Fat. F-a-t. Perhaps no other word in our language is despised as much, nor focused on so intensely. Americans are obsessed about fat–body fat–and how to get rid of it. We have been conditioned to view health and fitness in strictly black (fat) and white (fit) terms: A “fat” body cannot possibly be fit and healthy. This fat-versus-fit dichotomy, made popular in the 1970s with the publication of fitness guru Covert Bailey’s “Fit or Fat?” (5), has become the mantra of many a fitness and health professional. You don’t have to read any more than the title to grasp the fundamental message of this perennial best-selling fitness bible: A person is either fit, or fat–but not both.
The implications of this myopic fitness philosophy are obvious: The road to a fitter and healthier body is a very narrow one indeed. In order for a fat person to become fit and healthy, that person must lose weight and become lean. This of course implies that “lean” is inherently good and “fat” is inherently bad. Not only is this lipophobic paradigm overly simplistic, it does not stand up against a substantial amount of medical and scientific evidence.
Take coronary artery disease (atherosclerosis), for example–the number one killer in the United States. Conventional wisdom tells us that obesity itself is a major cause of clogged arteries–the rationale being that more fat on the body equals more fat in the blood stream equals more fat build-up in the arteries. However, most of the studies that have looked at the relationship between body weight (or body fat) and atherosclerosis–via coronary angiography or by direct examination of artery disease at autopsy–find that fat people are no more likely to have clogged arteries than thin people (4, 11,27). In some instances results entirely opposite to conventional wisdom are observed. For example, when researchers at the University of Tennessee (4) evaluated coronary angiograms of more than 4,500 men and women, they found that the risk of having a clogged artery actually decreased as body weight increased. In other words, it was the fat men and women who had the cleanest arteries. Although this finding is exceptional, the preponderance of angiography studies of this nature do undermine the notion that obesity inevitably results in clogged arteries.
Furthermore, the findings from angiography studies are consistent with countless autopsy studies–dating back to the middle of this century–of the link between body weight (or body fat) and arterial disease. The large-scale International Atherosclerosis Project (27), for example, conducted in the late 1950s and early 1960s, concluded after analyzing 23,000 sets of coronary arteries–obtained at autopsy–that no measure of body weight or body fat was related to the degree of coronary vessel disease. The obesity-heart disease link is just not well supported by the scientific and medical literature.
The same could be said for the notion that thin people are healthiest and can expect to live longer than everybody else. Contrary to the prevailing medical mind-set, the “thin-live-longest” studies frequently cited by the more vocal of the anti-fat crusaders (26) are far outnumbered by studies demonstrating that body weight–aside from the extremes–is not really all that strong a predictor of death rates, or overall health for that matter (10, 11,15, 29, 37, 38, 41). A 1996 publication by researchers at the National Center for Health Statistics and Cornell University illustrates perfectly (41). After analyzing the results from dozens of published reports on the impact of body weight on death rates, encompassing more than 350,000 men and nearly 250,000 women, the researchers found that moderate obesity (no more than about 50 pounds in excess of the so-called ideal body weight) increased the risk of premature death only slightly in men, and not at all in women, during follow-up periods lasting up to 30 years. In fact, the researchers found that thin men–even within the range recommended by the current U.S. government guidelines–had a risk of premature death equal to that of men who were extremely overweight. The researchers warned in their summary comments that “attention to the health risks of underweight is needed, and body weight recommendations for optimum longevity need to be considered in light of these risks.”
Ever since the Metropolitan Life Insurance Company introduced its tables of “ideal” weights in 1942 (21, 22)–the company called them “desirable” weights in 1959 (30), and did away altogether with the terms “ideal” and “desirable” in 1983 (31)–we have been operating under the weight loss industry-reinforced assumption that weighing more than what the height/weight charts say we should weigh is a sure sign of poor health and greatly increases risk of premature death. However, the majority of body weight-mortality investigations have shown that weighing 20 pounds, or 30 pounds, or even 50 pounds in excess of the height-weight chart recommendations is associated with little, if any, increased risk of an early check-out. For example, the current U.S. government guidelines indicate that a 5’4” woman should weigh between 111 pounds and 146 pounds, and a 5’10” man should weigh between 132 pounds and 174 pounds. According to the 1996 study previously mentioned (41), a 5’4” woman and 5’10” man could weigh close to 200 pounds before their risk of premature death goes up appreciably (excess body weight seems to be riskier in men than in women). This suggests that there are a great many “overweight” Americans–especially women–who are agonizing unnecessarily about those numbers on the bathroom scale.
So if being a little fatter than average might not be so bad, and being thin (at least for men) might not be so good, what does this say about body weight and health? If the concept of an ideal weight is little more than statistical fiction, should we just chuck the bathroom scale, kick back on the sofa with a bag of chips in one hand and the remote control in the other, and nestle into total couch-potato-hood? Of course not (although chucking the bathroom scale is probably a good idea). It’s just that body weight, and even body fat for that matter, do not tell us nearly as much about our health as lifestyle factors, such as exercise and the foods we eat. Consider the following scenario.
Randomly select a few hundred men and women (matched for age and smoking habits) and divide them into two groups based on body fat: lean and fat. Next take each person’s blood pressure, draw some blood and determine each person’s serum lipid levels, and have each person perform a glucose tolerance test (to get an idea of each person’s insulin sensitivity). I guarantee that you will find, on average, higher blood pressures, unhealthier blood lipid profiles, and poorer glucose tolerance/insulin sensitivity in the group of fat men and women.
Does this mean that the higher body fat levels caused the health problems? No. It just means that you are more likely to find these kinds of metabolic disorders in fat men and women. But associations do not prove cause-effect. Just because you are more likely to observe high blood pressure, elevated blood lipids and glucose intolerance in fat persons does not prove that body fat is the cause of these health problems, nor does it mean that a fat person has to become lean in order to resolve these health problems. The proof of this assertion is quite straightforward. Get these fat men and women to start an exercise program and eat healthier foods–and see how they do. Numerous research studies have done just that. A few examples are described below.
Results from the Dietary Approaches to Stop Hypertension (DASH) clinical trial, published in the New England Journal of Medicine in 1997 (3), proved that blood pressures can be effectively lowered by simple changes in diet, without losing weight. Among 133 men and women with high blood pressure, just eating more fruits and vegetables, and consuming low-fat dairy foods with reduced saturated fat, was sufficient to reduce systolic blood pressure by an average of 11.4 mmHg, and diastolic blood pressure by an average of 5.5 mmHg, within two weeks after changing their diets. The reductions in blood pressures were comparable to those observed with initiation of pharmacotherapy–but without the side-effects which sometimes accompany antihypertensive medications. Most significantly, the blood pressure reductions were achieved without any weight loss.
To prove that it’s fat in the diet–and not fat on the body–that is the primary cause of blood lipid abnormalities, such as high cholesterol, researchers at the National Public Health Institute in Helsinki, Finland, placed 54 middle-aged men and women on a low-fat (~24% of total calories) diet for six weeks (16). Total cholesterol dropped from 263 mg/dl to 201 mg/dl in the men, and from 239 mg/dl to 188 mg/dl in the women. Body weight did decrease modestly, by about 2 pounds. The subjects were then switched back to their usual diet (~39% of total calories from fat) for six weeks. Total cholesterol levels returned to their original levels–despite absolutely no change in body weight–requiring the researchers to conclude that the fat content of the diet, not weight change, was responsible for the changes in cholesterol levels.
Combined exercise and nutrition programs have provided even more compelling results, as illustrated by the changes observed in the more than 4,500 men and women who have completed a 3-week stay at the Pritikin Longevity Center in Santa Monica, California (6-9). The Pritikin program consists of eating a low-fat, high-complex starch, high-fiber diet (with no emphasis on rapid weight loss) and daily moderate-to-vigorous aerobic exercise. Within three weeks the average cholesterol level dropped from about 234 mg/dl to about 180 mg/dl; low-density lipoprotein cholesterol (the unhealthy kind) decreased from around 151 mg/dl to 116 mg/dl; and triglycerides were reduced by one-third (from 200 mg/dl down to 135 mg/dl) (6).
Pritikin program participants lowered their blood pressures by an average of 5-10%, and more than one-third of the men and women with high blood pressure were able to discontinue antihypertensive medications (7, 8). Those with type II (adult onset) diabetes also experienced tremendous improvements: 39% of those taking insulin and 71% of those on oral hypoglycemic agents were able to discontinue medication entirely (7, 8).
All of these improvements in health profile while on the Pritikin program were observed within three weeks. Although participants do lose weight (typically about 7-11 pounds, or about 5% of their initial body weight), statistical analysis indicates that less than 5% of the improvements in health can be attributed to changes in body weight. Most important to the question at hand is the fact that most men and women who enter the program obese leave the program obese–but with one major difference: They no longer have the health problems thought to be caused by excess body fat.
Just as risk factors for heart disease can be affected by changes in lifestyle independent of changes in body weight, the actual disease itself can be influenced by lifestyle modification–without changes in body weight. The results of the Cholesterol Lowering Atherosclerosis Study illustrate (14). Eighty-two moderately overweight middle-aged men with heart disease were placed in a two-year intervention program designed to reduce consumption of dietary fat. Men who reduced their fat intake to 27.5% of total calories showed no new fatty deposits in their coronary vessels (as determined by examination of coronary angiograms taken before and after the two-year study). On the other hand, men who failed to make significant changes in fat intake (34% of total calories from fat) didn’t do as well–they all showed some evidence of new lesions in their coronary vessels. Because neither group lost any weight during the two-year study, the researchers concluded, in a 1990 article published in the Journal of the American Medical Association, that “the appearance of new [coronary artery] lesions can be influenced without weight change by voluntary selection of acceptable foods.”
All this evidence suggests that as far as one’s health is concerned, lifestyle is far more important than body weight. This goes for longevity prospects as well, as the ongoing–since 1970–Aerobics Center Longitudinal Study at the Cooper Institute for Aerobics Research, in Dallas, Texas, demonstrates (10, 13). Data on more than 32,000 men and women indicate that the fittest men and women have the lowest death rates–regardless of what they weigh. In other words, a heavier-than-average person who is physically fit has a better chance of living a long life than does a thin couch potato. Furthermore, a separate analysis of nearly 10,000 of the men in this study who performed at least two exercise stress tests separated by an average of about 5 years (thereby allowing the researchers to evaluate the impact of changes in physical fitness on subsequent death rates), revealed that improving physical fitness level reduced death rates during the 5+ years of follow-up. Men who were initially classified as unfit (defined as being in the bottom 20% of fitness levels for a given age), but who–via increasing physical activity–improved their fitness level by the second fitness examination, reduced their mortality rate during the subsequent 5+ years of follow-up by 44%. Most significant in terms of the weight debate was the fact that the improved longevity prospects were not at all dependent upon weight loss. Results from the ongoing Harvard Alumni Study (33) provide similar results: Sedentary Harvard alums who increased their level of physical activity experienced a 23% reduction in all-cause mortality rate. Because alums who lost weight were no better off healthwise than those who did not lose weight, the reduction in all-cause death rate observed in the more physically active men was in no way attributable to slimming down.
Despite all this evidence suggesting that lifestyle is far more important than body weight in terms of health, and that it might be more prudent to focus on getting people fit and healthy rather than trying to make them thin, the weight loss industry still barrels along like a runaway freight train. Aside from the cultural obsession with slimness, health professionals have done much to sanctify this quest for a lean body–primarily by fueling a medical rationale for fat phobia: Obesity is a major killer. The most blatant–but unjustified–example of this scare tactic is the widely publicized claim that obesity kills 300,000 Americans every year. Former U.S. surgeon general C. Everett Koop asserted as much when he launched his Shape Up America! campaign in 1994. Since then, this figure has taken on a life of its own, appearing in scientific and medical journals (1) and mentioned repeatedly in the media–each time reminding us of the “fact” that obesity is the second leading cause of preventable death in America.
The problem, however, is that there is absolutely no way to prove this assertion. In fact, the most frequently cited source of this statistic, a 1993 article in the Journal of the American Medical Association (28), shows just how misinterpreted this statistic actually is. The article, titled “Actual Causes of Death in the Untied States,” attributes the 300,000 deaths per year to “diet/activity patterns”–not to obesity. Obesity is a physical trait; diet and physical activity are behaviors. To equate them not only is unjustified, it is absurd. While poor diet and lack of physical activity may lead to obesity, the truth of the matter is that the studies used to generate the 300,000 figure looked at the health impact of poor diet and sedentary lifestyle across the entire weight spectrum, not just among fat persons. [There are a great many less-than-healthy couch potatoes with poor dietary and exercise habits who–via luck of the genes–will never be fat.]
I am not advocating that we should be complacent about obesity. It’s just that continued focus on weight loss seems counterproductive, and may be quite hazardous to the health of those who continually battle their weight. Each year roughly 70 million Americans–nearly one-fourth of the entire U.S. population–attempt to lose weight, shelling out between $30 billion and $50 billion in the process (32). But despite our perennial efforts to shed pounds, our waistlines are getting bigger, not smaller. It seems what ever we lose, we gain back–and then some. Not only can this be damaging to our self-esteem and mental health, chronic fluctuations in body weight may also do physical harm (12, 17, 25). In fact, most of the epidemiological studies on weight loss alone show that weight loss increases risk for premature death, primarily from heart disease (2, 12, 20, 25, 34). This obviously represents a paradox, because weight loss is thought to improve cardiovascular disease risk factors. But this is not always the case.
One of the most popular weight reducing strategies of the past 35 years, the low-carbohydrate diet, actually raises cholesterol levels (especially low-density lipoprotein cholesterol) and reduces high-density lipoprotein cholesterol (the heart-healthy kind) despite weight loss (24, 36). This suggests that going on a low-carbohydrate diet may actually increase risk of atherosclerosis.
Another possible explanation for the paradoxical finding of weight loss being associated with increased risk of dying from heart disease is the recent evidence which shows that dieting depletes body reserves of heart-healthy omega-3 fatty acids, thus raising the possibility that weight loss via calorie restriction may actually make the body more vulnerable to atherosclerosis (39). The researchers who reported these findings warned that “a subtle but chronic risk state could be established if recurrent dieting depletes omega-3 reserves and intake during maintenance does not allow effective repletion.”
We need a new approach to health and fitness–one that places less emphasis on body weight (or body fat) and more emphasis on healthy metabolism–becoming “metabolically” fit. To achieve “metabolic fitness” does not require having a lean body, nor does it depend upon having the cardiovascular system of an endurance athlete.
In scientific/medical terms, metabolic fitness can be defined in terms of how the human body responds to the hormone insulin (9, 35). “Insulin sensitive” bodies tend to have excellent glucose tolerance, normal blood pressures, and heart-healthy blood lipid profiles. Therefore, insulin sensitive people tend to be at lower risk for type II diabetes and heart disease than people who are “insulin resistant”–a metabolic condition in which the body’s cells (mainly those in skeletal muscle, liver and adipose tissue) don’t respond normally to this hormone, and which ultimately may result in disordered lipid metabolism and elevated blood pressures. Insulin resistance is associated with high risk for type II diabetes and heart disease (9, 18, 35).
Although genes play a role, the major causes of insulin resistance are lack of exercise and consuming a diet high in fat (especially saturated fat) and refined sugar, and low in fiber–a description that fits many Americans (9). Because these behaviors also promote obesity, the “insulin resistance syndrome” (also known as the “metabolic syndrome”) is observed more often in fat people than it is in thin people. But as I have pointed out already, a fat person with the metabolic syndrome does not have to become lean in order to become insulin sensitive (i.e., obesity is not the underlying cause of the syndrome). Also, one does not have to be obese to be insulin resistant. An estimated one-fourth of non-obese men and women in the United States are insulin resistant and don’t realize it (35).
Substantial improvements in insulin sensitivity can be changed in a matter of days or weeks (7, 8, 19), which explains why dramatic improvements in glucose tolerance, blood pressures, and blood lipids can be observed so quickly after starting an exercise program or eating healthier foods. If we can accept the fact that metabolically fit and healthy bodies can come in all shapes and sizes (40), then the public health message becomes quite simple: be more physically active and consume a healthier diet.
As for exercise, moderate-to-vigorous activity (heart rate in the range of ~60-75 percent of maximum) for ~20-40 minutes per day on most days of the week is suitable for improving metabolic fitness (9, 23). Intensity and duration of exercise can be modified to suit individual needs. If time is not a constraint, duration can be emphasized while exercising at the lower end of the intensity range. Just as effective, however, is high-intensity exercise of only 20-30 minutes duration. As for nutrition, the best foods to boost metabolic fitness are those you find primarily near the base of the USDA food guide pyramid: Whole grains, fruits and vegetables, and legumes (beans). These foods have plenty of fiber and have been shown to improve health regardless of weight and independent of weight loss (3, 9, 19).
It may seem intuitive that exercising more and eating better will naturally result in weight loss. This generally is true, but with a major caveat. Not everyone will lose weight, and it is virtually impossible to tell how much any one person will lose. Most exercise programs and typical diets result in a weight loss of no more than 5-10 pounds (32); the average “overweight” U.S. adult wants to lose 20-30 pounds! This discrepancy between what Americans want and what exercise and healthy eating are able to deliver highlights the fundamental problem with using weight loss or reductions in body fat to judge the success of an exercise program or nutrition plan. Exercise and healthy eating should not be viewed merely as means to an end (weight loss), but rather as having their own intrinsic value. If someone quits an exercise program out of failure to reach a particular weight loss (or reduced body fat) goal, then all the benefits of the exercise are lost as well. And far too many people who start exercise programs don’t stay with them. Yo-yo fitness is becoming as common as yo-yo dieting.
In America today millions of men and women (and boys and girls) stigmatized as “too fat” are engaged in a perpetual war with their bodies. Isn’t it about time we called a truce? Let’s face biological reality. Some people are naturally meant to be thin, some naturally meant to be fat. Exercise and diet can modify our genetic destiny only so much. The human body is not an infinitely malleable mass of calories that can be burned down to any shape and size desired. But that doesn’t mean we can’t all be as metabolically fit as our lifestyle will allow. In terms of health and longevity, the scientific evidence is abundantly clear: It is far more important to be fit than it is to be thin. Contrary to prevailing dogma, the road to a fitter and healthier body is not so narrow after all.
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1. American Dietetic Association. Position of The American Dietetic Association: Weight management. J Am Diet Assoc 1997; 97: 71-74.2. Andres, R, DC Muller and JD Sorkin. Long-term effects of change in body weight on all-cause mortality: A review. Ann Int Med 119: 737-743, 1993.
12. Blair, SN, J Shaten, K Brownell, G Collins, and L Lissner. Body weight change, all-cause mortality, and cause-specific mortality in the Multiple Risk Factor Intervention Trial. Ann Int Med 119: 749-757, 1993.
13. Blair, SN, HW Kohl, III, CE Barlow, RS Paffenbarger, LW Gibbons, and CA Macera. Changes in physical fitness and all-cause mortality: A prospective study of healthy and unhealthy men. J Am Med Assoc 273: 1093-1098, 1995.
15.Carmelli, D, J Halpern, GE Swan, A Dame, M McElroy, AB Gelb, and RH Rosenman. 27-year mortality in the Western Collaborative Group Study: Construction of risk groups by recursive partitioning. J Clin Epidemiol 44: 1341-1351, 1991.
18. Fontebonne, A, MA Charles, N Thibult, JL Richard, JR Claude, JM Warnet, GE Rosselin, and E Eschwege. Hyperinsulinemia as a predictor of coronary heart disease mortality in a healthy population: The Paris Prospective Study, 15-year follow-up. Diabetologia 34: 356-361, 1991.
19. Fukagawa, NK, JW Anderson, G Hageman, VR Young, and KL Minaker. High-carbohydrate, high-fiber diets increase peripheral insulin sensitivity in healthy young and old adults. Am J Clin Nutr 52: 524-528, 1990
23. Lamarche B, Despres J-P, Pouliot M-C, et al. Is body fat loss a determinant factor in the improvement of carbohydrate and lipid metabolism following aerobic exercise training in obese women? Metabolism 1992; 41: 1249-1256.
33. Paffenbarger, RS, RT Hyde, AL Wing, I-M Lee, DL Jung, and JB Kampert. The association of changes in physical-activity level and other lifestyle characteristics with mortality among men. N Engl J Med 328: 538-545, 1993.
37. Rissanen, A, M Heliovaara, P Knekt, A Aromaa, and A Reunanen. Overweight and mortality in Finnish men. In: Obesity in Europe 88 (P Bjorntorp and S Rossner, editors). Paris: John Libbey. 1989, pp. 61-68.
39. Tang, AB, KY Nishimura, and SD Phinney. Preferential reduction in adipose alpha-linolenic acid (18:3n-3) during very low caloric dieting despite supplementation with 18:3n-3. Lipids 28: 987-993, 1993.
41. Troiano RP, Frongillo, Jr EA, Sobal J, Levitsky DA. The relationship between body weight and mortality: A quantitative analysis of combined information from existing studies. Int J Obesity, 20: 63-75, 1996.