For esophageal cancer, risk was indicated for those who are morbidly obese, but not for those who are moderately obese. Based on the evidence the report presents, do you share their conclusions? Or is this just more fearmongering from the “experts”?
Investigation by the Centers for Disease Control and Prevention also contradicts the obesity-cancer link.
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In the words of the CDC epidemiologists, there is “little or no association of excess all-cancer mortality with any of the BMI categories.”
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While there are some associations between specific types of cancer and obesity as well as mechanisms through which fat tissue affects cancer, it is clear that obesity has been greatly misrepresented and exaggerated as a cancer risk.
“Obesity costs us millions of dollars in healthcare expenditures.”
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So say some pundits in another well-publicized report. How did they arrive at this figure? They calculated the expenses associated with treating a host of conditions, including type 2 diabetes, coronary heart disease, hypertension, gallbladder disease, and cancer, assuming that susceptibility to all of those is caused by fat. Nowhere did they account for mitigating factors that might cause these conditions, such as genetics, activity habits, or diet—nor did they account for the fact that thin people are subject to these conditions as well.
Get Fat: It’s Good for You?
Less well publicized is the idea that body fat may actually protect us from many diseases. There is a long list of conditions less common in heavy people than their thinner counterparts, among them lung cancer, chronic bronchitis, tuberculosis, mitral valve prolapse, anemia, type 1 diabetes, premature menopause, and osteoporosis.
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Good Fat/Bad Fat?
There are two different types of body fat, which in part explains the ambiguity of the effects of body fat: One is more apt to give us benefits, and one more likely presents us with health risks, though the picture is not as clear-cut or as well understood as we’d like to believe. The two types are differentiated by their location. So-called “bad body fat” is known to scientists as visceral fat and is located around abdominal organs, in particular the liver. It is more metabolically active in terms of both storing and releasing fat, which can be dangerous in two ways: First, because the fat it releases can end up clogging your arteries, and second, much of the released fat can go directly to the liver, impairing its ability to carry out other functions. Women are not as susceptible to high levels of “bad body fat” as men are.
So-called “good body fat” is known to scientists as subcutaneous fat. The cells have high levels of an enzyme (lipoprotein lipase) which cause them to store fat easily and hold on to it more tightly. This means that the fat stays in the fat cells where we believe it has a positive effect on health.
Our body shape tells us a lot about how our fat is distributed. If you have an “apple-shaped” body distribution—fat around the belly rather than below the waist—you are more likely to have a high level of visceral body fat, the stuff more highly associated with risk. If instead you have a “pear-shaped” body distribution—fat on your thighs and hips (much more typical for women), you probably get more benefits from your fat.
Obesity is also associated with improved survival in several diseases. For example, obese persons with type 2 diabetes,
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hypertension,
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cardiovascular disease,
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and chronic kidney disease
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all have greater longevity than thinner people with these conditions.
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And obese people who have had heart attacks, coronary bypass,
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angioplasty,
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or hemodialysis
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live longer than thinner people with these histories.
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Also, obese senior citizens live longer than thinner senior citizens!
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3. The “Obesity Epidemic” Myth
No doubt Americans have gained weight over the last few decades. But if we are so concerned about an epidemic, why aren’t we celebrating its apparent end? The incidence of obesity is no longer increasing.
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According to government statistics, obesity rates for women have leveled off and stayed steady since 1999,
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sufficient time to consider it a plateau. They also have leveled off for men, having been stable since 2003.
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Same is true for kids: The prevalence of obesity for children and teens is no different today than it was in 1999.
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It may just be that we’ve reached our metabolic limit; our bodies have adjusted to our current lifestyle habits and environmental conditions and are now kicking in to maintain us at a new setpoint, albeit a higher one than our ancestors, who experienced different conditions.
In addition to having gained weight over the last few decades, we’re also growing taller. American men are over an inch taller than they were in the 1960s
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and nearly three inches taller than they were 100 years ago! Why isn’t that subject to the same media attention and concern? It may be that both the height and weight increase are the result of
improved
nutritional status and health.
What’s even more important to notice than our weight gain is that there is no evidence this weight gain is a crisis. As mentioned earlier, life expectancy has increased dramatically during the time period in which weight rose.
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The very diseases that are linked to obesity, like heart disease, are the ones that are declining.
We are simply not seeing the catastrophic consequences predicted to result from the “obesity epidemic.”
4. The “Lose Weight, Get Healthy” Myth
The idea that health will necessarily improve with weight loss is dubious at best.
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No one has ever proved that losing weight prolongs life.
There is great controversy as to whether weight loss is necessary or even desirable for improved health. While it is clear that research indicates a short-term improvement in health risk factors with weight loss, no randomized clinical studies have observed the long-term effects of weight loss, and the observational research (epidemiological studies) has typically found weight loss to be associated with dying younger.
For example, well-respected physiologist Glenn Gaesser examined the research and found fifteen studies published between 1983 and 1993 that show that weight loss actually
increases
the risk of dying early.
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Only two studies published during that same period showed weight loss reducing the risk of dying early, and one of these only showed an eleven-hour increase in longevity for each pound of weight loss!
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Even when subjects with unintentional weight loss (such as might occur with cancer or AIDS) are excluded, the research is ambiguous at best.
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When the National Institutes of Health convened a conference to review the evidence about dieting, they concluded: “Most studies, and the strongest science, shows weight loss . . . is actually strongly associated with increased risks of death—by as much as several hundred percent.”
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Note, of course, that just because the research indicates an association between weight loss and decreased longevity doesn’t mean that weight loss
causes
early death. I suspect the explanation for this association lies in the unhealthy methods people use to achieve weight loss, as well as the difficulty in separating weight loss from weight gain.
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Many people who do achieve weight loss go through cycles of weight loss and gain before finally stabilizing at a lower weight, damaging their health in the process.
Also, when people lose weight through dieting, particularly the more extreme diets, they shed lean tissue (from muscle and organs) in addition to fat. There may be a cost associated with losing lean tissue that offsets any possible benefits of shedding the fat. (Weight loss that results from increased activity may present a different picture, as exercise helps to preserve or increase lean mass, at least when sufficient calories are consumed.)
Nonetheless, extensive evidence documents that attempts at dieting typically result in weight cycling, not maintained weight loss. Weight fluctuation is strongly associated with increased risk for diabetes, hypertension, and cardiovascular diseases, independent of body weight.
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In other words, the recommendation to diet may be causing the very diseases it is purported to prevent!
In contrast, whether the concern is type 2 diabetes, atherosclerosis, hypertension, cancer, or a host of other conditions, the evidence is clear: An abundance of studies indicate improvement through nutrition or activity habits, independent of weight loss.
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We’re on much firmer ground when we promote lifestyle change. Lifestyle improvements may also result in weight loss, but this is not a given.
5. The “You Control Your Weight” Myth
Many genes interact to determine whether the food you eat gets stored as fat or burned for energy—whether that dash to catch the bus will get its fuel by lightening your fat stores or by emptying your carbohydrate stores and driving you to eat more. It’s a biological fact that identical eating and activity habits can result in thinness in one person and chubbiness in another.
Studies of adoptees provide good data on the degree to which your weight is inherited. After all, if there is a strong genetic component, you would expect a child’s weight to be similar to his or her biological parents regardless of how he or she was raised. The research supports this. For example, one study, published in the
New England Journal of Medicine
, looked at 540 adults who had been adopted when young: 55 percent in their first month and almost 90 percent within their first year.
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The study found that adoptees were similar in size to their biological parents, and their size had
no
relation to their adoptive parents.
A similar study, published in
JAMA
, compared twins who were reared apart to twins reared together, and had similar findings.
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The identical twins in this study had nearly identical BMIs regardless of whether they were brought up together or in different environments. There was a little more variation among the fraternal twins, who share some but not all genes. The researchers concluded that 70 percent of weight variation can be accounted for by genetics—making the heritability of obesity
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greater than that of almost any other condition, including breast cancer, schizophrenia, and heart disease!
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Thin people may think they stay thin because they are morally superior. The data suggests it is more likely that they’re genetically lucky (in this time when thinness is valued). The most direct route to thinness is to choose your parents well.
Your Genes Determine the Result of the Habits You “Choose”
Think again of two people with similar eating and activity habits, one of whom may be lean and the other heavy, one of whom may lose weight from consuming the same foods that result in creeping weight gain in another. In the past, experts believed this discrepancy was explained by a lack of honesty in reporting, rarely believing the fat person who claimed to eat like a bird. But today, that blame-laying is on shaky ground. Now experts recognize that the way in which people respond to diet and exercise is genetically determined.
Morgan Spurlock’s
Super Size Me
experiment is currently being replicated, this time under scientific conditions.
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Research volunteers are eating double their normal calorie intake in the form of “junk food” and avoiding physical activity. Preliminary results confirm that a certain type and number of excess calories don’t result in the same across-the-board weight increase. There is huge variability in their weight gain (and in health risk factors).
This is not surprising when one is acquainted with the research conducted on twins on the effects of diet and exercise. An example: