Read Aloud the Text Content

This audio was created by Woord's Text to Speech service by content creators from all around the world.

Text Content or SSML code:

Lipoprotein Lipase Some of the research investigating genetic influence on obesity focuses on the enzyme lipoprotein lipase (LPL), which promotes fat storage in fat cells and muscle cells.11 People with high LPL activity are especially efficient at storing fat. Obese people generally have much more LPL activity in their fat cells than lean people do (their muscle cell LPL activity is similar, though). This high LPL activity makes fat storage especially efficient. Consequently, even modest excesses in energy intake have a more dramatic impact on obese people than on lean people. Leptin Researchers have identified a gene in humans called the obesity (ob) gene. The obesity gene codes for the protein leptin. Leptin is a hormone primarily produced and secreted by the fat cells in proportion to the amount of fat stored. A gain in body fatness stimulates the production of leptin, which, by way of the hypothalamus, suppresses the appetite, increases energy expenditure, and produces fat loss.12 Fat loss produces the opposite effect—suppression of leptin production, increased appetite, and decreased energy expenditure. As Figure 7-1 shows, mice with a defective obesity gene do not produce leptin and can weigh up to three times as much as normal mice. When injected with leptin, the mice lose weight. (Because leptin is a protein, it would be destroyed during digestion if given orally; consequently, it must be given by injection.) Although it is extremely rare, researchers have identified a genetic deficiency of leptin in human beings as well. An error in the gene that codes for leptin was discovered in two extremely obese children whose blood levels of leptin were barely detectable. Without leptin, the children had little appetite control; they were constantly hungry and ate considerably more than their siblings or peers. Given daily injections of leptin, these children lost a substantial amount of weight, confirming leptin’s role in regulating appetite and body weight. Most obese people do not have leptin deficiency, however. In fact, most obese people produce plenty of leptin, but they fail to respond to it, a condition called leptin resistance.13 Researchers speculate that blood leptin rises in an effort to suppress appetite and inhibit fat storage when fat cells are ample. Obese people with elevated leptin concentrations may be resistant to its satiating effect. The absence of or resistance to leptin in obesity parallels the scenario of insulin in diabetes: some people have an insulin deficiency (type 1), whereas many others have elevated insulin but are resistant to its glucose-storing effect (type 2). Ghrelin Another protein known as ghrelin works in the opposite direction of leptin. Ghrelin is synthesized and secreted primarily by the stomach cells but works in the hypothalamus to promote a positive energy balance by increasing smell sensitivity, stimulating appetite and promoting efficient energy storage.14 The role ghrelin plays in regulating food intake and body weight is the subject of much intense research.15 Pharmaceutical companies are eager to develop products that mimic ghrelin to treat wasting conditions, as well as products that oppose ghrelin’s action to treat obesity.16 Ghrelin powerfully triggers the desire to eat. Blood levels of ghrelin typically rise before and fall after a meal—reflecting the hunger and satiety that precede and follow eating. In general, fasting blood levels correlate inversely with body weight: lean people have high ghrelin levels and obese people have low levels. Ghrelin fights to maintain a stable body weight. On average, ghrelin levels are high whenever the body is in negative energy balance, as occurs during low-kcalorie diets, for example. This response may help explain why weight loss is so difficult to maintain. Ghrelin levels decline again whenever the body is in positive energy balance, as occurs with weight gains. Fat Cell Development When “energy in” exceeds “energy out,” much of the excess energy is stored in the fat cells of adipose tissue. The amount of fat in adipose tissue reflects both the number and the size of the fat cells.* Thus, obesity develops when a person’s fat cells increase in number, in size, or quite often both. The number of fat cells increases most rapidly during the growing years of late childhood and early puberty. After growth ceases, fat cell number may continue to increase whenever energy balance is positive.17 Fat cells can also expand in size. After they reach their maximum size, more cells can develop to store more fat. Obese people have more fat cells than healthy-weight people; their fat cells are also larger. Figure 7-2 illustrates fat cell development. With fat loss, the size of the fat cells shrinks, but their number cannot. For this reason, people with extra fat cells may tend to regain lost weight rapidly. Prevention of obesity is most critical, then, during the growing years of childhood and adolescence when fat cells increase in number most profoundly. As mentioned, excess fat first fills the body’s natural storage site—adipose tissue. If fat is still abundant, the excess is deposited in organs such as the heart and liver and plays a key role in the development of heart failure and fatty liver, respectively.18 As adipose tissue produces adipokines, metabolic changes that indicate disease risk— such as insulin resistance—become apparent and chronic inflammation develops.19 Set-Point Theory One popular theory of why a person may store too much fat is the set-point theory. The set-point theory proposes that body weight, like body temperature, is physiologically regulated.20 Researchers have noted that many people who lose weight quickly regain it all. This suggests that somehow the body chooses a preferred weight and defends that weight by regulating eating behaviors and hormonal actions. After weight losses, the body reduces its metabolic rate. The decrease in metabolic rate after weight loss is greater than would be expected based on body composition alone.21 This adaptation helps to explain why it can be difficult for an overweight person to maintain weight losses. While set point answers some questions regarding the biology of energy balance, it fails to explain the many other influences contributing to the population’s obesity epidemic.22 Environmental Stimuli As discussed earlier, genetic factors play a partial role in determining a person’s susceptibility to obesity, but they do not fully explain obesity. Obesity rates have risen dramatically during recent decades, but the human gene pool has remained unchanged. The environment must therefore play a role as well. Obesity reflects the interaction between genes and the environment.23 An obesogenic environment includes all of the circumstances that people encounter daily that push them toward fatness. Over the past four decades, the demand for physical activity has decreased as the abundance of food has increased. Overeating People may overeat in response to stimuli in their surroundings— primarily, the availability of many delectable foods. Most people in the United States find high-kcalorie foods readily available, relatively inexpensive, heavily advertised, and reasonably tasty—thanks largely to fast food. With around-the-clock access to rich palatable foods, we eat more and more often than in decades past—and energy intakes have risen accordingly.2 Most alarming are the extraordinarily large serving sizes and ready-to-go meals offered in supersize combinations. Eating large portion sizes multiple times a day accounts for much of the weight increase seen over the decades.25 People buy the large sizes and combinations, perceiving them to be a good value, but then they eat more than they need. Research shows that people eat more if they’re served more.26 “Portion distortion” is a term used to describe the perception that large portions are the appropriate amounts to eat at a single sitting.27 And portion sizes of virtually all foods and beverages (and even sizes of plates, glasses, and utensils) have increased markedly in the past several decades, most notably at fast-food restaurants. The increase in portion sizes parallels the growing prevalence of overweight and obesity in the United States, beginning in the 1970s, rising sharply in the 1980s, and continuing today. Research suggests that fast-food consumption contributes significantly to the development of obesity.28 Fast food is often energy-dense food, which increases energy intake, BMI, and body fatness. The combination of large portions and energy-dense foods strikes a double blow. Reducing portion sizes is helpful, but the real kcalorie savings come from lowering the energy density. Satisfying portions of foods with low energy density such as fruits and vegetables can help with weight loss. and offering more fruits, vegetables, legumes, and whole grains. In an effort to help consumers make healthier choices, national legislation now requires restaurants with 20 or more locations to provide menu listings of an item’s kcalories, grams of saturated fat, and milligrams of sodium.29 Once such information displays become standard throughout the country, perhaps restaurants will have greater incentives to offer healthier choices. Learned Behavior Psychological stimuli also trigger inappropriate eating behaviors in some people. Appropriate eating behavior is a response to hunger. Hunger is a drive programmed into people by their heredity. Appetite, in contrast, is learned and can lead people to ignore hunger or to over-respond to it. Hunger is physiological, whereas appetite is psychological, and the two do not always coincide.