Ap stats chapter 15 homework answers

Human Growth And Development Discussions

15 Learning Outcomes After reading this chapter, you will be able to:

15.1 Explain why weight management is important to health and well-being.

15.2 Define the terms appetite, hunger, and satiety, and describe the physiological factors involved in regulating food intake.

15.3 Describe the role of hyperplasia and hypertrophy of adipocytes in the development of obesity.

15.4 Discuss the role of genetics and the environment in the development of underweight, overweight, and obesity.

15.5 Describe the role of diet and exercise in achieving a reasonable rate of weight loss.

15.6 Design a food and exercise plan to maintain a healthy weight.

15.7 Describe the role of diet and exercise in achieving a healthy weight gain.

15.8 Describe the role of weight-loss drugs and surgery for reducing obesity.

True or False? 1. Healthy weight loss occurs only with at least 2 hours of daily exercise. T/F 2. The body stops synthesizing fat cells after adolescence. T/F 3. Grazing throughout the day helps curb appetite and control body weight. T/F 4. Losing even 10 pounds can improve health. T/F 5. Genetics and the environment both affect body weight. T/F 6. Eating more vegetables and fruits can help an individual lose weight. T/F 7. Obesity is the result of consuming more energy than is expended. T/F 8. The nutrient that has the most effect on satiety is fat. T/F 9. You don’t need to diet and exercise if you are taking a weight-loss drug. T/F

10. Bariatric surgery results in weight loss without restricting food intake. T/F See page 572–573 for the answers.

Weight Management

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Why Is Weight Management Important? LO 15.1 Explain why weight management is important to health and well-being.

The term weight management means maintaining body weight within a healthy range. Achieving a healthy body weight is essential for physical and emotional well-being. It helps you feel good about yourself, provides the energy you need to enjoy life, and lowers the risk of chronic disease. In addition, weight management reduces costs to society. The costs for treating obese individuals are several thousand dollars higher than for their lean counterparts. It has been estimated that each additional pound of extra body weight above healthy body weight could add up to $13 a year per pound in added medical costs for men and up to $45 for women.6

Being Overweight or Obese Increases Health Risks As you learned in Chapter 14, a healthy weight is a body weight that doesn’t increase the risk of developing any weight-related health problems or diseases.7 In contrast, over- weight—and especially obesity—is associated with numerous health problems. In fact, in 2013, the American Medical Association declared obesity a disease in itself—specifically a multi-metabolic and hormonal disease state.8 This new classification of obesity as a disease helps focus attention and resources on the problem, opening the door for the 90 million obese Americans to receive treatment for their obesity. It may also be changing the way physi- cians approach obesity management, increasing the use of drug therapies and surgery. Alternatively, the obesity-as-a-disease message suggests that body weight is uncontrollable, and—if it discourages patients—might hinder weight management efforts that focus on healthy eating and exercise.

weight management Maintaining a healthy body weight; defined as having a BMI of 18.5–24.9.

Weight management is such a hot topic in the United States that the mainstream media frequently covers it.

In the last two decades, rates of overweight and obesity have exploded in the United States. In the early 1960s, fewer than 32 percent of Americans were overweight.1 Today, that number has risen to an alarming 67 percent of Americans classified as overweight, and more than 33 percent of adults

(about 72 million people) and 17 percent of children are obese.2 Not surprisingly, as more and more

individuals cross the threshold from a healthy body weight to being overweight, the topic has garnered

much interest in popular culture. In fact, people often turn to social media sites such as Facebook,

Pinterest, and Twitter to talk about weight management and locate helpful tools to help manage their

body weight.3

Despite its prevalence, people do not enjoy being overweight, and regularly spend large amounts of

money in search of a “cure.” In fact, Americans annually spend over $60 billion4 on everything from

over-the-counter diet pills to books, magazines, online support groups, and commercial dieting centers to

help shed their excess weight. It has been estimated that 21 percent of the total U.S. health care budget is

spent to treat the medical complications associated with being overweight.5

If you are currently struggling with your weight or know someone who is, don’t despair. Weight

loss takes work, but it is achievable. This chapter emphasizes the key components of how to achieve and

sustain a healthy body weight.

Why Is Weight Management Important? 539

People who are overweight or obese have an increased risk for cardiovascular disease— including hypertension, heart disease, and stroke—and the risk increases as BMI increases.9 This increased risk may be due in part to the fact that overweight people tend to have high blood levels of both triglycerides and LDL cholesterol and low levels of HDL cholesterol. 10

Overweight and obesity are also strongly linked to type 2 diabetes. Excessive adipose tissue contributes to insulin resistance, which forces the pancreas to work harder to pro- duce more insulin. Eventually, the pancreas can stop producing insulin altogether, caus- ing diabetes. Nearly 85 percent of people with type 2 diabetes are overweight or obese.11

A higher BMI can also increase the risk of gallbladder disease, joint stress, sleep apnea, reproductive problems, and some cancers, including endometrial, breast, and colon cancer. Central obesity is especially harmful: It is one of the five risk factors that comprise metabolic syndrome, a condition that in turn increases the risk for cardiovascular disease and type 2 diabetes. Obesity also increases the risk for osteoarthritis, a condition in which the tissue that protects the joints of the knees, hips, and lower back wears away.

Carrying extra body weight is so detrimental to health that for overweight individuals, losing as little as five to ten percent of body weight can be lifesaving.12 For example, if you currently weigh 200 pounds, a weight loss of 10–20 pounds can reduce your risk of type 2 diabetes and other chronic diseases.

Being Underweight Also Increases Health Risks As with being overweight, being underweight can lead to numerous diseases and condi- tions. These include anemia, heart irregularities, and amenorrhea (loss of menstruation in women). Underweight older adults are at risk for low body protein and fat stores and a depressed immune system, which makes it more difficult to fight infections. Injuries, wounds, and illnesses that would normally improve in healthy individuals can result in serious complications in individuals with a depressed immune system.

Individuals who are underweight are more likely to lack vital nutrients, such as cal- cium, which is important to maintain strong, dense bones. Being underweight increases the risk for osteoporosis and bone fractures later in life.13 Sustaining a normal, healthy body weight can reduce this risk.

Certain diseases, such as cancer, inflammatory bowel disease, and celiac disease, can cause malabsorption and result in significant weight loss. Other inadvertent causes of underweight include certain medications—such as some antidepressant, osteoporosis, and blood pressure drugs—all of which can decrease appetite. Smoking and substance abuse can also lead to unhealthy weight loss.

Overweight and Underweight Have Social and Psychological Risks Beyond the physical effects of carrying too much body weight, obese and overweight individuals are often at a social, educational, and economic disadvantage. Overweight people suffer more discrimination and are more likely to be denied job promotions and raises than normal-weight individuals.14 Obese females are less likely to be accepted into college, especially higher-ranked schools.15 Social situations, such as attending movies or sporting events, and travel on buses and airplanes may be limited for obese individuals due to restrictive seat sizes.16 These prejudices and limitations can result in lower self-esteem.17

Popular perceptions of overweight individuals as being lazy or weak-willed can fur- ther affect their feelings of self-confidence and self-worth.18 Images of slender models as the ideal in advertising and other media help perpetuate the notion that overweight individuals are less desirable. Living in an antagonistic environment may compromise

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attempts at achieving a healthy body weight. For example, obese and overweight people are less likely to exercise because they are embarrassed to change in the locker room or work out at a gym.19 Obese people have higher rates of suicide than healthy-weight people20 and are more likely to use alcohol and drugs when compared with their normal-weight peers.21

The psychological consequences of being underweight can be just as debilitating. Research has suggested that people who are underweight are at greater risk for irritability, anger, and depression.22 For example, underweight males are reported to have a 12 percent increased risk of committing suicide compared with healthy- weight males.23 People who are underweight can be more socially withdrawn compared with those with a healthy body weight.24

LO 15.1: THE TAKE-HOME MESSAGE Weight management means maintaining a healthy weight to reduce the risk of specific health problems. Classifying obe- sity as a disease may improve treatment options but may also raise health care costs, increase drug and surgical procedures, and hamper lifestyle changes to lose weight. The physical risks of overweight and obesity include an increased risk for cardiovascular disease, type 2 diabetes, certain cancers, and other dis- orders, whereas underweight increases the risk for anemia, heart irregularities, amenorrhea, and osteoporosis. The social and psychological effects of obesity and underweight include discrimination, low self-esteem, depression, suicide, and alcohol and drug problems.

How Is Food Intake Regulated? LO 15.2 Define the terms appetite, hunger, and satiety, and describe the physiological factors involved in regulating food intake.

Why do you feel hungry or full? A variety of factors influence not only how much we eat, but also the type of food we choose to eat. These factors include strong physiological and psychological influences that go beyond the need for energy.

Appetite Often Triggers Eating for Unnecessary Reasons Distinguishing between true hunger and appetite, or the desire to eat based on sig- nals other than hunger, can be difficult. Have you ever groaned after a huge meal, “I’m so full!” only to turn around and eat a thick slice of apple pie with ice cream? Appetite is often stimulated even when we are satiated. This desire to eat the apple pie may be triggered by the smell, taste, texture, or color of the food, or by external cues such as time of day, social occasions, or other people. Appetite can also be triggered by learned behavior and by emotions such as stress, fear, and depression. Identifying the triggers that affect your desire to eat is one of the key strategies in maintaining a healthy body weight.

appetite Desire to eat food whether or not there is hunger; a taste for particular foods and cravings in reaction to cues such as the sight, smell, or thought of food.

Overweight and obese people are often embarrassed to exercise in a gym or change clothes in a locker room because of their body weight.

How Is Food Intake Regulated? 541

Hunger and Satiation Affect the Desire to Eat and Stop Eating Two strong physiological factors, hunger and satiety, affect the amounts of food individu- als consume. Hunger is the physical sensation associated with the need or intense desire for food. Physiological signals such as low blood sugar or an empty stomach trigger hunger and searching for food. Once eating begins, hunger subsides as the feeling of fullness, or satiation, sets in and you stop eating. Satiety describes how you feel after a meal and before hunger is triggered again.

Satiety and hunger are both controlled by hormones produced in the brain and the gastrointestinal tract. In the brain, two regions of the hypothalamus control the trig- ger mechanisms that stimulate hunger and satiety: the ventromedial nucleus and the lateral hypothalamus. These regions receive signals from both inside and outside the brain. Focus Figure 15.1 explains the signals that control hunger and satiation.

Regulation of Satiety Satiety is triggered in the ventromedial nucleus in response to a variety of physiological cues. After a meal, the stomach becomes distended, sending signals from stretch recep- tors in the lining of the stomach to the brain to suppress hunger. As protein, fatty acids, and monosaccharides reach the small intestine, two hormones, cholecystokinin (CCK) and peptide YY (PYY), are released, sending feedback to the hypothalamus to increase satiety and decrease hunger.25 Once these nutrients are absorbed, the hormone insulin is released, which also results in a decrease in hunger.26

Other hormones, including leptin, produced in adipose tissue, influence satiety. The production of leptin is controlled by the obese gene (ob) and increases in amount as the fat stores increase. Leptin is a satiety signal. It acts on receptors found in the hypothalamus to decrease hunger and food intake, probably by inhibiting neuropeptide Y, a hormone that stimulates hunger. At the same time, leptin creates a negative energy balance by rais- ing the body temperature, which in turn increases energy expenditure and stimulates the oxidation of fatty acids in the liver and muscles. Thus, leptin regulates the amount of fat stored in the adipose tissue.27

In addition to the influence of hormones, certain macronutrients, especially protein, influence satiety and reduce the intake of food. Researchers have reported that protein intake ranging from 15 to 30 percent of total kilocalorie intake significantly reduces food intake.28

Regulation of Hunger Whereas the ventromedial nucleus affects satiety, the lateral hypothalamus controls hun- ger. The hormone ghrelin, produced in the gastric cells of the stomach, stimulates the lateral hypothalamus. Thus ghrelin has the opposite effect of leptin—it stimulates hunger. Ghrelin concentrations rise in the blood before a meal. Ghrelin travels through the blood to the hypothalamus, where it activates neuropeptide Y to stimulate hunger.

The production of ghrelin changes throughout the day. More ghrelin is produced between meals, during sleep, or when you fast. This increase in ghrelin production sig- nals the hypothalamus that the body needs energy. Ghrelin levels drop following a meal, especially one that contains high amounts of carbohydrate and/or kilocalories. This drop in ghrelin levels signals satiety and decreases the urge to eat.

Lean individuals tend to have higher levels of ghrelin than individuals with more body fat, especially in the morning hours. Ghrelin levels increase when an individual is on a low-kilocalorie diet, a fact that might help explain why people on weight-reduction diets continually feel hungry and find it difficult to lose weight.29

Leptin may also be partly responsible for hunger. When adipocytes shrink during weight loss, leptin levels drop. This reduction in leptin stimulates hunger and may drive the body to eat more to reestablish fat stores.

hunger Strong sensation indicating a physiological need for food.

satiation State of being satisfactorily full during a meal, which inhibits the ability to eat more food.

satiety Feeling of satiation or “fullness” after a meal before hunger sets in again.

Hunger is stimulated by circulating hormones and signals from your intestinal tract.

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Head to Mastering Nutrition and watch a narrated video tour of this figure by author Joan Salge Blake.

Figure 15.1 The Brain Controls Hunger and SatiationFOCUS

Neuropeptide Y (NPY) is produced in the hypothalamus and stimulates hunger.

NEUROPEPTIDE Y

Ghrelin is secreted from the stomach when the stomach is empty to stimulate hunger.

GHRELIN

INSULIN

Two regions of the brain—the ventromedial nucleus and the lateral hypothalamus—control eating behaviors in response to hormones released from the stomach, pancreas, small intestine, adipocytes, and the hypothalamus. The ventromedial nucleus responds to hormones to stimulate satiety. Hunger is triggered by hormones that stimulate the lateral hypothalamus.

Insulin is released from the pancreas following carbohydrate ingestion.

LEPTIN Leptin produced in the adipocytes is released into the blood to stimulate satiety.

PEPTIDE YY Peptied YY (PYY) is released from the small intestine when kilocalories have been consumed.

CHOLECYSTOKININ Cholecystokinin (CCK) is released from the small intestine when chyme enters the duodenum.

HORMONES THAT STIMULATE SATIETY

HORMONES THAT STIMULATE HUNGER

GHRELIN

NPY

INSULIN

PYY

CCK

LEPTIN

The ventromedial

nucleus

The lateral hypothalamus

How Do Fat Cells Form and Expand? 543

Certain vitamins and minerals have been shown to lower leptin concentrations and affect hunger levels. For example, zinc supplements have been reported to lower leptin in obese individuals and may be responsible for overeating.30 On the other hand, ingesting too little vitamin A and C also appears to inhibit leptin secretion.31 The mechanism of how vitamin and mineral intake affects the hormone leptin and hunger is still unclear.

LO 15.2: THE TAKE-HOME MESSAGE Food intake is controlled by hunger, satia- tion and satiety, and appetite. Appetite is a desire for food prompted by fac- tors other than hunger. Hunger is a strong physiological need for food. Satiety is the physiological response to food intake, resulting in satisfaction. Hunger, satiation, and satiety are controlled by the hypothalamus and regulated by neu- ropeptides, hormones, and neural signals from the gastrointestinal tract and adipocytes. The hormones leptin and ghrelin play key roles in triggering hunger and satiety, with ghrelin triggering hunger and leptin triggering satiation.

How Do Fat Cells Form and Expand? LO 15.3 Describe the role of hyperplasia and hypertrophy of adipocytes in the development of obesity.

The increase in the stores of body fat occurs in two ways: (1) Adipocytes, like muscle cells and many other body cells, can grow in size. This process is known as hypertrophy. In adipocytes, hypertrophy is caused by increased storage of fat. (2) Once an adipocyte fills to capacity, the production of more adipocytes is stimulated. The stimulation of exces- sive cell division—which occurs in tumor formation and other physiological processes, is known as hyperplasia. Adipocyte hyperplasia causes a buildup of excess fat tissue, which is stored throughout the body (Figure 15.2).

The Number of Fat Cells in the Body Never Decreases The average nonobese adult’s body contains approximately 30 billion to 50 billion adipo- cytes, each of which holds between 0.4 and 0.5 micrograms of fat. Overweight or obese adults most likely have the same number of adipocytes as healthy-weight adults but their fat cells are much larger, holding between 0.6 and 1.2 micrograms of fat. Thus, when a healthy-weight adult gains weight, it is likely due to hypertrophy.

When an overweight or obese adult loses weight, the size of the fat cell shrinks, but the number of cells does not. After weight loss, the smaller fat cells remain and can easily be filled up again when energy intake is greater than energy output.

hypertrophy Increase in size; in adipocytes, hypertrophy refers to the increase in size of the cells.

hyperplasia Increase in the number of cells due to cell division.

▲ Figure 15.2 The Formation of Adipocytes

Preadipocytes are immature cells formed from stem cells. a Once the preadipocyte

begins to store fat, it becomes a mature adipocyte.

b Hypertrophy results in an increase in the size of adipocytes, which happens during weight gain.

d During hyperplasia the number of adipocytes increases.

c

Preadipocyte

Fat Fat droplet

Cutaway view of mature adipocyte

Nucleus Cell membrane Hypertrophy

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Although hyperplasia appears to slow with age,32 the growth and production of fat cells may continue throughout life, especially in obese individuals. Every year about 10 percent of fat cells die and are replaced by new ones. The number of fat cells you create as a child remains with you for life.33

Fat Cells Can Grow and Shrink The size of fat cells is regulated by the enzyme lipoprotein lipase (LPL), which is made in the adipose tissue and lies on the surface of the adipocyte. As you learned in Chapter 5, LPL increases lipogenesis, or the accumulation of fat in the adipocyte. Another enzyme, called hormone-sensitive lipase (HSL), plays the opposite role in fat metabolism. HSL stimu- lates lipolysis, or the hydrolysis of triglycerides inside the adipocyte, and frees the fatty acids, which are then released into the bloodstream. The balance between lipogenesis and lipolysis affects the size of the adipocyte. This is similar to a savings account—as you save money, the balance grows until you take it out and the balance shrinks.

The activity of LPL and HSL differs in overweight and lean individuals.34 Heavier people have much more LPL activity, especially after eating (Figure 15.3). This makes it much easier to store energy from the meal. The activity of LPL increases following weight loss, which makes it much easier to regain lost weight.

Differences in LPL activity are also noted between genders.35 In men, LPL is more active in the visceral, abdominal fat cells than in females, but females have higher LPL activ- ity rates in the hips and thighs than do males. This is probably the reason women deposit more fat in the lower body and why adipose tissue in these areas is more stable and takes lon- ger to lose. Overall, women oxidize more fat for fuel during exercise than men do and a male’s LPL activity is higher following exercise than a female’s. The reason for this remains unclear.

LO 15.3: THE TAKE-HOME MESSAGE The average adult body contains 30 billion to 50 billion adipocytes. Once adipocytes are formed, they can increase or decrease in size as fat storage needs change, but they can never decrease in number. Every year 10 percent of fat cells die and are replaced. The enzymes lipoprotein lipase and hormone-sensitive lipase influence the balance between lipolysis and lipogenesis, and thus the growing or shrinking of fat cells.

▲ Figure 15.3 Lipoprotein Lipase Activity in Lean, Obese, and Post-Weight-Loss Adults LPL increases lipogenesis, or the accumulation of fat in the adipocyte. Source: J. English. 2013. Reversing Altered Metabolic Functions to Enhance Long-Term Weight Control. Available at http://nutritionreview.org/2013/04/ reversing-altered-metabolic-functions-enhance- longterm-weight-control/. Accessed April 2017.

8

10

6

4

2

0 Lean

LP L

ac tiv

ity

Obese Post weight-loss

How Do Genetics and Environment Influence Obesity and Weight Management? LO 15.4 Discuss the role of genetics and the environment in the development of underweight, overweight, and obesity.

The relationship of genes to obesity was first demonstrated in studies on separated identi- cal twins raised in different home environments who have similar weight gain and body fat distribution.36 On the other hand, our genetic code has not changed since the obesity epidemic began. Therefore the environment in which we work and live must also influ- ence body weight. Indeed, most health professionals now agree that obesity arises from a gene–environment interaction.37 The question is, which is stronger, nature or nurture?

Nutrigenomics and Epigenetics May Influence Weight Control Two new areas of study introduced in Chapter 1, nutritional genomics and epigenetics, may help answer this question. The science of nutrigenomics has identified specific genes that are involved in the body’s response to certain nutrients, such as how we absorb,

gene–environment interaction Interaction of genetics and environmental factors that increases the risk of obesity in susceptible individuals.

How Do Genetics and Environment Influence Obesity and Weight Management? 545

store, or break down dietary fat, and can pinpoint the variation in the gene that may be responsible for the body’s response. However, even with identical twins that have the same genetic makeup, the response to overeating or restricting kilocalories varies.

Researchers are still unclear what mechanism causes genes and nutrients to interact. This is where epigenetics comes into play. Recall that epigenetics studies changes in gene activity and gene expression that occur without changing the DNA sequence itself. The DNA in the body is wrapped around proteins called histones, much as thread is wrapped around a spool. Both the DNA and the histones are covered with chemical tags that can react to signals within the body, such as diet, stress, toxins, and physical activity. These chemical tags are collectively called the epigenome (Figure 15.4). The epigenome can cause the DNA-histone structure to tightly wrap, hiding genes. These genes are not accessible to the cell and therefore are not translated into proteins. However, the epigenome can also cause the DNA-histones to partially unwind, exposing the genes that were hidden and allowing them to be used to assemble proteins.

Food is one epigenetic factor that can cause the DNA-histones to partially unwind and expose inactive genes. For example, the B vitamins thiamin, riboflavin, and vitamin B12 donate methyl groups during metabolic reactions. These methyl groups tag the DNA-histones and thereby influence the expression of certain genes. These genes may, for example, trigger or inhibit fat synthesis, although how the mechanism might work is still unknown.38 In other words, while we can’t alter the genetic makeup we are born with, we may eventually be able to control the factors that turn obesity genes on or off.

People who share genes often have similar body weights.

▲ Figure 15.4 The Epigenome The epigenome consists of chemical tags that influence the use of genes to assemble proteins. The epigenome can cause the genome to wind more tightly, thereby hiding genes, or unwind, making genes accessible for expression as proteins.

DNA alpha-helixa

DNA wraps around proteins called histones. This DNA-histone structure is covered with chemical tags (the epigenome), some of which are derived from foods.

b

The epigenome can cause the genome to wrap tightly and hide genes or to unfold and reveal genes.

c

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Genetic Variants Can Influence Body Weight Scientists currently associate more than 40 genetic variants with obesity.39 Some of these gene variants influence your levels of hunger-satiety hormones. Others affect eating behavior, insulin response, thermogenesis, and other factors.40 But how do these gene variants occur?

Recall that even small changes in a gene can affect its ability to code for protein assembly. Among the most common of these small changes are single-nucleotide polymor- phisms, referred to as SNPs, or “snips.” Unlike epigenetic factors, which don’t change the structure of the DNA itself, SNPs are copy errors that occur during DNA replication and do change the building blocks—the nucleotide bases—of DNA. For example, in a gene with an SNP, a length of DNA might have the nucleotide thymine (T) in place of the nucleotide cytosine (C). This shift in a single nucleotide changes the way the gene behaves. This is similar to dialing a telephone number with one wrong digit. Most SNPs have no direct effect whatsoever on body weight, but some play an important role in how individuals respond to food intake.

SNPs of certain genes can influence the level or the functioning of some hormones that influence hunger, satiety, and appetite.41 Earlier in the chapter, you learned that the hypothalamus regulates hunger and satiety by responding to signals from the adipocytes, the pancreas, the stomach, and the small intestine. These signals are conveyed to the brain by the hormones leptin, insulin, CCK, peptide YY, and ghrelin. The hypothalamus then instructs you to eat more or eat less. Multiple gene variants can influence the way the body receives and responds to these signals. For example, an SNP of the ghrelin gene may cause high levels of ghrelin secretion, which could cause some people to overeat and become obese.42 Individuals who are genetically prone to a leptin deficiency (remember, leptin suppresses hunger) become massively obese, yet when they are given leptin, their hunger decreases and their weight falls to within a healthy range.43 Ironically, many obese people have adequate amounts of leptin, but the brain has developed a resistance to it, rendering its hunger control ineffective.44 For these individuals, other mechanisms prevent leptin from functioning as a regulator of hunger.

The adipocytes also secrete another hormone called adiponectin, which improves the body’s response to insulin, reduces fat accumulation in the liver and muscle, and enhances energy expenditure.45 The levels of this hormone are higher in lean people but are low in people who are obese and those with type 2 diabetes. This difference may be explained by SNPs involving the adiponectin gene and may explain why obesity increases the risk for diabetes.

Genetics may also affect thermogenesis, which in turn affects energy expenditure. Gene variants may cause different rates of thermogenesis in brown adipose tissue and in nonexercise activity thermogenesis (NEAT). When some individuals overeat, they burn rather than store excess kilocalories and are thus better able to manage their energy bal- ance.46 Many overweight individuals don’t appear to have this compensatory mechanism.

Gene Theories May Help Explain Weight Variations Some researchers have described a genetic “set point” that determines body weight. This theory holds that the body fights to remain at a specific body weight and opposes attempts at either weight loss or weight gain. In other words, a person’s weight remains fairly constant because the body “has a mind of its own.” Given that the average weight of Americans has increased dramatically over the last few decades relative to previous decades, this theory either isn’t true or the set point can be overridden.47

Other researchers have observed that, when excessive amounts of food are available, some people store more fat than others, and in environments where food is scarce, they lose less fat than others.48 Research comparing the Pima Indians in Arizona with their

adiponectin Hormone produced in the adipocytes that controls the body’s response to insulin and may be involved in reducing the risk of obesity and type 2 diabetes.

set point Weight-control theory proposing that each individual has a genetically established body weight and that significant deviation from this point stimulates changes in body metabolism to reestablish the normal weight.

How Do Genetics and Environment Influence Obesity and Weight Management? 547

ancestors in Mexico reveals that the environment can encourage weight gain in genetically susceptible populations; that is, populations with so-called thrifty genes.49 The Arizona Pima Indians are descended from the Pima Indians of northwestern Mexico. The original population of Mexican Pima Indians passed their genetic heritage on to their Arizona descendants, but not their lifestyle. This genetic inheritance is theorized to have included genes that have helped the Pimas expend less energy during times of famine and store more energy in times of plenty. However, as compared to the Arizona Pimas, the traditional Mexican Pimas engage in more physical activity and consume a diet higher in complex carbohydrates and lower in animal fats. Mexican Pimas have, on average, a BMI of about 25, compared with Arizona Pimas who have, on average, a BMI of over 33.50 Because they have a healthier lifestyle, the traditional Pimas have lower rates of obesity than the Arizona Pimas. This suggests that even if you have a genetic predisposition to being overweight, it’s not a done deal. If you are determined to make healthy dietary choices and engage in regular physical activity, you can overcome your genetic predisposition.

Environmental Factors Can Increase Appetite and Decrease Physical Activity As we saw with the Mexican and Arizona Pimas, the environment around us has changed in ways that have made it easier for people to gain weight. To explain how genetics and environment interact to produce obesity, researchers have used the analogy that genes load the gun but an obesity-promoting environment pulls the trigger.51 Environmental factors that seem particularly important include lack of time, an abundant food supply coupled with portion distortion, and lack of physical activity. Take the Self-Assessment: Does Your Environment Affect Your Energy Balance? to consider how your environment influences the lifestyle decisions you make throughout the day.

Self-Assessment

How Much Does Your Environment Affect Your Energy Balance? 1. Do you eat out at least once a day?

Yes □ No □

2. Do you often buy snacks at convenience stores or vending machines?

Yes □ No □

3. Do you buy the supersized portions of fast foods or snacks?

Yes □ No □

4. When you order pizza, do you have it delivered?

Yes □ No □

5. Do you drive around the parking lot to get the closest parking space to the entrance?

Yes □ No □

6. Do you get off at the subway or bus stop that is nearest to your destination?

Yes □ No □

7. Do you take the elevator when stairs are available in a building?

Yes □ No □

Answer All of the above habits contribute to an obesity-promoting environment. If you answered “yes” to three or more, you should think about how you can improve your lifestyle habits.

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Lack of Time Research shows that adults spend more time traveling to work and devote more of their daily hours to work than in previous decades.52 This longer workday means there is less time to devote to everyday activities, such as food preparation. Today, almost a third of Americans’ daily kilocalories come from ready-to-eat foods that are not pre- pared at home.53 Between 1972 and 1995, the prevalence of eating out in the United States increased by almost 90 percent, a trend that is expected to increase steadily to the year 2020.54 To accommodate this demand, the number of food service establish- ments in the United States has almost doubled—to nearly 900,000—during the last three decades.55

Dining out frequently is associated with a higher BMI.56 An Economic Research Service study found an average increase in kilocalorie intake for adults of 134 kilocalories for every meal eaten away from home.57 Eating out also reduces fruit and vegetable intake and adds more fat, sugar, and alcohol.58 The top foods selected when eating out, especially among college-age diners, are energy-dense French fries and hamburgers.59 Dining out also tends to displace nutrient-dense vegetables and fruits.

An Abundant Food Supply and Portion Distortion In the United States food is plentiful, there’s a lot to choose from, and portion sizes are generous. All of these factors are associated with consuming too many kilocalories.60

Years ago, people went to a bookstore for the sole purpose of buying a book. Now they go to a bookstore to sip a vanilla latte and nibble on biscotti while they ponder which book to buy. Americans can grab breakfast at a fast-food drive-through, lunch at a museum, a sub sandwich at many gas stations, and a three-course meal of nachos, pizza, and ice cream at a movie theater.

This access to a variety of foods is problematic for weight-conscious individuals. The appeal of a food diminishes as it continues to be eaten (that is, the first bite tastes the best and each subsequent bite loses some of that initial pleasure), but having a variety of foods available allows the eater to move on to another food once boredom sets in.61 The more good-tasting foods that are available, the more a person eats. For example, during that three-course meal at the movie theater, once you’re tired of the nachos, you can move on to the pizza, and when that loses its appeal, you can dig into the ice cream. If the pizza and ice cream weren’t available, you would have stopped after the nachos and consumed fewer kilocalories.

As you learned from Chapter 2, the portion sizes of many foods, such as French fries and sodas, have doubled, if not tripled, compared with the portions listed on food labels. Consumers perceive “supersized” portions as bargains because they often cost only slightly more than the regular size. Research shows that people tend to eat more of a food, and thus more kilocalories, when larger portions are served.62 In other words, when served a supersized soft drink, a person consumes more, if not all, of it even though a smaller drink would have provided the same level of satisfaction.

At home, the size of the serving bowl or package of food influences the amount that ends up on the plate. Serving from a large bowl or package has been shown to increase the serving size by more than 20 percent.63 This means that you are more likely to scoop out (and eat) a bigger serving of ice cream from a half-gallon container than from a pint container. To make matters worse, most people don’t compensate for these extra kilocalo- ries by reducing the portions at the next meal.64

You have probably heard competing claims about the superiority of diets high in either protein or carbohydrate for promoting weight loss. Does the macronutrient compo- sition of the diet really influence body weight? To find out, see Examining the Evidence: Do Diets Rich in Carbohydrates Make Us Fat?

Research has shown that women who dine out five or more times weekly consume close to 300 kilocalories more on dining-out days than do women who eat at home.

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EXAMINING THE

EVIDENCE

In recent years, there has been a renewed interest in altering the nutri-ent composition of diets to achieve weight loss. The recommended AMDR (Acceptable Macronutrient Distribution Range) is for 45–65 percent of daily kilocalories to come from carbohydrates, 20–35 percent of daily kilocalories to come from fat, and 10–35 percent of daily kilocalories to come from pro- teins. Some nutrition experts believe that people who wish to lose weight should increase their protein consump- tion to as much as 45 percent of total kilocalories, at the same time reducing carbohydrates to 25 percent.1 They cite studies reporting that high-protein diets produce greater weight loss when com- pared with high-carbohydrate diets of the same kilocalorie content.2 A diet lower in carbohydrate and higher in protein also was reported to prevent weight regain after weight loss had been achieved.3 Epidemiological evidence also suggests that carbohydrates may be contributing to America’s weight gain: According to a 2013 meta-analysis, our increased intake in carbohydrate-rich, sugar-sweetened beverages correlates with the weight gain observed in both children and adults in recent decades.4 This would suggest that as dietary intake of carbohydrates increases, so do our waistlines.

One big challenge is pinpointing the mechanism that might be responsible for weight gain with a higher carbohydrate intake. Some researchers argue that the culprit is insulin, while others suggest high-glycemic foods and beverages, such as sugary drinks, are the cause. A third theory is that carbohydrates alter appetite- suppressing hormones, causing hunger after a carbohydrate meal. Let’s take a closer look at the evidence.

The Insulin Connection As you learned in Chapter 4, the body requires insulin to facilitate the trans- port of glucose into body cells. But that’s not the only function of insulin. This pancreatic hormone also pro- motes the synthesis of fatty acids, or lipogenesis, in the liver. Excess glucose

not converted to glycogen in the liver, or used for energy, is converted to fatty acids and stored as fat. In theory, the more carbohydrate ingested, the more insulin the pancreas releases, the greater the potential for glucose to be stored as fatty acids in the adipocytes.

Insulin also prevents beta-oxidation of fatty acids by inhibiting lipolysis of stored fat in the adipose tissue, trap- ping fatty acids in the adipocytes.5 Thus, the effects of insulin on lipid metabolism tend toward conservation of fat. To avoid elevated insulin levels, a diet lower in carbohydrates would be a logical strategy.

Hunger Control and Carbohydrate Intake The composition of the diet may influ- ence the release of hunger-suppressing hormones. Recall that hunger is stimu- lated when ghrelin levels increase or is reduced when leptin levels increase. In one study, total ghrelin levels were shown to decrease significantly when protein was consumed, compared with carbohydrates or lipids.6 The research- ers also noted that after 3 hours, ghrelin levels rebounded following carbohydrate intake but not following

protein intake, supporting the theory that protein suppresses hunger for lon- ger than does carbohydrate.

Ghrelin levels may be regulated by insulin, at least initially. In one study, a higher carbohydrate intake, which increased the amount of insulin released, led in turn to a reduction in the amount of ghrelin in the blood.7 Researchers suggest that this may be due to the impact of insulin on circulating ghrelin levels. Or insulin may be affected by whether the carbohydrates ingested were simple or complex carbohydrates.8 The theory is that the release of insulin following a meal regulates the reduction of ghrelin, thus influencing satiety.

Carbohydrate and protein may also affect the satiety hormone peptide YY. PYY levels have been shown to increase gradually without declining after consumption of a high-protein meal, whereas PYY levels peak and then begin to decline after consump- tion of a high-carbohydrate meal.9 Researchers suggest that the increase in PYY following a high-protein/low- carbohydrate meal leads to more sus- tained feelings of satiety and may play a role in promoting a reduction in over- all food intake and weight loss.

Glycemic Index and Weight Loss The typical Western diet, based on high-glycemic-index staples such as potatoes, bread, and rice, may affect hunger and ultimately body weight. Foods with a high glycemic index are digested quickly, and in turn quickly raise blood glucose, thereby increas- ing insulin secretion to a greater extent compared with lower-glycemic foods. Consumption of high-glycemic foods has also been shown to be followed by hunger earlier than consumption of low-glycemic foods.10 The increase in satiety with low-glycemic, high-fiber foods also results in lower kilocalorie intakes and potential weight loss.

Consuming a low-glycemic-index diet may also be effective in reducing total body fat. As noted above, increased levels of insulin may increase lipogenesis

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6. Vancleef, L., T. Van Den Broeck, T. Thijs, S. Steensels, L. Briand, J. Tack, and I. Depoortere. 2015. Chemosensory signalling pathways involved in sensing of amino acids by the ghrelin cell. Scientific Reports 5:15725. doi: 10.1038/srep15725.

7. Steensels, S., L. Vancleef, and I. Depoortere. 2016. The Sweetener-Sensing Mechanisms of the Ghrelin Cell. Nutrients 8(12):795. doi: 10.3390/nu8120795.

8. Penaforte, F. R., C. C. Japur, L. P. Pigatto, P. G. Chiarello, and R. W. Diez-Garcia. 2013. Short-Term Impact of Sugar Consumption on Hunger and Ad Libitum Food Intake in Young Women. Nutrition Research and Practice 7(2):77–81.

9. Sedlackova, D., J. Kopeckova, H. Pape- zova, V. Hainer, H. Kvasnickova, M. Hill, and J. Nedvidkova. 2012. Comparison of a High-Carbohydrate and High-Protein Breakfast Effect on Plasma Ghrelin, Obestatin, NPY and PYY Levels in Women with Anorexia and Bulimia Nervosa. Nutrition and Metabolism 9:52. doi: 10.1186/1743-7075-9-52.

10. S. Wang, L. Yang, J. Lu, and Y. Mu. 2014. High Protein Breakfast Promotes Weight Loss by Suppressing Subsequent Food Intake and Regulating Appetite Hormones in Obese Chinese Adolescents. Hormonal Research in Paediatrics. doi: 10.1159/000362168.

11. A. M. Goss, L. L. Goree, A. C. Ellis, P. C. Chandler-Laney, K. Casazza, M. E. Lockart, and B. A. Gower. 2013. Effects of Diet Mac- ronutrient Composition and Fat Distribution During Weight Maintenance and Weight Loss. Obesity 21(6):1139–1142.

12. J. Halkjaer, T. I. Sorensen, A. Tjonneland, et al. 2004. Food and Drinking Patterns as Pre- dictors of 6-year BMI-Adjusted Changes in Waist Circumference. British Journal of Nutri- tion 92:735–748.

13. Naude, C. E., A. Schoonees, M. Senekal, T. Young, P. Garner, and J. Volmink. 2014. Low Carbohydrate versus Isoenergetic Balanced Diets for Reducing Weight and Cardiovas- cular Risk: A Systematic Review and Meta- Analysis. PLoS ONE 9(7):e100652. doi: 10.1371/journal.pone.0100652.

14. Astrup, A., and J. Brand-Miller. 2014. Obesity: Have New Guidelines Overlooked the Role of Diet Composition? Natural Review of Endocrinolog y 10(3):132–133.

with a smaller waist circumference.12 The results of these studies suggest that con- suming low-glycemic foods reduces the impact of insulin on lipid metabolism and may enhance fat loss.

The evidence supporting the prem- ise that a high-carbohydrate diet may promote weight gain is promising; however, when researchers compare the effects of isocaloric diets that are low in carbohydrate (less than 45 per- cent carbohydrate) versus moderate in carbohydrate (45–65 percent carbohy- drate), the weight loss is similar.13 Until more conclusive evidence is presented, a healthy weight-loss diet should include lean meats, low-fat dairy, whole grains, legumes and other vegetables, and fresh fruits and limit high-glycemic refined carbohydrates.14

References 1. Astrup, A., A. Raben, and N. Geiker. 2015.

The Role of Higher Protein Diets in Weight Control and Obesity-Related Comorbidities. International Journal of Obesity 39(5):721–726. doi: 10.1038/ijo.2014.216.

2. Bray, G. A., D. H. Ryan, W. Johnson, et al. 2017. Markers of Dietary Protein Intake Are Associated with Successful Weight Loss in the POUNDS Lost Trial. Clinical Obesity. doi: 10.1111/cob.12188.

3. M. P. Lejeune, E. M. Kovacs, and M. S. Westerterp-Plantenga. 2005. Additional Protein Intake Limits Weight Regain After Weight Loss in Humans. British Journal of Nutrition 93:281–289.

4. V. S. Malik, A. Pan, W. C. Willett, and F. B. Hu. 2013. Sugar-Sweetened Beverages and Weight Gain in Children and Adults: A Sys- tematic Review and Meta-Analysis. American Journal of Clinical Nutrition 98(4):1084–1102.

5. DiPilato, L. M., F. Ahmad, M. Harms, P. Seale, V. Manganiello, and M. J. Birnbaum. 2015. The Role of PDE3B Phosphorylation in the Inhibition of Lipolysis by Insulin. Molecular and Cellular Biolog y 35(16):2752– 2760. doi: 10.1128/MCB.00422-15

and decrease lipolysis, thereby preserv- ing body fat. A 2013 study measured the impact of a low-glycemic diet (average 49 on the glycemic index) compared with a high-glycemic diet (average 60 on the glycemic index) for 16 weeks. Results showed that at the end of the 16-week study, the low-glycemic group had dropped 4.4 percent more intra-abdom- inal fat compared with the high-glycemic group (Figure 1).11 Another study reported that a low- glycemic diet is associated

▲ Figure1 The Effects of a High versus Low Glyce- mic Diet on Fat Loss A low-glycemic diet resulted in a greater loss of abdominal fat compared to a high-glycemic diet. Source: A. M. Goss, L. L. Goree, A. C. Ellis, P. C. Chandler-Laney, K. Casazza, M. E. Lockart, and B. A. Gower. 2013. Effects of Diet Macronutrient Composition and Fat Distribution during Weight Maintenance and Weight Loss. Obesity 21(6):1139–1142.

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Lack of Physical Activity Since 1985, Americans have been consuming about 300 more kilocalories daily while also expending less energy during their entire day.65 The increase in “kilocalories in” and decrease in “kilocalories out” is a recipe for a positive energy imbalance and weight gain. Compared with years past, Americans expend less energy both at work and in the little leisure time that they have.

When your great-grandparents went to work in the morning in the 1940s, chances are good they headed out to the fields or into factories. Your parents, though, are more likely to head to an office and sit in front of a computer, and you will probably sit at a desk for much of your workday. This shift in work from jobs that required manual labor to jobs that are sedentary has contributed to the rising rates of overweight and obesity in

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How Can You Lose Weight Healthfully? LO 15.5 Describe the role of diet and exercise in achieving a reasonable rate of weight loss.

The easiest way to avoid having to lose weight is to not gain weight in the first place. But for people who do need to shed pounds, following the principles discussed here can help.

America.66 One study found that men who sit for more than 6 hours during their workday are at higher risk of being overweight than those who sit for less than an hour daily.67

Technology in the workplace now allows us to communicate with everyone without having to leave our desks. This means that people no longer have to get up and walk to see the colleague down the hall or the client down the street. Researchers estimate that a 145-pound person expends 3.9 kilocalories for each minute of walking, compared with 1.8 kilocalories per minute sitting. Thus, walking 10 minutes during each workday to com- municate in person with coworkers would expend 10,000 kilocalories annually, yet only about 5,000 kilocalories would be expended if the person sat in the office sending e-mails or calling colleagues on the phone. Over the course of a year, these extra 5,000 kilocalories not expended could add up to over a pound of body weight. After 5 years in the workforce, there would be around seven extra pounds of body weight sitting in the chair.

Another form of technology, mechanized transportation, may negatively affect your weight-management goals. Research on urban sprawl has shown that the greater the dis- tance between home and school or work, the more people drive or use public transporta- tion and the less they engage in biking or walking. In addition, the more you drive, the more you weigh.68 For each hour you spend driving to work or school, the likelihood of obesity increases 6 percent, whereas for each half-mile walked per day, the likelihood of obesity is reduced by almost 5 percent.69 This may be one of the factors in the increase in obesity rates among children. In a recent study in Canada, only 25–30 percent of chil- dren and youth reported walking or bicycling to school.70 Changing these behaviors while providing a safe way for children to arrive at school requires creative solutions. One such solution is the “walking school bus.” A walking school bus is similar to a car pool except students walk to school with one or more adults. Children arrive at school safely and increase their daily physical activity.71

As technology continues to advance and allows for less energy expenditure during the day, planned physical activity at another time of day must make up the difference. Unfortunately, more than 20 percent of Americans report no daily leisure-time physical activity.72 Research shows that those age 2–18 years old spend over 5 hours daily, on aver- age, on a combination of “screen-time” activities. These include watching TV, playing video games, and non-work/school-related computer time—even though experts have suggested limiting screen time to 2 hours daily.73

Students who walk to school accompanied by their parents demonstrate the concept of a “walking school bus.”

Increased amounts of “screen time” are con- tributing to decreased amounts of physical activity.

LO 15.4: THE TAKE-HOME MESSAGE Many genetic influences play a role in obe- sity and weight management. Nutrigenomics has identified specific genes that are involved in how we absorb, store, or break down dietary fat. Epigenetics— changes in gene expression rather than DNA—may help to explain the effects on body weight when certain foods are eaten. Gene variants, such as single- nucleotide polymorphisms that affect hormone levels, can influence body weight, as can so-called thrifty genes. Several environmental factors—which include lack of time, easy access to a variety of energy-dense foods and large portions, and lack of physical activity—also encourage obesity.

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Avoid Fad Diets The low-carbohydrate, high-protein, and high-fat diets of the 1970s (Dr. Atkins’ Diet Revolution) were replaced by the very high-carbohydrate and very low-fat diets of the 1980s and early 1990s (Pritikin and Dr. Ornish’s diets), which were in turn replaced by the carbohydrate-restricted, moderate-protein and -fat diets of the late 1990s (the Zone diet), only to flip back to the low-carbohydrate, high-protein and high-fat diets in the early 2000s (Dr. Atkins’ New Diet Revolution, South Beach). Fifteen years later, we’re back to lower-carbohydrate and higher-protein diets (Paleo and New Atkins diets).