Quote of the Day

Scientists who study obesity at the cellular level say genetics determines people’s natural weight range, right down to the type and amount of food they crave, how much they move and where they accumulate fat. Asking how someone got to be so fat is as meaningless as asking how he got to be so tall. “The severely obese have some underlying genetic or metabolic difference we’re not smart enough to identify yet,” says Dr. Rudolph Leibel of Columbia University Medical Center. “It’s the same way that a 7-foot-tall basketball player is genetically different from me, at 5-foot-8.”

Fat has been blamed for cardiac trouble, diabetes and some forms of cancer. But fat-acceptance activists argue that the epidemiological studies that link fatness to disease often fail to adjust for non-weight-related risk factors found more often in fat populations. Poverty, minority-group status, too much fast food, a sedentary lifestyle, lack of access to health insurance or to nonjudgmental medical care, the stress of self-loathing and being part of a stigmatized group — all are more common among fat people, and all are linked to poorer health outcomes at any weight. This makes it harder to say to what extent an association between obesity and disease is due to the fatness itself or to the risk factors that tend to go along with being fat.

Robin Marantz Henig in the New York Times Magazine

19 thoughts on “Quote of the Day

  1. I am one of the obese, and a firm believer that fat loss for the obese is impractical and not nearly as beneficial as the diet industry would like us to believe.

    However, I do have to think there is more than genetics involved in the increase in obesity rates in the US from the 1970s to today. I realize the average age of the US population is getting higher, and I realize that the threshold for being overweight (but not, as far as I can tell, obesity) was lowered in 1998. I also realize that smoking levels have dropped in that same time. Those things all account for some of the statistical difference in obesity today versus 40 years ago.

    But it’s my impression it doesn’t account for all of it. What are the possibilities? I have guesses: 1.) I’m wrong, and those three things do account for the entire difference. 2.) The spread of food stamps has allowed enough people that were previously having problems getting adequate nutrition to eat, and reach their natural body weight. 3.) The start of the dieting frenzy actually _caused_ some portion of the obesity epidemic, as the majority of the people that starved themselves ended up gaining more weight than they lost. What have I missed?

    • Check out the CDC PDF of data on average heights and weights from 60-2002. Assuming they use the same methods of data gathering, the average adult height in the US has increased about an inch between the 60s and 2002. Average adult body weight in the US has increased about 24 pounds. Average adult BMI in the US has gone from 25 in the 60s to 26 in the early 90s to 28 now. That’s average (mean) values.

      When the US changed the definition of overweight in 97, it was from a BMI of 27+ (when the average BMI was 26) to a BMI of 25+. So…the statistical “average person” was defined as overweight.

      • Living400lbs, I think you mean 26 in the early 90s.
        Mike S, following up Living400lbs’ info on average BMIs, Jeffrey Friedman often points out that looking at the change in the average BMI/average amount of weight gained is more meaningful than looking at the increase in the overweight/obesity rate; because most people are near the cutoffs for either “overweight” or “obese”, a relatively small shift in average weight can result in a large increase in the number of people categorized as “overweight” or “obese”.

        Endocrine-disrupting chemicals are one change in our environment that could be causing changes in weight. It’s also possible that changes in either what or how we eat (including dieting-related changes–the feast-famine cycle) are having some effect on BMIs, but the strength of the effect is modified by genetic differences.

  2. I can’t help but wonder, how much fatter people may have gotten due to the failure of diets and being told they aren’t “doing enough” to control their weight they just threw up their hands and essentially said to heck with it and sat on the couch and ate since that’s what they were being accused of anyway, leading them to a heavier weight than they would be if just left alone. I don’t know, that behavior certainly reflects my own experiences.

    • “The majority of people — up to two thirds — regained all the weight they had lost, plus more … several studies indicated that dieting was actually a consistent predictor of future weight gain.” — news article discussing the Mann study.

      And from the Mann study (PDF) itself:

      Reviews of the scientific literature on dieting (e.g., Garner & Wooley, 1991; Jeffery et al., 2000; Perri & Fuller, 1995) generally draw two conclusions about diets. First, diets do lead to short-term weight loss. One summary of diet studies from the 1970s to the mid-1990s found that these weight loss programs consistently resulted in participants losing an average of 5%–10% of their weight (Perri & Fuller, 1995). Second, these losses are not maintained. As noted in one review, “It is only the rate of weight regain, not the fact of weight regain, that appears open to debate” (Garner & Wooley, 1991, p. 740).

      The more time that elapses between the end of a diet and the follow-up, the more weight is regained. For example, in a study in which obese patients were starved in the hospital for an average of 38 days, patients were followed for varying lengths of time after the starvation period. Among patients who were followed for under two years, 23% gained back more weight than they had lost. Among patients who were followed for two or more years, 83% gained back more weight than they lost (Swanson & Dinello, 1970). Even in the studies with the longest follow-up times (of four or five years postdiet), the weight regain trajectories did not typically appear to level off (e.g., Hensrud, Weinsier, Darnell, & Hunter, 1994; Kramer, Jeffery, Forster, & Snell, 1989), suggesting that if participants were followed for even longer, their weight would continue to increase. It is important for policymakers to remember that weight regain does not necessarily end when researchers stop following study participants.

      Some of this may be due to people deciding to “get fat” because they can’t get thin, but regaining can happen even when you continue to follow the diet/exercise program where you lost weight in the first place. It’s very dispiriting.

    • That behavior reflects my experiences too. Otherwise I’m sure I’d be a little overweight but probably not over 400 pounds as I am now. Food and fat were control issues when I was a girl. I love my mother but she’s such a control freak. Her many failed attempts to make me lose weight only made me regain it all and then some, mainly because she’d put me on a diet and then sabotage it. Lose the weight but clean your plate, that sort of thing. As a teenager I finally rebelled and ate whatever I wanted out in the open just for spite and of course that made me gain even more weight which I also flaunted just to annoy her.

      I haven’t felt well the last few days so my mother invited herself over to cook for me, even though I’m now 55 and she’s 80, because she convinced herself that my husband and I will starve. He’s thin but I doubt he’s in any danger. Wait, this is a good thing. Maybe Mom will clean the house for me today?

    • One thing to keep in mind, that is not often widely publicized, is that prolonged calorie restriction does dramatically slow your metabolism, far beyond the amount you would expect just from loss of lean muscle mass. Read about the Minnesota Starvation Study conducted during World War 2 – the average study participant had been followed for eight weeks before the starvation period started and had a 3200 calorie maintenance intake (neither gaining nor losing fat at that level of calories per day). During the study, they were restricted to under 1600 calories per day with the same exercise level, and they lived in the study laboratory and had no opportunity to cheat.

      A 1600 calorie deficit per day would predict that the study participants would lose 84 pounds over the course of the study. They lost closer to 40, on average. Their metabolisms dropped some 30% and they became depressed and obsessed with food.

      That’s what happens to most of us obese when we’re put on a prolonged diet. We’re not moody and tired and hungry all of the time because we’re lazy whiny weak-willed losers. It’s because we are locked in an ongoing battle of wills against our own bodies. People who do successfully keep the fat off for more than five years have to make calorie restriction and exercise effectively a religion – check the National Weight Control Registry (just do a web search on it). For those of thus that can’t or won’t do that, for better or worse we’re stuck.

      I gained less fat since I gave up on dieting than I gained on the rebound from diets. I firmly believe some of the obesity epidemic is from the rebounds.

  3. Also, we can’t forget that the baby boomers are now into their late 50s and 60s. Most people gain about 10% of their body size in their 40s and 50s. This alone may be enough to skew the numbers.

    Linda Bacon argues that the very fat have gotten significantly bigger. If you take those numbers out, I think the average population gain is more like 7-10 lbs. We can pretty much guarantee that very fat folks have gotten that way from dieting with a bit of giving up sprinkled in (weight interventions in childhood don’t help). I also think most bodies gain weight under stress and being fat in this society is a stress-maker! If society would leave us fat folk alone, the majority of us would probably be smaller.

      • Hensrud and Klein (Mayo Clin Proc. 2006;81(10, suppl):S5-S10) found that for most people, gaining weight causes resistance against gaining more weight because the additional tissue consumes energy, increasing total metabolism. For some reason, some people seem to gain fat only and not additional lean tissue, So their added weight doesn’t consume as many additional calories and they can continue their previous level of intake and exercise, but keep gaining weight indefinitely. The additional weight makes physical activity harder and harder, so they do it less, and modern technology makes that process easier. They become more likely to suffer from diabetes, secondary infection, heart problems, etc. Even 50 years ago, we were less able to treat those. Moderate obesity isn’t itself a health risk, but morbid obesity does seem to be. What I’m saying is that I think that people who have this physical trait start gaining earlier because of environmental factors, and live longer than they would have in the past.

        It makes me angry that people see others in that position and judge them, when it’s an accident of genetics that their weight gain stabilized after 10 or 15 pounds.

      • I have a theory… I suspect that as you go out towards the “long tail” of the BMI distribution, metabolic/weight regulation problems become more and more common. An extreme example, and one which we’re able to diagnose, is lack of leptin receptors. This basically makes people hungry all the time. If someone is hungry all the time and there is greater availability of food and of high-calorie food, their weight will be impacted more by that than the weight of someone who is able to feel full normally. I think that there are probably less extreme ways that the weight regulation system can be out of whack, that are currently undiscovered and undiagnosed, and perhaps changes in the availability of food in general or of calorie-dense food specifically, or changes in how much or what type of exercise we get, also increases the weight of people with such conditions more strongly than people without such conditions. People with “normal” weight-regulation systems won’t gain much weight, but people who were already much fatter than average are more affected by small changes in how we eat.

  4. It’s possible to reconcile 1) that weight is mainly determined by genetics and largely out of an individual’s control, and 2) that people overall are much bigger today than they were 100 years ago (or 50 years ago). There’s no conflict there, despite what some people claim. Genes don’t operate in opposition to environment, but along with it. Genetics isn’t a perfect map that exists in stasis from conception to death. Genes switch on and off based on environmental factors, and are programmed in different ways by early experiences, behavior, and chemical exposure. We have barely begun to understand how that works. An oncology journal talked about links between certain chemicals and weight gain plus cancer in lab animals — http://jnci.oxfordjournals.org/content/99/11/835.full.

    I say that we need to stop talking about obesity as a behavioral problem and start looking at it as a data point that could help lead us in the direction of identifying environmental causes of disease. Obesity seems to correlate with (but does not cause) cancer, heart disease, high blood pressure, diabetes, etc. Let’s figure out what genes are involved in common, see how different toxins and chemicals interact with those genes, and focus on treating the actual diseases.

  5. When I worked as a carpet cleaner it was amazing that my weight stayed above 250lbs. My weight range did increase as I got older and took a desk job, but my weight does increase or decrease in any substantial amount unless I go on a “crazy diet”.

    My body has other quirks, my hormone levels vary (thyroid is all over the place), but my insulin level is always perfect. This is just the way I am built. .

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