a result, most nutritional scientists contend, as they did in the days before leptin was discovered, that eating and exercise behaviors - not genes - are the predominant factors in determining whether someone gains or loses weight.

Still, as Albright - who agrees with the set-point idea - notes, genetic contributions cannot be overlooked. In many overweight people, societal factors have simply served to bolster innate ones. "I think genetics pulls the hammer back on the obesity gun," Albright says. "Behavior is what pulls the trigger."

Regardless, the set-point theory maintains plenty of support. Its contemporary proponents suggest that increased leptin levels in obese people imply that their brains' leptin receptors are simply refractory to its effects, like insulin receptors in the pancreas in type 2 diabetics. Thus leptin resistance, not leptin deficiency, may mediate weight gain in some obese people. (Faulty leptin receptors have already been observed in certain rats.) Newer research by Friedman and others has shown that leptin influences the way brain neurons concerned with feeding are integrated during early development. Rather than being viewed as a substance that could be administered to obese people to promote weight loss, as it once was, leptin is now regarded as more of an "anti-starvation" hormone, with low levels of the chemical - or the brain's lack of response to it - triggering starvation-like effects, e.g., a decreased metabolic rate. Scientists have also honed in on a gene called lipin, which, when overexpressed in mice, results in weight gain even in the face of stable food intake. In any event, the precise contributions of leptin and genetics to weight management has yet to be elucidated.

Outside the lab, many cite examples of yo-yo dieters who have shed pounds over and over, only to return to their former, heavier weight, as evidence in support of the set-point concept. However, it seems equally plausible that this is as much a function of behavior as physiology: If someone abandons lifestyle changes that enabled them to lose weight (e.g., "goes off a diet" and ceases exercising after reaching some predetermined target weight), then it naturally follows that his or her weight, now at the mercy of old habits, will creep back toward previous levels. In such a scenario no set point is needed. Many an alcoholic drinker has been known to return to the bottle after long periods of abstinence, but no one is proposing the existence of an "ethanol set point" in such individuals. In a nutshell, merely highlighting the many people who have dropped pounds only to regain them to support the idea that long-term weight loss is widely unattainable seems logically tantamount to fingering the 1986 space shuttle Challenger disaster as proof that manned flights to outer space are impossible.

Some fat advocates, such as Portnick, are proponents and purveyors of exercise, and are wont to point out that being overweight and burning plenty of calories are far from mutually exclusive; NAAFA's official position is that "fitness is a desirable and attainable goal for most fat people." Certainly, physical activity is desirable for anyone, fat or thin, and exercise confers a variety of physical and psychological benefits regardless of whether it engenders significant weight loss. But the unfortunate truth is that significantly overweight people who are regular exercisers are a statistically rarity. (It's worth nothing that relatively few normal-weight Americans exercise regularly, either.) A study published in the New England Journal of Medicine in 2004 aroused the ire of fat advocates after Frank Hu, M.D. and a team of Harvard researchers, including Stampfer, concluded after looking at the body weights and activity levels of 116,500 nurses over 24 years that exercise does not, in fact, do away with the need for people to be vigilant about their weight. The study found that compared to women who were both active and lean, sedentary and obese were almost 2½ times more likely to die, physically active but obese women twice as likely, and sedentary but slender women 55 percent more likely. Among the study's critics was Gaesser, who claimed that the researchers used only baseline BMI's in their statistical analysis and failed to explain why. Hu's claim is that the researchers used baseline BMI valued alone in order to control for the effects of subsequent diseases.

Regardless, an important ancillary finding of the study was that only 2% of participants with BMI's over 30 reported amassing a total of even 30 minutes of moderate exercise (e.g., brisk walking) per day. So with fat-yet-fit Americans such as Portnick decidedly hard to come by - in no small part because heavier people who take up exercising often weed themselves out of the overweight population - it appears that getting significant amounts of exercise is simply one more weight-loss recommendation that fat advocates acknowledge when pressed but for the most part ignore.

In addition, fat advocates assert that extremely active overweight people are much healthier than their sedentary-but-lean counterparts. This is surely true, but as Albright points out, there are potential hazards in making interpersonal rather than intrapersonal comparisons. "There are obese people out there who can run circles around me and have VO2 max levels at extremely high levels," Albright notes. "But, are they optimally healthy? If, with the plethora of protective genes that allow them to function at a high level despite their obesity, would they would actually be able to perform at an even higher level if "less fat?'"

In addition, there are reasons other than the New England Journal of Medicine study to doubt the widely trumpeted refrain that fat is not, in and of itself, problematic. For example, studies examining the long-term effects of bariatric surgery have shown that solely as a result of weight loss from the surgery, diabetes symptoms were completely resolved in 77% of patients and 70% or more saw improvements in blood cholesterol. It has also been reported that two-thirds of hypertensive people who undergo bariatric surgery see their high blood pressure disappear. All of these changes occur in the absence of significant amount of exercise. While patients undergoing these procedures are at the far right of the obesity scale, doctors are confident that people who are "merely" overweight or obese can reap the same benefits from simply shedding pounds. "You can extrapolate the benefits of weight loss to 'regular obese' folks," says Michael Mollod, M.D., a cardiologist from Sarasota, Florida. "Those who lose less weight (than bariatric surgery patients) can lose their diabetic symptoms too."