“Fat” – Part 2 Understanding Obesity – Reasons for Hope

“Fat prejudice is the primary impediment to understanding—or wanting to understand what obesity is all about,” says a public health nurse who appears in “Fat: What No One Is Telling You,” a 2007 PBS home video documentary.

In the first installment of this post, I explained how little physicians know about what causes obesity—in part because, as this nurse points out, “blaming the victim has stood in the way of understanding.” Here, I am reminded of how, in the past, we blamed patients suffering from depression and other forms of mental illness. For centuries, this prejudice stood in the way of understanding that mood disorders are caused by a flaw in chemistry, not character

In “Fat,” patients describe how even some doctors treat them with contempt. “When I went to get a Pap smear, the doctor said, ‘You’re too fat; come back when you’ve lost weight,’” one woman recalls. 
The documentary also points out that “while everyone dies . . . it should perhaps come as no surprise that in our society, obese people are blamed for dying. If a thin patient comes into the hospital, has a heart attack, and dies, cause of death is labeled ‘heart disease’, a public health nurse who appears in the film tells the filmmakers. “If an obese patient has a heart attack and dies, cause of death is ‘obesity’.”

Nevertheless, despite the bias, today scientists have begun to look past the old-fashioned notion that obesity is merely a matter of gluttony, and have made real progress in beginning to understand a terribly complicated chronic disease.

Granted, obesity doesn’t look like “a subtle disease,” acknowledges Harvard’s Dr. Lee Kaplan, who heads the Weight Reduction Program at Mass General Hospital. Conventional wisdom says that if you put too much food in your mouth, and don’t exercise enough, you’ll wind up fat. Period.

As is so often the case, the conventional wisdom is wrong. The truth is that “more than 400 genes are involved in weight regulation. And that doesn’t include the environmental factors,” Kaplan points out. The experts report that some people eat rich, fatty foods, never exercise, and remain thin. Others exercise daily, diet religiously and are seriously overweight. Of course many overweight people who need to lose 20 or 25 pounds take it off and keep it off. But they are not obese—they are not fighting a chronic condition.

Ninety-five percent of obese patients who remain in medically supervised treatment regain whatever pounds they lose. Physicians don’t know why. They have not been able to figure out how to help these patients because medical science has not yet sliced through the tangle of genetic, metabolic, social, psychological and environmental factors that cause obesity.

A Unique Disease—the Body Undermines the Cure
 
What we do know is that “Obesity is the one disease where your body fights the cure,” says Dr. Michael Rosenbaum, a Columbia University researcher working on an NIH-funded study on weight control.

By and large, the body is programmed to help you heal. But not in this case. People think that dieting is “a matter of choice,” says Arthur Frank, medical director of the George Washington University Weight Management Program. But in fact, losing weight requires overcoming powerful brain signals that are working against you.

If you have ever dieted you may already know that, once you lose some weight, your metabolism slows down and you burn fewer calories. For all your body knows, you are stranded on a desert island, starving to death. So it tries to “help.” The brain is wired to eat and store fat to protect against starvation. In fact, when you lose weight, the human body has redundant systems to try to save you. That’s how the human species has survived.

In “Wired to Eat,” a 2005 article published in MIT Technology Review, Jeffrey Friedman, an obesity researcher at Rockefeller University, explains that the mechanism that drives us to eat is located in the hypothalamus at the base of the brain, where two types of neurons appear to be the chief regulators of appetite. These neurons tell us when we're hungry and when we're not. The so-called NPY neuron stimulates hunger, and the POMC inhibits appetite. Each neuron is turned up or down by chemicals that wash over them. "A dominant factor in controlling weight is this basic neural circuit," says Friedman.

The chief chemical involved is leptin, a hormone produced by fat cells in the belly. When people gain weight, fat cells increase the levels of leptin, and as leptin washes over the POMC neuron, their appetite is suppressed. When people start to lose weight, body fat is reduced, which decreases the levels of leptin. Less leptin means the POMC turns down and the NPY neuron predominates, which ramps up hunger. Other chemicals—fats, sugars, and neural transmitters—also influence the actions of these neurons, but leptin seems to be the key.

Friedman is famous for his 1994 discovery of the gene that codes for leptin. And for a brief moment in the mid-1990s, the MIT Technology Review explains, “leptin seemed to be a potential wonder cure for obesity.” Researchers hoped that leptin injection would turn up the POMC neuron that inhibits hunger. But leptin injections work for only a small percentage of the obese. It turns out that the majority [of obese people] do produce leptin, but their bodies actually resist the effects of the hormone by blocking its ability to turn up the hunger-suppressing action of the POMC neuron. So their appetites remain large, and they keep eating—and gaining weight—until they reach the point at which the resistance stops. Where that point lies, Friedman believes, is determined by genetic makeup.

Some people appear to be hardwired to be particularly ravenous. When access to food is unlimited, say hunger-gene experts, these people can will themselves to eat less, but their efforts will almost inevitably be overridden by the far more powerful force of genetics. Studies show that invariably, weight loss is followed by weight gain, making obesity a life-long struggle. “You just have to keep falling off the horse and getting back on again,” says one woman who appears in “Fat.” A physician in the film points out that trying to continue eating less is like trying to run upstairs without breathing faster. “You can do it for a while, but not for that long.”

This explains why appetite suppressants have a minimal effect in helping obese patients according to Dr. Robert Lustig of the Division of Pediatric Endocrinology at the University of California, San Francisco. “These medications become less and less effective after just 4 months,” Lustig explains. This is not because of a lack of compliance on the part of the patient, but rather due to leptin resistance, which persists even in the face of pharmacotherapy. When appetite suppressants foil one set of receptors, another mechanism kicks in, and hunger returns.”

Looking for the Needle in a Small Gene Pool        

Friedman did some of his most important obesity research on Kosrae, a tiny volcanic island in the Pacific Ocean some 4,670 kilometers southwest of Hawaii. There, he led a Rockefeller University team that worked in a joint project with the Kosrae State health authorities and the U.S. Department of Health and Human Services to discover why not everyone on the island was overweight.

Until the United States took control of Kosrae and the rest of Micronesia after World War II and began shipping in canned and processed foods, the people of this island were predominately lean—eating fish, bananas, coconuts, and taro. Most islanders lived a near-subsistence life, suffering through frequent droughts and stormy seasons that decimated crops. And they stayed thin.

But after World War II, their diet changed. San Francisco Chronicle reporter David Ewing Duncan visited the island in 2005, and describes grocery store shelves stocked with “Frosted Flakes, pork and beans, canned peas, soft drinks, and Spam . . . Today well over half of the adult population is overweight,” he observes. This comes as no shock; we know that as environment changes, and foods high in carbs and fat become widely available, an entire population is likely to gain weight.

The surprise is that some on the island remained lean despite the change in diet. And this is what attracted molecular biologists at Rockefeller searching the human genome for genes and mechanisms that influence how we eat.

This diversity in a small population, with only 7,600 people on an isolated island where most people are descended from a few families, is what intrigued Friedman. Having just a few genetic lineages on the island means that each person's genomic makeup is far more similar to his or her compatriots' than, say, an American's would be. “Looking for a gene is like searching for a needle in a haystack," he says. "On Kosrae, the small gene pool makes the haystack smaller."

The MIT Technology Review
explains Friedman came to believe that the Kosraeans' ballooning weight is a manifestation of what geneticist James Neel in 1962 dubbed the ‘thrifty gene’ theory. Neel posited that in an environment prone to famine, hunter-gatherers gained a selective advantage if their genes predisposed them to storing fat when food was available. Those with such ‘thrifty genes’ were more likely to survive famines and pass on their genes. But in modern times, the thrifty gene has proved a liability.

“The theory also posits that people who lived in early agricultural societies, such as those in the Fertile Crescent in the Middle East, had a steady supply of food from plants and domesticated animals and thus didn't need to store fat. So in our world today, people with lean genes are protected from obesity, and those with fat genes are at the mercy of DNA.”

“Why leptin resistance occurs in some people is poorly understood, Friedman says.  It may be a relic of the thrifty-gene response, ramping up appetite in those whose ancestors lacked adequate food. The Rockefeller team measured leptin levels in the Kosraean population; Friedman is using that data to help correlate leptin resistance with genes that might be responsible for it. According to Friedman, each of us has a ‘set point’ of hunger and satiation, which we inherited from our individual forebears. We are born with this setting, and we are driven to keep eating until we reach it.”

“People whose ancestors, like most Kosraens', had to work hard to get enough to eat, had their hunger-volume—analogous to a specific setting on a radio dial—turned up to 8 or 10.” Duncan adds. “Those whose ancestors had plenty of food—for instance, the agriculturists of the Fertile Crescent and Europe, and parts of India and China, people who have basically had stable food supplies for as many as 10,000 years—have inherited a setting of two or three.”

Friedman concedes that more work is needed to understand the role of exercise in weight gain. But, according to the MIT Technology Review, he does believe that “the weight increases of the past 20 years in the United States represent a steady progression of people eating enough food to reach their set points, rather than a sudden spike in bad eating habits or more sitting around. What really intrigues Friedman is why everyone doesn't get chubby when there is plenty to eat. Analyses show that the number of lean people has remained steady for the past 30 years, he says. ‘One's size is not an environmental effect. Nor is it a matter of willpower.’”

There is of course much money to be made if entrepreneurs can convince the obese that they have the secret to weight loss. As Duncan notes, “the diet industry [is] skeptical of Friedman's claim that obesity is as over-determined [as he claims. The industry] insists that people can overcome the hunger impulse and trim down with healthy diets and reduced calories. Friedman says this is true, but that even a heavy person in most cases can lose only 10 or 20 pounds and keep it off. But even a small amount of weight loss can be healthy, he says. ‘You can lose more for a period of time,’ he says, but the biology will eventually force you to eat in most cases, and ‘you will regain the weight.’”

“Friedman acknowledges that what he suggests is counterintuitive, since people can resist jelly beans up to a point. But he insists that, for the majority of the obese, free will in weight control is an illusion. ‘This is a way of thinking that needs to change.’"

One might wonder why the “thrifty gene” has survived. After all, how many Americans die because they don’t get enough food? Granted, many of America’s poor are malnourished, which in turn leads to diseases that can be fatal, few succumb because they simply can’t get enough calories.

But as the documentary “Fat,” points out , Americans “have gone from having very little to eat to being able to eat a lot—with a few bucks in our pocket—in just 75 years.

Panning a fast-food restaurant, the film points out, “how many calories you can get for just four bucks.” This wasn’t true during the Great Depression of the 1930s. Indeed, the film’s narrator observes “there are millions of people who are here today who wouldn’t have been here 60 years ago” because they couldn’t have “gotten this much food for that amount of money in yesterday’s dollars.” 

Little wonder that the brain still sounds an alarm when we lose weight.

What We Are Learning From Gastric Bypass Surgery

And “leptin resistance” is just one of many mechanisms that protects us. “The gut has a nervous system—and a mind of its own—that decides what and how much we eat,” says Michael Gershon a bowel expert at Columbia University who appears in “Fat.” 

At Mass General, Dr. Lee Kaplan agrees: “We have two brains—in the stomach and ‘upstairs.’ The brain in the gut can disturb the brain in the head.”

“Neuro-chemical signals that flow between the two brains,” Kaplan adds and we have discovered that gastric bypass surgery (a.k.a. “stomach-stapling”) interrupts that flow.

Until recently, physicians believed that patients lost weight because the surgery reduced the size of the stomach, forcing them to eat less. But once again, it’s not that simple. Researchers performing gastric bypass surgery on rats have discovered that the surgery severs nerves in the bowel that communicate with the brain—and that this is tied to weight loss.

Today, the surgery is giving researchers valuable new information about how the brain and gut manage obesity. “In the next 5 or 10 years, we’ll find that there are many, many other things we didn’t know,” Kaplan predicts.

“Gastric bypass surgery is not a solution for obesity—it’s only appropriate for the sickest of our patients,” he adds. “But it’s given us an enormous hope that, through what we learn, we’ll be able to solve the problem.”

In Part 3 of this post, I’ll reveal what happened to the characters from “Fat” that I described in Part 1, why exercise may be far more important than diet for obese people who want to be healthy—and what society is and isn’t doing to promote  exercise for children.

12 thoughts on ““Fat” – Part 2 Understanding Obesity – Reasons for Hope

  1. In this analysis, thus far, there’s no mention of changes in the micro nutrient quality of food intake due to a general increase in sugar (fructose) consumption. Nor is there discussion of the universal admonition to consume fewer fat calories.
    I’ve been studying nutritional issues for more than 30 years and weight control for at least half that time and my view is that excessive carbohydrate consumption and inadequate fat intake are the major factors behind the expansion of America’s gross national waistline.
    The research of Peter Havel and Stephen Phinney from the University of California-Davis, Richard Fineman from SUNY Downstate, Jeff Volek from the University of Connecticut, Eric Westman from Duke University, and Mary Vernon from the University of Kansas supports the low-fat/fructose explanation for the obesity epidemic. A minor factor in the obesity epidemic but a major one in cancer is the proliferation of omega 6 vegetable oils. “Health Beat” readers who Google the above names or “fructose omega 6 oils hazards” or “saturated fats truth benefits” will likely gain a different perspective on the obesity epidemic than can be furnished by Drs. Lustig, Kaplan, Rosenbaum, Frank, and Friedman.
    David Brown
    Nutrition Education Project

  2. Fully recognizing that the singular of data is not anecdote, I’ve found it fascinating to understand the interactions, in my own body, between blood glucose and food intake. Yes, I understand that transient blood glucose and total caloric intake are different issues.
    If I eat ice cream or yogurt that is low-fat but has appreciable amounts of monosaccharide and disaccharide sugars, my glucose will spike. If I eat a full-fat ice cream, I have a minor rise. Eating a variant that is low fat and noncalorically sweetened is not a problem.
    I don’t have that much of a sweet tooth, so that’s not a sacrifice. The surprising things come with ostensibly high-fiber, high-carbohydrate foods such as oatmeal, which I do love. Plain oatmeal, or with skim milk, gives me an enormous rise in blood sugar, but adding a fat slows the rise.
    In the last year, I’ve been getting better and better at bread baking, and now am at a point where I can create recipes that work for my metabolism. Glycemic index is a starting point, but soluble and insoluble fiber, fat content, etc., are all areas to experiment. Using pure gluten to help the rising of low-carbohydrate flours, such as buckwheat, may be a promising route.

  3. “Until the United States took control of Kosrae and the rest of Micronesia after World War II and began shipping in canned and processed foods, the people of this island were predominately lean—eating fish, bananas, coconuts, and taro. Most islanders lived a near-subsistence life, suffering through frequent droughts and stormy seasons that decimated crops. And they stayed thin.”
    This seems to confirm what I’ve been saying (repeatedly) that in societies where people don’t have access to manufactured foods there is less obesity. Theoretically some of these islanders could have stuffed themselves with taro and gotten fat, but it seems that they didn’t. I don’t think the reason was a lack of an adequate supply, but because one just can’t eat enough of a food like this to gain weight. There is just too much fiber and water compared to the amount of carbohydrates. So one gets filled up before one has consumed many calories. One cup of taro has only 116 calories.
    So even if there is a genetic disposition toward weight gain, it won’t be activated in a meaningful way if the foods which trigger over eating are not available.
    One can make similar arguments about diabetes, which used to be a fairly rare disease. Now we have an epidemic which is linked to the huge rise in sugars and high fructose corn syrup used in foods.
    Both problems can be lessened by reversing the social incentives that have been put in place which favor junk food.
    This is a public policy problem first, a public health problem second and a personal medical problem third.
    This country is unwilling to get in the way of any moneymaking scheme that has a large lobbying base. How else can one explain the continued existence of cigarettes 50+ years after their health problems were revealed?
    Those in a position to change public policy don’t want to, there is just too much money at stake.

  4. Robert, Howard and David, thanks for your comments.
    Robert: you wrote “Theoretically some of these islanders could have stuffed themselves with taro and gotten fat, but it seems that they didn’t. I don’t think the reason was a lack of an adequate supply” . . .
    Se the post where I wrote: “Most islanders lived a near-subsistence life, suffering through frequent droughts and stormy seasons that decimated crops.”
    The fact is that the people of Kosrae often lacked an adequate supply of food. The island was known for famines that wiped out large sections of the population.
    As recently as the end of WW II many natives as well as Japanese soliders who were living on the island died for lack of food.
    I did a little reading–apparently fishing was hard there, and it was also difficult to harvest the coconuts. To try to fend off starvation, the natives dug deep breadfruit pits to serve as semi-refrigerators. They tried to keep fermented breadfruit in the pits to eat during times of famine . . . but obviously that didn’t work out.
    The thrifty gene theory seems to apply in areas where agriculture was difficult and there was often an insufficient supply of food.
    You don’t find evidence of thrity genes in populations who lived where farming was relatively easy.
    That said, the thrifty gene is not the only cause of obesity. Like other complex diseases (cancer, etc.) it has many causes.
    Junk food contributes to obesity not just because it is high carb and high fat, but because it is cheap. It’s the abundance of food that allows people to eat until they’re more than full.
    Such abundance really is a recent development. In the past, only affluent Americans were fat (this was seen as a sign of status) while the poor and middle-class were thin. (See pictures of Americans at the turn of the 20th century)
    “Thin” didn’t really became fashionable until the 1920s — the era of the “Flapper”– a woman with a straight, thin boyish figure.
    But in the 1950s, the “hourglass figure” (busty and full-hipped) was agan considered the ideal. Jayne Mansfield was far from slender.
    Then in the 1960s, Twiggy served as the model for beauty. (In the Sixties fashion models were supposed to be super-skinny so that their bodies “wouldn’t distract from the clothes.”
    And ever since then, the rule has been “you can never be too thin.”
    But back to your point–yes, junk food is hugely profitable. . . and a public health problem. We need subsidies to make healthier food widely available and affordable.
    And yes, it is extraordinary that cigarettes are still on the market.
    Howard- Glad to hear you’re baking bread!
    David–
    I’ve read about the fructose theory — it’s also connected to leptin.
    Readers with find both sides of the argument here:
    http://www.sfgate.com/cgi-bin/article.cgi?f=/chronicle/archive/2004/02/18/FDGS24VKMH1.DTL
    Some say that fructose has a special effect on metabolism; others argue that we simply consume too much of it–it is in many foods.
    Since the early 1980s, food manufacturers have been putting more and more fructose in our food. But to say that it is the major cause of increased obesity is like saying that the advent of the computer and video games is the main cause of obesity.
    Again, it’s a complicated disease, and nutritonists, biologists sociologists, epidemiologists and psychologists all contribute to our understanding.
    Finally, I’d note that the low-carb, high fat diet is controversial becaue of the emphasis on fat. (Many doctors feel more comfortable recommending high-protein, low carb diets.)
    But this post is about obesity, and the point of the post is that, for the truly obese, none of these diets work for long.This is why they deserve sympathy rather than harsh
    judgment.

  5. Maggie,
    I agree with you that people who struggle with weight issues “deserve sympathy rather than harsh judgment.” In nature, both humans and animals exhibit tremendous genetic variations in physiology and body chemistry that give rise to many configurations of food preference, appetite, and body size and shape. Consequently, for some people (as well as animals and fish) it is normal to have a high fat content. Note that researchers utilize obesity prone laboratory animals to test various therapeutic (drug) approaches to weight control. Scientists developed a reservoir of such animals through selective breeding.
    In the USA there is a growing reservoir of over weight and obese people who retain excess fat for a variety of reasons. For some it is genetic. These find it impossible to lose fat no matter what they do. Others would lose weight if they simply consumed less food. Others would lose weight if they consumed better quality food. And still others would lose weight if they consumed food matching their metabolic needs. If this seems confusing to you, I suggest you read these two books by Roger J. Williams, PhD: “Biochemical Individuality” and “Nutrition Against Disease.”
    You mentioned that “the low-carb, high fat diet is controversial because of the emphasis on fat.” At this stage of the game there should be no controversy because there’s plenty of solid research demonstrating that high-fat intake can be healthy. I say “can be” because some people, due to metabolic makeup, should not use the high fat approach. One of the reasons why high-fat can be healthy is because it conserves biochemicals required for conversion of energy molecules from one form to another. I’m talking about converting carbohydrate or protein to fat. Few seem to realize that muscle tissue derives 60 to 80 percent of its energy needs from fat. To supply enough fat energy for muscle function a low-fat diet forces the body to perform chemical reactions that utilize supportive nutrients such as proteins, vitamins, and minerals. Once the energy transformation is complete, the byproducts of this metbolic process are excreted in the urine. In India some people consume their own urine in order to recycle these nutrients.
    Personally, I think the reason nutritional controversies persist, after a hundred years of research, is because the biochemical individuality factor is generally ignored.
    Finally, I urge you to read “Good Calories, Bad Calories” by Gary Taubes. Taubes has thoroughly investigated the origins of the low-fat, high-carb dogma and suggests that it has never been properly tested by the research community.

  6. David:
    You write: “Personally, I think the reason nutritional controversies persist, after a hundred years of research, is because the biochemical individuality factor is generally ignored.”
    I think this cuts to the heart of the matter. This is why I keep stressing the complexity of obesity.
    Different causes (or a different combination of causes) account of obesity in different individuals.
    I also am convinced that there is a huge difference between appearing very heavy and being obesee in a way that is hurting your health.
    There are different body types. Men in some cultures are meant to be short and very stocky; Women in other cultures tend to be tall and have very broad hips. I doubt this means that they are all unhealthy.
    In other words, I very much doubt that the American ideal of beauty, circa 2008, should be taken as a global model for health.
    If someone is able to exercise easily, is flexible, and is carrying muscle as well as fatm he or she may well be healthier than someone who diets constantly, and gets little exercise.
    Finally on the question of high fat, high carbs . . . I probably am reacting based on what works for me (high protein, moderate fat, very little carbs.)

  7. I am embarassed to respond to such a well written piece with anecdote, but here goes.
    I’m covering the ER. Lady is there with tooth pain. I’m always suspicious of drug seeking but she looks legit. Late 20′s, 5’8″ maybe 180#. All her teeth are losing enamel.
    I ask about meth.
    “Nope,” she says,”Every body thinks that. But my teeth started rotting after I got my stomach surgery.”
    She’d had her stomach “stapled” down in California a couple years earlier. Lost 120# the first year. Has only gained back about 12# this year. But her teeth are going, gone.
    She mentioned how alot of the fellow patients she saw in the follow up clinic had become alcoholics. “They can’t eat anymore, but they can drink.”
    She got a look at the bill that Kaiser paid. $20k.
    I wonder if these complications are counted in the follow up data. Or are we just counting pounds?
    And pounds, as you said in you first piece quite well, do not necessarily equal health.

  8. ddx:dx–
    I have heard that the side effects from bariatric surgery can be extreme–though I’ve never heard of the enamel loss.
    That some people would becom alchoholics makes sense. For many people, eating provides great psychological comfort and pleasure. They would need another way to “celebrate.”
    It’s also risky surgery
    Moreover, today some of the doctors doing it don’t have much experience .(It’s also very lucrative surgery.)
    But for someone who is morbidly obese (i.e. obesity is killing him) this is the only answer we have right now.
    And I have real respect of the patients and doctors who embrace it as a last
    resort.
    Still, if I knew someone who was planning on it, I would urge them to find out how many such surgeries the doctor had done over what period of time, etc.

  9. I just wanted to say that my family through the generations (according to old pictures) does not tend to be fat at all, until the last two generations. My mother has a strong tendency for weight gain, as well as most of her children. I can only assume that much of this problem is dietary in nature. For me, as soon as I quit all forms of sugar, except for fresh fruit in season, my weight loss was easy and substantial. I also added exercise in the mix, but it believe it was largely due to the way we were raised and the way I eventually changed my eating habits.

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