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Fat Chance
The third problem with “a calorie is a calorie” is illustrated by the U.S. secretary of health and human services Tommy Thompson’s admonishment in 2004 that we’re “eating too damn much,” would suggest that we’re eating more of everything. But we’re not eating more of everything. We’re eating more of some things and less of others. And it is in those “some things” that we will find our answer to the obesity pandemic. The U.S. Department of Agriculture keeps track of nutrient disappearance. These data show that total consumption of protein and fat remained relatively constant as the obesity pandemic accelerated. Yet, due to the “low-fat” directives in the 1980s of the AMA, AHA, and USDA, the intake of fat declined as a percentage of total calories (from 40 percent to 30 percent). Protein intake remained relatively constant at 15 percent. But if total calories increased, yet the total consumption of fat was unchanged, that means something had to go up. Examination of the carbohydrate data provides the answer. As a percentage of total caloric intake, the intake of carbohydrates increased from 40 percent to 55 percent.[11] While it’s true we are eating more of both classes of carbohydrate (starch and sugar), our total starch intake has risen from just 49 to 51 percent of calories. Yet our fructose intake has increased from 8 percent to 12 percent to, in some cases (especially among children), 15 percent of total calories. So it stands to reason that what we’re eating more of is sugar, specifically fructose. Our consumption of fructose has doubled in the past thirty years and has increased sixfold in the last century. The answer to our global dilemma lies in understanding the causes and effects of this change in our diet.
There’s one lesson to conclude from these three contradictions to the current dogma. A calorie is not a calorie. Rather, perhaps the dogma should be restated thus: a calorie burned is a calorie burned, but a calorie eaten is not a calorie eaten. And therein lies the key to understanding the obesity pandemic. The quality of what we eat determines the quantity. It also determines our desire to burn it. And personal responsibility? Just another urban myth to be busted by real science.
Chapter 3
Personal Responsibility versus the Obese Six-Month-Old
Sienna is a one-year-old girl who weighs 44 pounds. She was 10 pounds at birth and was delivered by caesarean section due to her size. Her mother is not obese, but her father is overweight. Her mother tested negative for diabetes during the pregnancy. Since birth, Sienna has had an incredible appetite. Her mother could not breastfeed her because she could not keep up with the baby’s demand for food. An average infant of Sienna’s age will eat one quart of formula per day. Sienna consumed two quarts per day. When Sienna was six months old, we told her mother to start feeding her solid foods. Sienna eats constantly and will scream if her mother does not feed her. She already has high cholesterol and high blood pressure.
Is Sienna obese because of her behavior? Was this learned behavior? When would she have learned this behavior, and from whom? Has she, at age one, learned to control her mother to get what she wants? Should she accept personal responsibility for her actions?
Based on “a calorie is a calorie,” behaviors come first. Personal responsibility implies a choice: that there is a conscious decision leading to a behavior. This behavior is formed because of learned benefits or detriments (e.g., a child placing her hand on a stove and learning it is hot). But does this make sense with regard to obesity? In everyone? In anyone? There are six reasons to doubt “personal responsibility” as the cause of obesity.
1. Obesity Is Not a Choice
The concept of personal responsibility for obesity doesn’t always make sense. In our society today, one has to ask: Are there people who see obesity as a personal advantage? Something to be desired or emulated? Across the board, modern Western societies today value the thin and shun the obese. Obesity frequently comes with many medical complications, and those afflicted are more likely to develop heart problems and type 2 diabetes (see chapter 9). Obese people spend twice as much on health care.[12] Studies show that the obese have more difficulty in dating, marriage, and fertility. The obese tend to be poorer and, even in high-paying jobs, earn less than their peers.[13]
Now ask the same question about children. Did Sienna see obesity as a personal advantage? Did she become obese on purpose? Obese children have a quality of life similar to that of children on cancer chemotherapy.[14] They are ostracized by their peers and are the targets of bullies. Many obese children suffer from low self-esteem, shame, self-hatred, and loneliness. One study showed children pictures of potential playmates. Each looked different and some had physical handicaps, such as being deformed or in a wheelchair. The researchers asked the children with whom they would rather play. The obese child came in dead last. Clearly, obesity is not something to which people, especially children, aspire.
However, this view of obesity does not necessarily square with the beliefs of obese people themselves. They see themselves as perpetrators, not victims. They often state that they know their behavior is out of control and that this behavior is their own fault. They frequently experience yo-yo dieting. They lose weight for a period of time, and when they gain it back they blame themselves, seeing the gain as a character failing. They often recount binge eating, which suggests that a degree of dietary control is lost. These experiences of losing control make them think they had the control in the first place. Did they?
2. Diet and Exercise Don’t Work
If obesity were only about increased energy intake and decreased energy expenditure, then reducing intake (diet) and increasing expenditure (exercise) would be effective. If obesity were caused by learned behaviors, then changing those behaviors would be effective in reversing the process and promoting weight loss. Specific and notable successes have led to behavior/lifestyle modification as the cornerstone of therapy for obesity.
There are the anecdotal cases of weight loss by celebrities, such as Kirstie Alley or Oprah Winfrey, who publicly endorse their diets as if they were the latest fashionable handbags. They share their stories on TV and convince their viewers that this lifestyle change is possible for them, too, and that, as with adding the newest fall color to their wardrobe, losing weight will make them attractive and happy. There are reality television shows, such as The Biggest Loser, that document the weight loss (along with many a meltdown) of “normal people” through controlled diet and exercise. Publicity, cash prizes, and constant attention are often enough to change one’s diet and exercise response for a short time. In any magazine and many infomercials, peddlers of new weight-loss remedies provide before and after pictures of people who have lost 100 pounds.
Whether this constitutes a true lasting change in behavior is doubtful. After all, Kirstie Alley and Oprah, celebrities who live in the public eye, have gained their weight back several times (until their newest miracle diet began, countless new diet books were sold, new gurus were anointed, millions of dollars were made, and the cycle repeated itself). There have been numerous reports of contestants on The Biggest Loser regaining much of their weight after the show ended. Most notably, Eric Chopin, the Season 3 winner, appeared on Oprah to tell his sorry tale of gaining at least half the weight back after his victory. He wrote in one blog post, “I’m still not back on track totally. I don’t know what it is.” Significant weight regain has been seen in up to one third of patients who have had surgery for weight loss (see chapter 19), because the reason for the obesity is still there. Unless it’s dealt with directly, regaining will be the norm, not the exception.
Strict control of one’s environment through limiting caloric intake and increasing physical activity can result in weight loss. This is true as long as the environment remains regulated. A perfect example is the army recruit who consistently loses weight due to monitored diet and vigorous exercise. This also accounts for the number of “fat schools” and “fat camps” that have sprung up nationwide. Parents send their overweight child away for the summer and are thrilled when he returns thinner, if harboring parental resentment. There are numerous reports of Hollywood stars who bulk up for a role (remember Robert DeNiro in Raging Bull?) and then lose the excess weight after shooting. (Of course, they have the benefit of round-the-clock personal trainers and nutritionists to monitor their food intake.) While such results are dramatic, they usually cannot be sustained. Environmental control is different from behavioral control (see chapters 17 and 18).
The real problem is not in losing the weight but in keeping it off for any meaningful length of time. Numerous sources show that almost every lifestyle intervention works for the first three to six months. But then the weight comes rolling back.[15] The number of people who can maintain any meaningful degree of weight loss is extremely small (see figure 3.1). However, because behavior/lifestyle modification is the accepted treatment, the general explanation of weight regain is that it is the individual’s fault. Because he is “choosing” not to live a healthy lifestyle, the doctors and the insurance industry do not feel it their responsibility to intervene.
The same is true for children. Due to some notable and individual successes, behavior/lifestyle modification is the cornerstone of therapy. However, this is not a winning strategy for most obese children. Research shows that dietary interventions don’t often work. Exercise interventions are even less successful. And unfortunately for children like Sienna, at one year of age they are unable to run on a treadmill. Also, the effects of altering lifestyle for obesity prevention are underwhelming and show minimal effect on behavior and essentially no effect on BMI.
Fig. 3.1. The “Biggest Loser”—Not You. Percentage of obese individuals who were able to maintain their weight loss over nine years.
3. The Obesity Epidemic Is Now a Pandemic
If obesity were just an American phenomenon it would be an epidemic, an outbreak of illness specific to a certain area. One might then blame our American culture for promoting it. Due to our slippage in education and technological superiority, we’re labeled as “fat and lazy” or “gluttons and sloths.” Yet obesity is now a pandemic, a worldwide problem.
The United Kingdom, Australia, and Canada are right behind us. Also, in the past ten years, obese children have increased in France from 5 to 10 percent, in Japan from 6 to 12 percent, and in South Korea from 7 to 18 percent.[16] In fact, obesity and chronic metabolic diseases are occurring in underdeveloped countries that have never had such problems before.[17] Previously, poorer countries such as Malaysia had problems with malnutrition. Now Malaysia has the highest prevalence of type 2 diabetes on the planet. China has an epidemic of childhood obesity, at 8 percent in urban areas. Brazil’s rate of increase in obesity is predicted to reach that of the United States by 2020. Even India, which continues to have an enormous problem with malnutrition, is not immune – since 2004, the number of overweight children increased from 17 percent to 27 percent. Sienna is not a rarity; her obese peers are being born everywhere. The areas experiencing the greatest rise in obesity and type 2 diabetes include Asia (especially the Pacific Rim) and Africa, which are not wealthy areas.[18] No corner of the globe is spared.
This is not an American problem, an Australian problem, a British problem, or a Japanese problem. This is a global problem. Could each of these countries be experiencing the same cultural shifts toward gluttony and sloth that we are? Childhood obesity knows no intellect, class, or continent.
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Примечания
1
J. Kim et al., “Trends in Overweight from 1980 Through 2001 Among Preschool-Aged Children Enrolled in a Health Maintenance Organization,” Obesity 14 (2006): 1164–71.
2
S. J. Olshansky et al., “A Potential Decline in Life Expectancy in the United States in the 21st Century,” New Engl. J. Med. 352 (2005): 1138–45.
3
World Health Organization, Fact Sheet: Obesity and Overweight (2011), www.who.int/mediacentre/factsheets/fs311/en/.
4
UN General Assembly, “Prevention and Control of Non-Communicable Diseases,” New York, 2010.
5
J. M. Chan et al., “Obesity, Fat Distribution, and Weight Gain as Risk Factors for Clinical Diabetes in Men,” Diabetes Care 17 (1994): 961–69.
6
S. L. Gortmaker et al., “Changing the Future of Obesity: Science, Policy, and Action,” Lancet 378 (2011): 838–47.
7
K. C. Sung et al., “Interrelationship Between Fatty Liver and Insulin Resistance in the Development of Type 2 Diabetes,” J. Clin. Endocrinol. Metab. 96 (2011): 1093–97.
8
S. L. Gortmaker et al., “Changing the Future of Obesity: Science, Policy, and Action,” Lancet 378 (2011) 838–47.
9
R. Padwal et al., “Long-Term Pharmacotherapy for Obesity and Overweight,” Cochrane Database Syst. Rev., Art. No.: CD004094. DOI: 10.1002/14651858 (2004). PMID: 15266516.
10
C. B. Newgard et al., “A Branched-Chain Amino Acid-Related Metabolic Signature That Differentiates Obese and Lean Humans and Contributes to Insulin Resistance,” Cell Metab. 9 (2009): 311–26.
11
P. Chanmugam et al., “Did Fat Intake in the United States Really Decline Between 1989–1991 and 1994–1996?” J. Am. Diet. Assoc. 103 (2003): 867–72.
12
D. Thompson et al., “Lifetime Health and Economic Consequences of Obesity,” Arch. Int. Med. 159 (1999): 2177–83.
13
J. Bhattacharya et al., “Who Pays for Obesity?” J. Econ. Perspect. 25 (2011): 139–58.
14
J. B. Schwimmer et al., “Health-Related Quality of Life of Severely Obese Children and Adolescents,” JAMA 289 (2003): 1813–19.
15
T. A. Wadden et al., “Treatment of Obesity by Very Low Calorie Diet, Behavior Therapy, and Their Combination: A Five-Year Perspective,” Int. J. Obes. 13 (1989): 39–46; M. W. Schwartz et al., “Regulation of Body Adiposity and the Problem of Obesity,” Arterioscler. Thromb. Vasc. Biol. 17 (1997): 233–38.
16
S. Yoo et al., “Obesity in Korean Pre-Adolescent School Children: Comparison of Various Anthropometric Measurements Based on Bioelectrical Impedance Analysis,” Int. J. Obes. 30 (2006): 1086–90.
17
N. Gupta et al., “Childhood Obesity in Developing Countries: Epidemiology, Determinants, and Prevention,” Endocr. Rev. 33 (2012): 48–70.
18
A. Ramachandran et al., “Diabetes in Asia,” Lancet 375 (2010): 408–18.