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Institute of Medicine (US) Committee on Health and Behavior: Research, Practice, and Policy. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington (DC): National Academies Press (US); 2001.

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Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences.

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3Behavioral Risk Factors

Several behaviors that exert a strong influence on health are reviewed in this section: tobacco use, alcohol consumption, physical activity and diet, sexual practices, and disease screening. Although epidemiologic data on the relationships between these behaviors and various health outcomes were available in the early 1980s, many refinements in knowledge have occurred since then. Causal conclusions have been strengthened by more sophisticated research designs, dose/response relationships have been clarified, the influence of many of these behaviors on overall public health has been quantified, and scientific guidelines have been formulated. This chapter summarizes the important recent epidemiologic evidence on the health effects of these behaviors.

TOBACCO USE

Since the release in 1964 of the surgeon general's first report on smoking, there has been a tremendous increase in scientific knowledge about the health consequences of tobacco use (U.S. Department of Health and Human Services [USDHHS], 1989; U.S. Department of Health and Human Services [USDHHS], 1990; U.S. Department of Health and Human Services [USDHHS], 2000). Cigarette-smoking is the major cause of preventable mortality and morbidity in the United States (National Center for Health Statistics [NCHS], 1998a; USDHHS, 2000). Not only does smoking lead to an increased risk of the two leading causes of death in the United States—heart disease and cancer (NCHS, 1998b; USDHHS, 2000)—but smoking during pregnancy has been linked to adverse pregnancy outcomes (DiFranza and Lew, 1995; Hebel et al., 1988; LeClere and Wilson, 1997; Li et al., 1993; Shu et al., 1995; USDHHS, 2000; Ventura et al., 1997; Walsh, 1994). Nonsmoking people are not immune to tobacco's health hazards, inasmuch as exposure to second-hand smoke has serious health consequences for adults and children (USDHHS, 1986, 2000; U.S. Environmental Protection Agency [USEPA], 1992).

Although cigarette-smoking among adults leveled off in the 1990s, tobacco use among adolescents increased in that period (USDHHS, 2000). That cigarette-smoking among younger people has increased is particularly alarming for several reasons. Evidence shows not only that tobacco is addictive (USDHHS, 2000) and that only a relatively small percentage of smokers can stop smoking permanently each year (Centers for Disease Control and Prevention [CDC], 1993; Centers for Disease Control and Prevention [CDC], 1996b; USDHHS, 2000), but also that nicotine addiction develops in most smokers during adolescence (Institute of Medicine [IOM], 1994; USDHHS, 1988a, 1994, 2000). Curbing or eradicating tobacco use might remain a daunting task. Prevention is the primary objective, but many benefits are associated with smoking cessation, and such efforts should not be ignored.

Measuring the Public Health Burden of Cigarette-Smoking

There is widespread agreement in the public health and medical communities that cigarette-smoking is the biggest external (nongenetic) contributor to death in the United States. Tobacco-related diseases account for more than 400,000 deaths among adults in the United States each year (CDC, 1993; NCHS, 1998b; USDHHS, 2000). Deaths attributable to tobacco use have been found to exceed deaths from acquired immunodeficiency syndrome (AIDS), traffic accidents, alcohol use, suicide, homicide, fire, and use of illegal drugs combined (IOM, 1994). One World Health Organization report showed that the burden of disease and death attributable to tobacco in developed countries was substantially higher than that attributable to any other risk factor, including alcohol use, unsafe sex, hypertension, and physical inactivity (Murray and Lopez, 1996).

Because there is a long delay between the onset of persistent smoking and the full development of its adverse health consequences, current tobacco-attributable mortality and morbidity are consequences of smoking that began decades ago. If current U.S. tobacco use patterns persist, it is estimated that 5 million persons who were under the age of 18 in 1995 will die from a smoking-related disease (CDC, 1996a; USDHHS, 2000).

Major Smoking-Related Diseases

Cigarette-smoking leads to an increased risk of heart disease, the leading cause of death in the United States (USDHHS, 2000); and the surgeon general's 1983 report (USDHHS, 1983) concluded that cigarette-smoking is the most important modifiable risk factor for coronary heart disease. Cigarette-smoking is also linked with cancer, the second-leading cause of death in the United States (NCHS, 1998b). Smoking causes cancers of the lung, larynx, esophagus, pharynx, mouth, and bladder, and contributes to cancer of the pancreas, kidney, and cervix (USDHHS, 2000). Tobacco use is the leading contributor to lung cancer incidence, and refraining from smoking could prevent most lung cancer cases (National Cancer Institute, 1986; NCHS, 1998b). In 1996, lung cancer accounted for about 28% of all cancer deaths (NCHS, 1998b; Ries et al., 1996; Ventura et al., 1997). An estimated 172,000 new cases are diagnosed each year, and lung cancer causes an estimated 153,000 deaths each year (NCHS, 1998b). Smoking also causes other lung diseases, such as chronic bronchitis and chronic obstructive pulmonary disease (USDHHS, 2000).

According to the Surgeon General's 1990 report (USDHHS, 1990), smoking is the most important modifiable cause of poor pregnancy outcome in the United States, It is estimated that 15–30% of all pregnant women smoke (Chandra, 1995; Ventura et al., 1997). Pregnancy complications associated with maternal smoking include premature detachment of the placenta, development of the placenta in the lower uterine segment, which can cause hemorrhaging in the last trimester; bleeding during pregnancy; premature membrane rupture; and premature delivery. Maternal smoking also has been associated with spontaneous abortions and low birthweight (DiFranza and Lew, 1995; Hebel et al., 1988; LeClere and Wilson, 1997; Li et al., 1993; Shu et al., 1995; USDHHS, 2000; Ventura et al., 1997; Walsh, 1994). Evidence indicates that in some groups of pregnant women smoking one to six cigarettes a day increases by about two-thirds the risk of giving birth to a low birthweight infant (LeClere and Wilson, 1997; Ventura et al., 1997). Smoking in the last few weeks of pregnancy has the biggest impact on fetal weight gain. Women who stop smoking before becoming pregnant or who quit in the first 3–4 months of pregnancy have infants of the same birthweight as those born to women who never smoked. Women who stop smoking later in pregnancy have higher birthweight infants than do women who smoke throughout pregnancy.

The complex issues associated with the real and perceived risk of tobacco and tobacco harm-reduction products are explored in an IOM report (2001).

Consequences of Second-Hand Smoke

Exposure to second-hand smoke has serious health consequences (USDHHS, 1986, 2000; USEPA, 1992). At least 43 of the roughly 4000 chemicals identified in tobacco smoke have been shown to cause cancer in humans and animals (USDHHS, 2000; USEPA, 1992). About 3000 nonsmoking Americans die of lung cancer and 150,000–300,000 children suffer from lower respiratory tract infections each year because of exposure to second-hand smoke (USDHHS, 2000; USEPA, 1992). Second-hand smoke exposure exacerbates asthma and leads to 500,000 child visits to physicians each year (DiFranza and Lew, 1996; USDHHS, 2000). Second-hand smoke exposure also has been linked to increased risk of heart disease among adults (Glantz and Parmely, 1995; Howard et al., 1998; USDHHS, 2000). Data gathered in a study of the U.S. population over the age of 3 showed that almost 88% of nonusers of tobacco had detectable serum cotinine, a biological marker of exposure to second-hand smoke (Pirkle et al., 1996; USDHHS, 2000). Another study showed that almost 22% of Americans under the age of 18 (about 15 million people) were exposed to second-hand smoke in their homes (CDC, 1997b; USDHHS, 2000). A 1996 study showed that home and workplace environments contribute significantly to the widespread exposure to second-hand smoke in the United States (Pirkle et al., 1996; USDHHS, 2000).

Socioeconomic Characteristics of Smokers

Although smoking among adults declined steadily from the middle 1960s through the 1980s, it leveled off in the 1990s (USDHHS, 2000). In 1995, the prevalence of smoking among adults was almost 25% (CDC, 1997a; NCHS, 1998b; USDHHS, 2000). Men are more likely to smoke than are women—27% and 22%, respectively (CDC, 1997a; USDHHS, 2000)—although those rates could change because cigarette use among high school senior girls almost equals that among boys (NCHS, 1998a; USDHHS, 2000). American Indians and Alaska Natives are more likely (34%), and Hispanics, Asians, and Pacific islanders are less likely (16%), to smoke than are other racial and ethnic groups (African American, 26%; White, 25%) (USDHHS, 2000). Cigarette-smoking was about twice as common among poor men and women as among more affluent persons in 1995 (NCHS, 1998a). One study showed that non-Hispanic White and African Americans living in poverty were more likely to smoke than were people with middle and high incomes in 1995 (NCHS, 1998a).

Among adolescents, tobacco use increased in the 1990s, after decreasing in the 1970s and 1980s (USDHHS, 2000). Several factors place young people at an increased risk of initiating tobacco use (USDHHS, 2000). Sociodemographic risk factors include low socioeconomic status of one's family. Environmental risk factors include accessibility and availability of tobacco products, cigarette advertising and promotion, the price of tobacco products, perceptions that tobacco use is normative, use and approval of tobacco use by peers and siblings, and lack of parental involvement. Personal risk factors include poor self-image and low self-esteem relative to peers, the belief that tobacco use is functional (useful or providing a benefit), and lack of confidence in one's ability to refuse an offer to use tobacco (USDHHS, 1994, 2000).

Primary Prevention of Cigarette-Smoking

When the surgeon general's first report on smoking was released in 1964, 42% of American adults smoked tobacco; in 1995, use had declined to 24.7% (47 million) of American adults (CDC, 1997a). Among adults, the number of former smokers (43 million) is now almost the same as current smokers (46 million) (IOM, 1994). Given the progress since 1964, it is possible to envision a smoke-free society; however, maintaining the current rate of progress will be challenging. There is overwhelming evidence that the nicotine in tobacco is addictive (USDHHS, 1988a, 2000). Almost 70% of current smokers want to quit smoking, and about 45% quit smoking for at least a day (Howard et al., 1998). However, only 2.5% of smokers stop smoking permanently each year (CDC, 1996b, 1993; USDHHS, 2000).

Nearly all first-time use of tobacco occurs before high school graduation. That is important because nicotine addiction occurs in most smokers during adolescence (IOM, 1994; USDHHS, 1988a, 1994, 2000). Smoking patterns among American youth and the short- and long-term health consequences of initiating smoking in adolescence were described in the Surgeon General's 1994 report Preventing Tobacco Use Among Young People (USDHHS, 1994). The same report provides a summary of efforts to prevent tobacco use among young people; such prevention emerged as a major focus of tobacco control efforts (IOM, 1994; USDHHS, 2000).

Benefits of Smoking Cessation

Given the addictive nature of nicotine and the cumulative nature of health damage due to smoking, strategies to reduce tobacco use should emphasize primary prevention rather than smoking cessation. However, smoking's prevalence in the U.S. population points to the need to continue cessation efforts.

Scientific data on the benefits of smoking cessation were reviewed in the surgeon general's 1990 report (USDHHS, 1990). In the 25 years between 1965 and 1990, half of all living Americans who had ever smoked had stopped. The 1990 report concluded that smoking cessation has major and immediate health benefits for men and women of all ages. Former smokers live longer than continuing smokers. For example, on the average, people who quit smoking before reaching the age of 50 have half the risk of dying before the age of 65 than those who do not quit before the age of 50 (USDHHS, 2000, 1990).

OBESITY: PHYSICAL ACTIVITY AND DIET

Recent years have seen an epidemic in obesity in the United States (Mokdad et al., 1999). Obesity is a major health risk for diabetes (Must et al., 1999), and the relationship of weight to the disease has been extensively reviewed in the literature (Kopelman, 2000; Leong and Wilding 1999; National Task Force on the Prevention and Treatment of Obesity, 2000; Scheen, 2000; USDHHS, 1980). Overweight adults also are at an increased risk for hypertension, coronary heart disease, and some forms of cancer (NCHS, 1998a; Pi-Sunyer, 1993). They also run the risk of developing gallbladder disease, osteoarthritis, sleep apnea, respiratory problems (USDHHS, 2000), and a variety of musculoskeletal problems (Foreyt et al., 1996). There is some disagreement about whether the principal threat to health is from an increase in body fat per se, or from a lack of physical activity, but there is no disagreement that major behavioral change is needed to correct this increase in obesity (Hill and Peters, 1998; Taubes, 1998).

Although genetic factors are important, physical activity and diet contribute significantly to maintenance of appropriate body weight. The combination of inactivity and detrimental dietary patterns has been ranked as the second leading factor contributing to mortality in the United States, after tobacco use (McGinnis and Foege, 1993). In addition, both diet and physical activity, in and of themselves, influence health. Studies show that men and women who are physically active have, on the average, lower mortality than people who are inactive (Kaplan et al., 1987, 1996; Kujala et al., 1998; Kushi et al., 1997; Leon et al., 1987; Lindsted et al., 1991; Paffenbarger et al., 1993; Sherman et al., 1994; Slattery et al., 1989). A sedentary lifestyle has been linked to 23% of deaths from major chronic diseases (Hahn et al., 1990). Furthermore, studies show that dietary factors are associated with 4 of the 10 leading causes of death, including coronary heart disease, stroke, some forms of cancer, and non-insulin-dependent diabetes mellitus (CDC, 1997c; USDHHS, 2000).

This section will review some of the factors that influence obesity, with a particular emphasis on physical activity and diet, and describe the relevance of body weight, physical activity, and diet to cardiovascular disease, cancer, and musculoskeletal problems. It is not meant to be a comprehensive review but rather a sampling of the influences these behaviors can have on health and disease.

Prevalence and Trends

Obesity and overweight are increasing in the United States. Currently, “overweight” is defined as a body mass index (BMI)1 of 25–30 while “obesity” is defined as a BMI greater than 30 (National Heart Lung Blood Institute Obesity Task Force, 1998).2 For most of the 1960s and 1970s the

prevalence of overweight adults (25–74 years of age) was nearly constant at about 25%. However, by 1988–1994, that rose to approximately 35% (NCHS, 1998a), and the prevalence continues to increase. Obesity increased from 12% in 1991 to almost 18% in 1998 and 19% in 1999 (Mokdad et al., 1999; 2000). Obesity in children over the age of 6 and in adolescents also is increasing (Troiano and Flegal, 1998; USDHHS, 2000). Because overweight and obesity that develop in childhood or adolescence can persist into adulthood, this trend increases the risk for chronic disease later in life (USDHHS, 2000).

Relatively few Americans participate in regular physical activity. Only 11% of the U.S. adult population reported regular, vigorous physical activity for 20 minutes or longer more than twice each week (USDHHS, 2000). Furthermore, physical activity tends to decline during adolescence (CDC, 1998; Pate et al., 1994), and a major decrease in vigorous physical activity (much more for girls than for boys) occurs in grades 9–12 (USDHHS, 2000). A consensus is emerging that physical activity does not need to be vigorous to be beneficial to health.3 For people who are inactive, even small increases have been associated with measurable health benefits (USDHHS, 2000).

In 1994–1996, the proportion of Americans who ate away from home was approximately 57%, or an increase of about one-third from the late 1970s (USDA, 1997; USDHHS, 2000). Recent data indicate that 40% of the family food budget is spent at restaurants and carry-outs (USDA, 1996; USDHHS, 2000). Food purchased from restaurants, fast-food outlets, school cafeterias, and vending machines generally is higher in saturated fat, cholesterol, and sodium and lower in fiber and calcium than is food prepared and eaten at home (Lin and Frazao, 1997; USDHHS, 2000). And people tend to eat larger portions of higher calorie foods when they eat out. The larger food portions in restaurants further exacerbate this problem (McCrory et al., 2000). One study pointed to an association between the frequency of eating restaurant food and elevated BMI (McCrory et al., 1999). A 1995 survey found that school meals and snacks had the highest saturated-fat density of all foods people eat away from home, including food from restaurants, fast-food outlets, and vending machines (Lin and Frazao, 1997; USDHHS, 2000). Although schools are required to plan menus that comply with U.S. dietary guidelines, these standards do not apply to a la carte foods or to foods sold in snack bars, school stores, or vending machines (USDHHS, 2000). Because many dietary habits are established during childhood (CDC, 1996c; Kelder et al., 1994; USDHHS, 2000), educating school-aged children about nutrition can help them establish healthy eating habits early in life. Implementation of curricula that encourage healthy eating and that provide students with the skills they need to adopt and maintain healthy eating habits has led to positive changes in student dietary behaviors and to reductions in cardiovascular disease risk factors (CDC, 1996c; Contento et al., 1995; Lytle and Achterberg, 1995; USDHHS, 2000).

Similar increases in the incidence of overweight and obesity are evident throughout the world, although rates differ (Flegal, 1999). In Europe obesity is especially prevalent in Southern and Eastern countries, particularly among women (Seidell, 1995). In Sweden, between 1980 and 1996 the prevalence of obesity rose from 9% to 12% in women and from 6.6% to 10% in men (Lissner et al., 2000). Between 1982 and 1994, the percentage of overweight people in New Zealand increased from about 53% to 64% for men and 36.5% to 45% for women (Simmons et al., 1996). In many countries, as in the United States, obesity is an increasing concern in children (for example, Great Britain: Chinn and Rona, 2001; Germany: Kromeyer-Hauschild et al., 1999; Singapore: Ho et al., 1983). Even in the developing world, the rates of obesity are showing increases (Shetty, 1997). As reviewed above for the United States, these international trends are attributed to high fat, energy dense diets and reduced physical activity (Shetty, 1997; Seidell, 1995).

Socioeconomic Characteristics

Although overweight and obesity are increasing among all sociodemographic groups, the prevalence is influenced by specific sociocultural variables, including gender, ethnicity, socioeconomic status, and education. From 1988 to 1994, about one-third of U.S. adults were overweight, with a higher prevalence among poor women (46%) (NCHS, 1998a). A clear gradient with family income exists for the prevalence of overweight in women (but not in men). Poor women are 1.4 times more likely to be overweight than are middle-income women and 1.6 times more likely to be overweight than are women with high incomes (NCHS, 1998a). Obesity is particularly common among Hispanic, African American, Native American, and Pacific Islander women (USDHHS, 2000).

Populations also differ in amount of physical activity. The proportion of the population reporting no leisure-time physical activity is higher among women than men, among Hispanics than among Whites, among older than younger adults, and among the less affluent than the wealthier (USDHHS, 1996, 2000). A sedentary lifestyle is less likely with increasing income. African American men living in poverty are 3 times more likely to be sedentary than were those with high family incomes. For Hispanic and non-Hispanic White men, a sedentary lifestyle was about 2.5 times more prevalent among the poor than among those with a higher family income. Women had similar income-related gradients in sedentary lifestyle, with higher income groups experiencing a lower prevalence of sedentary lifestyle (NCHS, 1998a).

Adult Weight Gain

Adult weight gain is observed in many industrialized societies. Because full adult height generally is attained by age 18, weight gain in adulthood is almost exclusively through the addition of adipose tissue. Lack of weight gain, particularly among men over 50, does not imply an absence of gain in fat. Above this age, muscle mass is, to varying degrees, redistributed to fat, much of it within the abdomen (Rimm et al., 1995).

Avoiding weight gain as an adult is a high priority because treatment of obesity has poor long-term success, and lost weight often is regained (Chapter 5). Several studies show that greater leisure-time physical activity is associated with lower weight gain (Ravussin et al., 1988; Rissanen et al., 1991), and it reduces the weight gain often observed after cessation of cigarette-smoking (Kawachi et al., 1996). Although many people try to lose weight, most regain the weight within 5 years (NIH, 1993; USDHHS, 2000). In order to maintain weight loss, permanent lifestyle changes that combine good dietary habits, decreased sedentary behavior, and increased physical activity are essential. Changes in the physical and social environment can help people maintain the necessary long-term lifestyle changes both for diet and for physical activity (USDHHS, 2000). Preventing weight gain in the first place also substantially reduces the likelihood that conditions such as hypertension and diabetes will develop (Colditz et al., 1995). A reduction of even 10–15% of body weight in substantially overweight people has been shown to ameliorate hyperglycemia, hyperlipidemia, and hypertension (see Mertens and Van Gaal, 2000; Oster et al., 1999; de Leiva, 1998; Goldstein, 1992).

Weight and Disease

Several authors have pointed out the consequences of overweight and obesity for morbidity and mortality (Allison et al., 1999; Calle et al., 1999; Must et al., 1999). A linear relationship exists between adiposity and most health conditions. The shape of the curve for mortality has been debated, in part because of excess mortality among the leanest people. The positive relationship between leanness and mortality is confounded by cigarette-smoking (smokers tend to be leaner but also are at higher risk of disease), and by reverse causation—the major illnesses that predispose to death lead first to weight loss. The effect of disease on weight might result in the leaner segment of the population being overrepresented among those at a higher risk of death.

Observed statistical associations between weight and mortality have driven recommendations for weight guidelines, but setting the guidelines has been problematic because of the U-shaped relationship described above, and recommendations have varied over time. The Dietary Guidelines Advisory Committee (USDA and USDHHS, 1995a) concluded that mortality risk increased significantly among persons with a BMI of 25 or higher (Lee and Paffenbarger, 1992; Rimm et al., 1995; Willett et al., 1995), whereas a linear increase in risk of diabetes, hypertension, and coronary heart disease begins well below that value (Chan et al., 1994; Colditz et al., 1995; Willett et al., 1995). A 2- to 4-fold increase in risk of these diseases is observed among those with BMI 24–25, compared with those whose BMI is 21. The lower cut-point for the healthy weight range is set at a BMI of 19, below which a person is considered excessively thin and at risk of other health complications (USDHHS, 2000; USDA, 1995a; USDA and USDHHS, 1995a, b).

Diet and physical activity are behaviors that have a direct influence on weight. However, they may also have direct effects on diseases. These direct and indirect actions are explored below in examples of diseases.

Cardiovascular Diseases

Several cohort studies have documented the adverse cardiovascular health effects experienced by overweight adults. In part, cardiac failure develops as a consequence of the increased demands on the heart to supply blood to the increased body fat (Kopelman, 2000). The Nurses Cohort Study (Willet et al., 1995) demonstrated a 2-fold increase in coronary heart disease in overweight women and a 3.6-fold increase with obesity. Similarly, the Framingham Heart Study showed increased incidence in heart disease proportionate to excess weight (Hubert et al., 1983). Adult weight gain is an additional risk (Hubert et al., 1983). For example, compared with men and women who maintained weight to within 2 kg of their weight at age 18–20, those who gained 5–9.9 kg experienced a 1.5-to 2-fold higher risk of coronary heart disease (Rimm et al., 1995; Willett et al., 1995) and hypertension (Ascherio et al., 1992; Huang, 1998).

Many studies show that physically active people have a substantially lower risk of coronary heart disease than do the inactive (Berlin and Colditz, 1990; Kaplan et al., 1987; Kushi et al., 1997; Leon et al., 1987; Lindsted et al., 1991; Slattery et al., 1989). Prospective data from a cohort study of 72,000 female nurses (40–65 years old in 1986) indicated that walking and vigorous physical activity reduce the incidence of coronary events (Manson et al., 1999). Brisk walking for 3 hours or more each week reduced the risk of coronary disease by 30–40%, and increasing the time or intensity of the physical activity produced even greater reductions in risk (Manson et al., 1999). Several clinical trials suggest that moderate physical activity can produce a similar, or even larger, reduction in blood pressure than vigorous activity does (Hagberg et al., 1989; Marceau et al., 1993; Matsusaki et al., 1992). Although vigorous physical activity rarely is associated with myocardial infarction or sudden cardiac death (USDHHS, 1996), some risks exist. Even persons who exercise regularly have a transient increase in the risk of sudden cardiac death during and immediately after vigorous physical activity (Kohl et al., 1992).

More than 20 prospective studies have addressed components of diet and risk of coronary heart disease (Willett, 1998). Research in humans and laboratory animals shows that diets low in saturated fatty acids and cholesterol are associated with low risks and rates of coronary heart disease (USDHHS, 2000). Although consumption of trans-fatty acids increases the risk of coronary heart disease (Ascherio et al., 1994; Expert Panel on Trans Fatty Acids and Coronary Heart Disease, 1995; Hu et al., 1997; Willett et al., 1993, Willett and Ascherio, 1994), eating foods higher in polyunsaturated fat and monounsaturated fat decreases the risk of coronary heart disease. In addition, fiber intake is strongly protective against coronary heart disease (Willett, 1998). Emerging evidence suggests that low folate and high circulating concentrations of homocysteine are major contributors to risk of coronary heart disease and stroke (Boushey et al., 1995; Chasan-Taber et al., 1996; Rimm et al., 1996; Selhub et al., 1995). Vitamin E appears to reduce the risk of coronary heart disease (Rimm et al., 1993; Stampfer et al., 1993).

Cancer

Obesity has been associated with an increased risk for some forms of cancer. The data have been most consistent for postmenopausal breast cancer (Barnes-Josiah et al., 1995; Huang et al., 1997) and endometrial cancer (Le Marchand et al., 1991). A prospective study by Sonnenschein et al, (1999) reported a relative risk for breast cancer of 2.36 in postmenopausal women in the fourth quartile of BMI. Women in this weight range also showed a 4-fold greater risk for endometrial cancer (Goodman et al., 1997). The mechanisms of these effects are not known, but they could be related to levels of sex hormones.

Physical inactivity has been examined as a contributing factor in a variety of cancers. Many studies conducted in men show an inverse relationship between physical activity and risk of colon cancer (Giovannucci et al., 1995; Lee et al., 1991; Severson et al., 1989; Slattery et al., 1988; Whittemore et al., 1990; Wu et al., 1987). A large prospective cohort study in women found a similarly strong inverse association between physical activity and colon cancer (Martinez et al., 1997). Physical activity not only increases intestinal motility (Thor et al., 1985) and aids in the suppression of colon cell proliferation (Lee, 1994; Shephard et al., 1991), but it is hypothesized to decrease gastrointestinal transit time (Lee, 1994; Shephard, 1993) and thus the duration of contact between the colon mucosa and potential carcinogens.

Increased physical activity has been hypothesized to prevent breast cancer by reducing cumulative lifetime exposure to circulating ovarian hormones (Kramer and Wells, 1996). However, the epidemiologic findings are inconsistent. Several studies report reductions in breast cancer risk with more physical activity (Bernstein et al., 1994; D'Avanzo et al., 1996; Mittendorf et al., 1995; Thune et al., 1997); others found a modest association at best (Albanes et al., 1989; Chen et al., 1997; Friedenreich and Rohan, 1995; Gammon et al., 1998; McTiernan et al., 1996; Rockhill et al., 1998) or even increased risk (Albanes et al., 1989; Dorgan et al., 1994). Similarly, findings from studies on the relationship between physical activity and prostate cancer are inconsistent (USDHHS, 1996).

Diet also could be an etiologic factor in cancer. For instance, evidence indicates that low folate intake works a role in the development of colon cancer (Freudenheim et al., 1991; Giovannucci et al., 1998; Mason and Levesque, 1996). A consistent relationship between intake of fruit and vegetables and lower risk of many malignancies supports an anticancer effect of some component of these foods (Steinmetz and Potter, 1991). Yet, despite epidemiologic evidence that fruits and vegetables that contain carotenoids reduce the risk of lung cancer (Ziegler et al., 1996), randomized trials of the specific carotenoid, ß-carotene, fail to show any benefit (Albanes et al., 1996; Hennekens et al., 1996). In fact, the ß-Carotene and Retinol Efficacy Trial (Omenn et al., 1996) found an increase in mortality in patients taking supplements of ß-carotene and vitamin A. Evidence linking high-fatty-acid diets with cancer are inconclusive, and there is continuing debate about the relationship between colorectal, prostate, and breast cancers and total fat content or type of fat in the diet (NRC 1989; Ip and Carroll, 1997; USDHHS, 2000). Randomized clinical trials are attempting to clarify the relationship between dietary total fat and the risk of cancer (Freeman et al., 1993; Schatzkin et al., 1996; USDHHS, 2000).

Musculoskeletal Health

Physical activity contributes to the development of bone mass during childhood and adolescence and to the maintenance of skeletal mass during adulthood (USDHHS, 1996). Increased bone mineral density is positively associated with aerobic exercise (Snow-Harter et al., 1996; USDHHS, 2000). Through its load-bearing effect on the skeleton, physical activity influences bone density and bone architecture—the higher the load, the greater the bone mass (Lanyon, 1987, 1993). Conversely, if the skeleton is unloaded, because of inactivity or immobility, bone mass declines.

Calcium intake is essential for the formation and maintenance of bones (USDHHS, 1988b; USDHHS, 2000). Higher calcium intake has been linked to increased bone density in short-term studies, but high protein intake and high dairy calcium intake are both related to increased risk of fractures in long-term prospective studies of men and women (Feskanich et al., 1996, 1997; Owusu et al., 1997, 1998). Because ideal calcium intake for development of peak bone mass has not been determined, it has not been established to what extent increased calcium intake will prevent osteoporosis.

Although most young children meet the dietary requirements for calcium, the intake of calcium declines precipitously with age (USDHHS, 2000). In part as a consequence of inadequate calcium in the diet, osteoporosis is prevalent, affecting more than 25 million people in the United States alone. It is the principal underlying cause of bone fractures in postmenopausal women and the elderly (NIH, 1994; USDHHS, 2000). Physical activity can help. Strength training has been shown to help post-menopausal women preserve bone density (Nelson et al., 1994; USDHHS, 2000).

In addition to strengthening bone, physical activity reduces the risk of fractures in the elderly by increasing muscle strength and balance, thus reducing the risk of falling. Muscle strength has been shown to decline with age, and studies have documented a relationship between muscle strength and physical function (Brown et al., 1995; USDHHS, 2000). However, age-related loss of strength can be attenuated with strengthening exercises and this can help the older population maintain a threshold of strength necessary to perform basic weight-bearing activities, such as walking (Evans, 1995; Tseng et al., 1995; USDHHS, 2000). Thus, regular physical activity can help to maintain the functional independence of the elderly population (Buchner, 1997; LaCroix et al., 1993; Nelson et al., 1994).

Osteoarthritis, the most common form of arthritis, increases with age, and it is the leading cause of activity limitation among older persons (USDHHS, 1996). Although some competitive athletic activities (such as running, soccer, football, and weight-lifting) are associated with increased risk of osteoarthritis in specific joints (USDHHS, 1996), regular noncompetitive physical activity is not harmful to joints (Lane, 1995; Panush and Lane, 1994) and might actually relieve symptoms and improve functioning among persons who already have osteoarthritis or rheumatoid arthritis (Ettinger et al., 1997; Ettinger and Afable, 1994; Fisher and Pendergast, 1994; Minor, 1991).

Physical activity poses some potential risks. Musculoskeletal injury is the most common. Increased risks of roadway accidents also could be associated with running or bicycling on roads, and various sports are associated with specific hazards, such as downhill skiing at high velocities and collisions with other players in football and hockey.

ALCOHOL CONSUMPTION

Alcohol has been identified as a top contributor to death in the United States (McGinnis and Foege, 1993), after tobacco use and diet and activity patterns. Compared with other threats to human health, alcohol causes the widest variety of injuries (Rose, 1992). Approximately 100,000 deaths are related to alcohol consumption in the United States each year (McGinnis and Foege, 1993; Rose, 1992), which translates into 15% of potential years of life lost before the age of 65 (Rose, 1992).

A significant proportion of the U.S. population drinks alcohol. Among current drinkers, 46% report having been intoxicated at least once in the past year, and almost 4% report having been intoxicated weekly (USDHHS, 2000). Almost 10% of current drinkers (approximately 8 million people) meet diagnostic criteria for alcohol dependence, and an additional 7% (more than 5.6 million people) meet diagnostic criteria for alcohol abuse (National Institute on Alcohol Abuse and Alcoholism [NIAAA], 1993; USDHHS, 2000). In 1995, the cost of alcohol abuse and alcoholism was estimated at $167 billion in the United States, of which more than two-thirds was due to lost productivity (Harwood et al., 1998; USDHHS, 2000).

Alcohol use and alcohol-related problems are common among adolescents (O'Malley et al., 1998; USDHHS, 2000). Research shows that the age at which a person starts drinking strongly predicts development of alcohol dependence over a lifetime. Approximately 40% of people who begin drinking before the age of 15 develop alcohol dependence at some stage in their lives. About 10% of people who begin drinking at age 21 or older develop alcohol dependence at some stage in life (Grant and Dawson, 1997; USDHHS, 2000). People with a family history of alcoholism have a higher prevalence of lifetime alcohol dependence than do those with no such history (Grant, 1998; USDHHS, 2000).

Socioeconomic Factors

Studies conducted in 1994–1996 showed that people of both sexes and all races and ethnic groups—with the exception of Hispanic women— displayed a strong inverse relationship between education and heavy alcohol consumption (NCHS, 1998a). Generally, heavy drinking tends to decrease with education, and moderate alcohol use increases with education (NCHS, 1998a; Substance Abuse and Mental Health Services Administration, 1993). In 1994–1996, African American men and women with less than a high school education were almost twice as likely to report heavy alcohol use as were those who had more than a high school education (NCHS, 1998a). White men with high school diplomas were 20% more likely to report heavy alcohol use than were those with more education. White women with less than a high school diploma were 40% more likely to report heavy drinking than were women with more education.

Negative Health Effects

As early as 1926, a U-shaped relationship was described between mortality and consumption of alcohol (Pearl, 1926). The wide range of alcohol-induced illnesses and injuries is primarily attributable to differences in the amount, duration, and patterns of alcohol consumption as well as to differences in genetic vulnerability to particular alcohol-related consequences (USDHHS, 1997a; 2000). Long-term excessive drinking increases risk for high blood pressure, irregularities of heart rhythm (i.e., arrhythmias), disorders of the heart muscle (i.e., cardiomyopathy), and stroke (USDHHS, 2000). Long-term, heavy drinking also increases the risk of developing cancer of the esophagus, mouth, throat, and voice box and of the colon and rectum (NIAAA, 1993; USDHHS, 2000). Alcohol consumption appears to increase the risk of breast cancer in women (Smith-Warner et al., 1998); consumption of two or more drinks per day has been shown to slightly increase women's risk of developing breast cancer (Reichman, 1994; USDHHS, 2000).4 The Dietary Guidelines for Americans (USDA, 1995a) advises women to consume no more than 1 drink per day; while men are advised to consume no more than two per day. Because men and women have less body water as they age, older persons can lower their risk of alcohol problems by drinking no more than one drink per day (Dufour et al., 1992; USDHHS, 2000). Heavy and chronic alcohol use is a cause of poor pregnancy outcomes (NCHS, 1998a; USDHHS, 1993), including fetal alcohol syndrome, a major nongenetic cause of mental retardation (American Academy of Pediatrics, 1993; Bagheri et al., 1998; IOM, 1996). Sustained heavy alcohol consumption worsens the outcome for patients with hepatitis C (NIH, 1997a; USDHHS, 2000) and increases the risk for cirrhosis and other liver disorders (Saadatamand et al., 1997; USDHHS, 2000). Cirrhosis, primarily attributable to heavy drinking, is one of the 10 leading causes of death in the United States (Bureau of the Census, 1997; Hasin et al., 1990; Popham et al., 1984; Saadatamand et al., 1997; Schmidt, 1980).

Progress has been made in reducing the rate of alcohol-related driving fatalities, but it is still a serious problem. Overall, the rate of alcohol-related driving fatalities declined from 9.8 deaths per 100,000 people in 1987 to 6.5 per 100,000 in 1996 (USDHHS, 2000). It is estimated that even at current rates, 3 out of every 10 Americans will be involved in an alcohol-related crash sometime during their lives. The populations of greatest concern for alcohol-related driving fatalities include Native Americans and those between the ages of 15 and 24. In 1994, the alcohol involvement rate in fatal traffic crashes for American Indian and Alaska Native males was 4 times higher (28 per 100,000 population) than for the general population, and, for 15- to 24-year olds, the rate was almost 13 per 100,000 population (USDHHS, 2000).

The consequences of excessive alcohol consumption extend beyond death rates. Alcohol consumption also contributes to risk of injury. In addition to injuries and deaths from traffic accidents, a significant proportion of injuries and deaths from falls, fires, and drowning has been linked with use of alcohol (Saadatamand et al., 1997; USDHHS, 2000). Alcohol consumption contributes to destruction of personal and social relationships (Brookoff et al., 1997); it is a factor in homicide, suicide, marital violence, and child abuse (Roizen, 1993; USDHHS, 2000); and it contributes to high-risk sexual behavior (Strunin and Hingson, 1992, 1993; USDHHS, 2000).

Positive Health Effects

In contrast with those harmful effects, however, evidence is overwhelming of a beneficial effect of moderate consumption of alcohol (1–2 drinks per day) on reducing risk of coronary heart disease and thrombotic stroke. Light-to-moderate drinking can have beneficial effects on the heart, especially among people at greatest risk for heart attacks, including men over age 45 and women after menopause (USDHHS, 2000; Zakhari, 1997). Moderate alcohol-drinking reduces the risk of death from those cardiovascular causes, on the average, by approximately 20–40% (Doll, 1997; Thun et al., 1997). A reduction in cardiovascular disease mortality will translate into a reduction in total mortality in many populations because cardiovascular disease is by far the leading cause of death in middle and old age. The inverse association between alcohol consumption and cardiovascular disease risk is causal: ethanol has been shown in short-term experimental studies to increase the serum concentration of high-density lipoprotein cholesterol (Rimm et al., 1999), and it also appears to affect platelet function and other components of clotting and fibrinolysis (Hendriks et al., 1994; Meade et al., 1987; Renaud et al., 1992).

Quantifying Net Public Health Benefit

The positive and negative effects of alcohol on mortality raise the question, “Is alcohol consumption good for health?” The answer is conditional. The net benefit of alcohol consumption in a population depends on age distribution of the population, because the ratio of mortality from conditions that are prevented by alcohol to mortality from conditions that are made more common by it varies greatly with age. The net benefit also will vary with the population prevalence of factors that predispose to (or protect from) cardiovascular disease, and they might differ in men and women.

Optimal public health guidelines on alcohol consumption are not the same across or even within populations, because the importance of cardiovascular disease and injuries or trauma varies significantly with age and sex as well as from one society to another. For instance, in Sub-Saharan and Latin American countries, the ratio of deaths from coronary heart disease to deaths from violence is close to 1.0, and sometimes even less than 1.0 among men (Murray and Lopez, 1996). Groups inherently at high risk from the detrimental effects of alcohol (such as adolescents and young adults, binge drinkers, and those with lower socioeconomic status) in which deaths from injuries (including motor vehicle injuries), violence, and other external causes are high, have not been included in epidemiologic studies that analyze the alcohol/mortality relationship. For example, among U.S. men aged 15–29, deaths from injuries and other external causes account for 75% of all deaths, compared with 4% from cardiovascular diseases (Schoenborn and Marano, 1988). In another study involving Swedish military recruits in the same age range, a linear increase in risk of death from all causes was found with increasing alcohol consumption (Andreasson et al., 1988).

Although alcohol consumption is unlikely to reduce total mortality in people under 45 (Doll, 1997), the optimal duration of moderate alcohol consumption is not known in terms of reducing risk of cardiovascular disease mortality in older people. Furthermore, even though some of the benefits of alcohol are the result of long-term, habitual consumption (Jackson et al., 1992), many of the important effects of ethanol on high-density lipoproteins and clotting components are acute; thus, it is likely that alcohol consumption beginning in middle age would suffice while avoiding much of the risk of injuries and other external causes of death (although not necessarily of cancers or cirrhosis of the liver).

Optimal alcohol consumption differs for men and women for several reasons. Women metabolize alcohol less efficiently than men do (making women more prone to some health problems than are men who drink the same amount), and because women have less body water than men (making them more prone to intoxication than men after drinking the same amount of alcohol) (USDHHS, 2000). Women also have lower age-specific risks of cardiovascular disease and greater susceptibility to liver damage than men, and women are prone to a relatively high risk of breast cancer, which appears to increase with consumption of any amount of alcohol (Smith-Warner et al., 1998). Although men might be at risk for alcohol-related problems if they consume more than 14 drinks per week or more than 4 drinks per occasion, women could be at risk if they consume more than 7 drinks per week or more than 3 per occasion (USDHHS, 1995, 2000).

The problem of alcohol consumption is frequently one of maldistribution, with many abstaining and many consuming at a hazardous level (Holman and English, 1996). There seems to be no precedent for a public health campaign that simultaneously seeks to “pull in” both tails of a risk factor distribution, in this case reduction of both the prevalence of abstention and of heavy drinking (Holman and English, 1996). There are risks in promoting a population wide alcohol policy that discourages abstention, even if the policy encourages only light-to-moderate regular consumption. First, there is no evidence that moderate drinking is harmless. Second, a public health recommendation that encourages even light drinking over abstention could increase the number of heavy drinkers in a population since it has been noted that population distributions of risk factors tend to shift, either downward or upward, as an entity (Rose, 1992). Researchers have noted that it is unethical for governments and other public institutions to promote low alcohol intake as a disease prevention measure because of the potential adverse risks at the population level, but they also note that it is similarly unethical to promote abstinence (Holman and English, 1996). In an editorial accompanying publication of a large study by the American Cancer Society, a question was raised about whether alcohol consumption is the method of choice for preventing cardiovascular disease. One important consideration is whether physical activity and diet would be as effective as moderate alcohol consumption-with lower risk of harm—in lowering cardiovascular disease mortality (Potter, 1997). The data on physical activity and some dietary factors would seem to suggest that they are equally effective, and they have the additional benefit of reducing risks of many other diseases.

SEXUAL PRACTICES

Sexual relationships and practices are complex to investigate, but their study is important because infectious disease has always been a possible outcome of sexual relationships, as has unwanted pregnancy. Both are crucial public health issues of our time. Recently released figures show that the United States is among the highest in incidence and prevalence of sexually transmitted infection (also called sexually transmitted disease) in the industrialized world (USDHHS, 2000).

Concern about AIDS has been an important motivation for recent studies of sexual behaviors, including a large national survey of sexual behaviors and attitudes (Laumann, 1994). Most of the issues that arise in relating sexual behavior to risk of infection with the human immunodeficiency virus (HIV) pertain to many other, far more common, sexually transmitted infections. But HIV has made unsafe sex a matter of life and death. In 1995, there were more than 43,000 deaths from AIDS in the United States, making it the eighth-leading cause of death in that year, and the leading cause of death among Americans 25–44 years old (Anderson et al., 1997). It is now the second-leading cause of death among all Americans aged 25–44, but it is the leading cause of death for African Americans in this age group (USDHHS, 2000). Other, more common sexually transmitted infections—human papilloma virus, gonorrhea, chlamydia, and genital herpes—vary in the severity of their consequences; but if left untreated, these diseases can compromise health and even become life threatening.

Prevalence of Sexually Transmitted Infections

In 1996, the United States had 15.3 million new cases of sexually transmitted infection. This was higher than the 12 million annual new cases estimated by the Centers for Disease Control and Prevention a decade before (Tanne, 1998). The increase is partly real and partly the result of more sensitive tests that can now identify asymptomatic infection.

More than 68 million Americans now have an incurable sexually transmitted infection (Tanne, 1998); for instance, 1 out of every 5 Americans has genital herpes (Tanne, 1998). Every year, 15 million people are infected with a sexually transmitted disease, almost 4 million of them teenagers (American Social Health Association, 1998; USDHHS, 2000). Sexually transmitted infections are more prevalent in teenagers and young adults than in older persons, partly because of the greater propensity of younger persons to engage in unprotected sex and to switch sexual partners relatively frequently (Laumann, 1994). Despite its prominence in the media, AIDS represents only a tiny proportion of sexually transmitted infections, basically less than half of one percent of all the new cases of sexually transmitted infection (Laumann, 1994). The most commonly reported sexually transmitted infection in the United States is chlamydia, with 3 million new cases each year (Tanne, 1998). The direct and indirect costs of the primary sexually transmitted diseases and their complications, including sexually transmitted HIV infection, are estimated at $17 billion each year (St. Louis et al., 1997; USDHHS, 2000).

Data from a University of Chicago national survey on sexual behaviors (Laumann, 1994) indicate that 16.9% of U.S. adults aged 18–59 years old have had a sexually transmitted infection (15.9% of men, 17.8% of women). The risk of sexually transmitted infection rises monotonically and dramatically with the number of sex partners. Lifetime occurrence of any sexually transmitted infection rises from 4% for those with only one partner after the age of 18 years to 40.4% for those with more than 20 partners. The number of sex partners is the most succinct measure of the extent of exposure to infection. Another important aspect of extent of exposure is type of sexual practice: anal intercourse is an especially efficient way of transmitting infections, especially HIV, because it often leads to small breaks in the skin.

Contributing Factors That Affect Transmission

Although sexually transmitted infections are behavior-linked diseases that result from unprotected sex (IOM, 1997; USDHHS, 2000), other factors contribute to their rapid spread in a population. Because most sexually transmitted infections are asymptomatic, or produce very mild symptoms, they often are disregarded, so infected persons do not seek immediate medical care. About 85% of women and about 50% of men with chlamydia have no symptoms (Fish et al., 1989; Handsfield et al., 1986; Stamm and Holmes, 1990; USDHHS, 2000). There is also a long interval between the acquisition of a sexually transmitted infection and the eventual recognition of a clinically significant health problem; it is sometimes several years before an infection manifests itself. Thus, because the original infection is often asymptomatic, there is frequently no perceived connection between the original sexually acquired infection and the health problem associated with it.

Another contributing biological factor is that women are at higher risk than men for most sexually transmitted diseases, and for some of these infections, young women are more susceptible than older women. This is especially alarming because analyses of adolescent females' sexual activity not only demonstrate the frequency of those behaviors, but also reveal that not all sexually experienced young females willingly enter into a sexual relationship (Abma et al., 1998; USDHHS, 2000). In 1995, more than 16% of females who experienced their first sexual intercourse when they were aged 15 or younger indicated that it was not voluntary (Abma et al., 1997; USDHHS, 2000). Sexual violence against women contributes both directly and indirectly to the transmission of disease. Directly, women who experience this type of violence are less able to protect themselves from sexually transmitted infections or pregnancy (USDHHS, 2000). Indirectly, studies show that sexually abused girls engage in high-risk sexual behaviors such as voluntary intercourse at earlier ages and multiple partners, which are risk factors for sexually transmitted diseases (Miller et al., 1995; Stock et al., 1997).

There is an association between sexually transmitted infections and substance abuse, particularly the abuse of alcohol and other drugs. The introduction of new, illicit substances into communities, for instance, often drastically alters sexual behavior in high-risk sexual networks, thereby causing an epidemic of sexually transmitted diseases (Marx et al., 1991; USDHHS, 2000). The epidemic in crack cocaine use intensified the U.S. syphilis epidemic in the late 1980s (Gunn et al., 1995; USDHHS, 2000).

One social factor that contributes to the spread of sexually transmitted infections in the United States is the stigma connected with them. Another is the overall discomfort many people have with discussing intimate aspects of life, particularly those related to sex (Brandt, 1985; USDHHS, 2000). This is what most significantly separates the United States from industrialized countries that have low rates of sexually transmitted infection. (USDHHS, 2000). Even in the most intimate relationships, talking openly and comfortably about sex and sexuality is difficult for many Americans. A recent survey indicated that approximately one-fourth of married women and one-fifth of married men had no knowledge about their partner's sexual history (EDK Associates, 1995; USDHHS, 2000). The secrecy surrounding sexuality hampers sexuality education programs for adolescents, and it discourages open discussion between parents and their children and between sex partners regarding sexually transmitted diseases. It also impedes balanced messages from mass media, health care professionals' education and counseling activities, and community activism (IOM, 1997; USDHHS, 2000).

Sexually Transmitted Infections and Cancer

Several sexually transmitted viral infections are known or strongly suspected to cause cancer. The most important of these are the sexually transmitted types of human papilloma virus. At least 90% of the approximately 16,000 cases of cervical cancer diagnosed each year are estimated to be attributable to infection with the human papilloma virus (Morrison et al., 1997).

A strong link between hepatitis B and hepatitis C viruses and hepatocellular carcinoma (liver cancer) became evident during the 1980s. Hepatitis B infection occurs more frequently among persons who have multiple sex partners and who also have a history of sexually transmitted infection. An estimated 53,000 cases of hepatitis B virus (out of a total of 200,000– 300,000 cases) were sexually transmitted in the United States in 1994 (IOM, 1997).

Disproportionate Affliction of Sexually Transmitted Infections

Although people in all communities—including all racial, cultural, economic, and religious groups—and sexual networks are at risk for sexually transmitted infections, some are disproportionately affected by these diseases and their associated complications. For instance, not only do sexually transmitted diseases occur more frequently in women than in men, but women also suffer more serious complications (USDHHS, 2000), including pelvic inflammatory disease, ectopic pregnancy, infertility, and chronic pelvic pain (Chandra and Stephen, 1998; USDHHS, 2000). In addition, women are biologically more susceptible to infection when exposed to a sexually transmitted disease agent, and sexually transmitted diseases are more difficult to diagnose in women because of female physiology and the anatomy of the reproductive tract (USDHHS, 2000).

Sexually transmitted diseases pose a risk to unborn children. The diseases not only cause serious health problems in pregnant women, but they can result in the death of the fetus or newborn (Brunham et al., 1990; USDHHS, 2000). Sexually transmitted disease in a mother also can result in congenital or perinatal infections that permanently damage the child's brain, spinal cord, eyes, auditory nerves, or immune system. Sexually transmitted infection can complicate a pregnancy even without directly reaching the fetus or newborn, causing spontaneous abortion, stillbirth, premature membrane rupture, or premature delivery (Goldenberg et al., 1997; USDHHS, 2000). Women with bacterial vaginosis, for instance, are 40% more likely than women without this condition to deliver a preterm, low-birthweight baby (Hillier et al., 1995; Meis et al., 1995; USDHHS, 2000).

Sexually transmitted infections disproportionately affect adolescents and young adults for several reasons, including behavioral, social, and biological (Alan Guttmacher Institute, 1994; USDHHS, 2000). In 1996, 15-to 19-year-olds had the highest reported rates of chlamydia and gonorrhea (USDHHS, 1997b; USDHHS, 2000), and the herpes infection rate of white adolescents between the ages of 12 and 19 was shown to have increased almost 5-fold over just 10 years (Fleming et al., 1997; USDHHS, 2000). Several factors contribute these incidences. Because many teenagers are sexually active, they are at risk for sexually transmitted infections; in 1995, just over 50% of females aged 15–19 indicated they had already had sexual intercourse, and more than 51% of high school males reported having experienced sexual intercourse by age 16. Teenagers are more likely than older persons to have serial sex partners who are active in a sexual network that already is infected with untreated sexually transmitted diseases (USDHHS, 2000).

Rates of sexually transmitted diseases are higher for minority and ethnic groups (primarily African American and Hispanic populations) than for whites. For example, although chlamydia is a widely distributed sexually transmitted infection in all racial and ethnic groups, the prevalence is higher in minorities. In 1996, African Americans accounted for approximately 78% of the total number of gonorrhea cases reported—32 times the rate for whites. These high rates also apply to African American adolescents and young adults, with the average about 24 times higher than that for 15- to 19-year-old white adolescents and 30 times higher than for 20- to 24 year-old whites in 1996. In 1996, the gonorrhea rate for Hispanics was 3 times the rate for whites. Since 1990, syphilis rates have declined in all racial and ethnic groups, except for American Indians and Alaska Natives, but the rates for African Americans and Hispanics continue to be greater than those for non-Hispanic whites. In 1996. African Americans accounted for approximately 84% of all reported cases of syphilis (USDHHS, 2000).

Young, heterosexual women, especially minorities, are increasingly acquiring HIV infection and developing AIDS. In 1996, 39% of the reported AIDS cases occurred in 13- to 24-year-olds and, of the AIDS cases reported in women, almost 4 of every 5 occurred in the minority population, consisting primarily of African Americans or Hispanics (USDHHS, 2000).

Prevention of Sexually Transmitted Infections

Behavioral means for prevention of sexually transmitted infections include delaying the onset of sexual activity, limiting the number of partners, abstaining from sex with people not known to be infection free, and using effective barrier contraception.

Community-focused interventions also are useful in reducing sexually transmitted infections. Such interventions generally aim to change behavioral norms. Research conducted in the past decade has shown that sexual behavior and sexual preference exhibit persistent social regularities, which implies that social forces are important in shaping sexual expression (Laumann, 1994). Thus, changing norms that encourage safe sexual behaviors holds great potential for reducing the population burden of sexually transmitted infections. Mass media campaigns, for example, have used reinforcing messages to increase knowledge about HIV infection and ways to prevent it. Because only a small percentage of adolescents receive any prevention information from parents, and because for most teenagers schools are the main source of information about sexually transmitted infections, school-based interventions can be significant in motivating young people to modify their behaviors (American Social Health Association, 1996; USDHHS, 2000). In fact, most states and school districts now require teaching about prevention of sexually transmitted infections (IOM, 1997). Curricula including information about both abstinence and contraceptive use appear to be effective in delaying the onset of sexual intercourse and in encouraging contraceptive use once intercourse has begun (IOM, 1997). Currently available contraceptives differentially affect risk of pregnancy and sexually transmitted infections. There is a contraceptive trade-off dilemma with currently existing methods: the contraceptives with the best record of preventing pregnancy have the worst record for preventing sexually transmitted infections (Cates, 1996). For instance, oral contraceptives are highly effective at preventing pregnancy, but offer no protection against sexually transmitted infections. Furthermore, they appear to increase risk of cervical chlamydial infection (Cottingham and Hunter, 1992). Intrauterine devices, also effective in preventing pregnancy, are associated with pelvic inflammatory disease, especially in the first month after insertion (Farley et al., 1992). The condom is effective at preventing sexually transmitted diseases, but it is less effective than are other contraceptive methods for preventing pregnancy (USDHHS, 2000). For such reasons, use of dual methods of contraception could help prevent unwanted pregnancies and transmission of infections (Cates and Stone, 1992; USDHHS, 2000).

DISEASE SCREENING PRACTICES

Screening asymptomatic persons to detect preclinical disease has become an important part of public health. But preclinical screening makes sense only if treatment initiated earlier in the disease process will reduce morbidity and mortality from the disease: there is no benefit in living with a diagnosis if a person's life or quality of life is not extended. Although some screening tests can be highly effective in reducing morbidity and mortality, others are of unproven benefit. Poor specificity can produce a large number of false-positives, which in turn can lead to unnecessary and potentially harmful follow-up with diagnostic testing and treatment and needless psychological distress.

The selection of appropriate tests for a given individual depends primarily on that person's age and sex. In addition, consideration of individual risk factors, such as lifestyle or family history, often is used to determine which tests are appropriate tests and how often testing should be done.

In 1984, the U.S. Public Health Service commissioned the U.S. Preventive Services Task Force. This panel was charged with developing recommendations for clinicians on the appropriate use of preventive interventions, including screening for preclinical disease and screening for disease risk, based on a systematic review of evidence of clinical effectiveness. In 1989, the first Guide to Clinical Preventive Services (U.S. Preventive Services Task Force, 1989) was published. In 1990, the task force was reconvened to continue and update the scientific review process through examination of new and emerging evidence on preventive interventions. The second edition of the Guide to Clinical Preventive Services (U.S. Preventive Services Task Force, 1996) was published in 1996. Much of the discussion below concerning screening tests for the major chronic diseases of middle and older age derives from that Guide.

According to the task force, screening must satisfy two major requirements to be considered effective for use in a population. First, the test must be able to detect the target condition earlier than would be possible without screening and with enough accuracy to preclude large numbers of false-positive and false-negative results. Second, screening for and treating persons with early disease should improve the likelihood of favorable health outcomes (e.g., reduced disease-specific morbidity or mortality) as compared with what would happen in treating patients who present on their own with signs or symptoms of the disease. In addition, the tests must be cost-effective and acceptable to the target population (fear of or distaste for colorectal screening and tests involving drawing of blood, for example, could prevent some people from participating). Documented effectiveness should be the most basic requirement for providing a health care service (U.S. Preventive Services Task Force, 1996).

Primary versus Secondary Prevention

Primary prevention aims to reduce the incidence of disease; secondary prevention attempts to prevent the prevalence of disease, usually by shortening the course of the disease through early and effective intervention. Screening, as a component of early detection of extant disease, is one aspect of secondary prevention. However, some forms of screening, such as high-blood-cholesterol or high-blood-pressure screening, can be thought of as primary prevention for cardiovascular disease—they are in essence screening for risk of disease. As the tests have become better able to detect very early stages of such diseases as cancer (for example, in situ breast cancer and very small colon polyps), the boundary between primary and secondary prevention has blurred.

The following is a summary of general guidelines for screening for the major chronic diseases of middle and older ages. For people with unusual family histories of disease, or other medical concerns, screening procedures can vary at the discretion of the physician.

Screening for Hypertension and High Blood Cholesterol

The U.S. Preventive Services Task Force recommends screening for hypertension for all children and adults (U.S. Preventive Services Task Force, 1996). The prevalence of hypertension increases with age, and it is more common in African Americans than whites. It is estimated that 40– 50 million Americans have hypertension (Burt et al., 1995). Office sphygmomanometry (use of the blood pressure cuff) is the most appropriate way to screen for hypertension in the general population. However, there are special problems with accuracy when testing children under the age of 3. (The definition of hypertension in childhood is somewhat arbitrary, based on age-specific percentiles.)

There is a positive relationship between the magnitude of blood pressure elevation and the benefits of treatment. In persons with malignant hypertension, the benefits of treatment are most dramatic: treatment increases 5-year survival from near 0 to 75% (Hansson, 1988). The efficacy of treating less severe hypertension has been demonstrated in randomized clinical trials. The greatest benefits are associated with reduction in morbidity and mortality from stroke. Improved detection and treatment of high blood pressure is responsible for a substantial portion of the greater than 50% reduction in age-adjusted stroke mortality that has been observed in this country since 1972 (Joint National Committee on Detection and Treatment of High Blood Pressure, 1993). The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure and the American Heart Association recommend blood pressure measurement at least once every 2 years for adults with a diastolic blood pressure below 85 mm Hg (millimeters of mercury) and a systolic pressure below 130 mm Hg. More frequent testing is recommended for persons with higher measures, with frequency depending on degree of elevation. The American Academy of Pediatrics, the American Medical Association, and the American Heart Association recommend that children and adolescents have their blood pressure monitored every 1 or 2 years during regular office visits to a physician (U.S. Preventive Services Task Force, 1996).

Along with hypertension, elevated blood cholesterol is a major modifiable risk factor for cardiovascular disease. Total cholesterol can be measured in venipuncture or fingerstick specimens from fasting or nonfasting individuals. Because of normal physiologic variation and measurement error, a single cholesterol measurement might not reflect a person's true average concentration. A single measurement of blood cholesterol can vary by as much as 14% from an individual's average value, under normal laboratory circumstances (Cooper et al., 1992). For this reason, some experts advise telling people their “cholesterol range,” rather than providing them with a single value (Belsey and Baer, 1990). When a precise estimate of blood cholesterol is needed, an average of two or three measures has been recommended.

Based on evidence from clinical trials showing that lowering serum cholesterol can reduce risk of coronary heart disease, periodic screening for high blood cholesterol (once every 5 years) is recommended for all men aged 35–65 (U.S. Preventive Services Task Force, 1996). Although there are few trial data pertaining to women, the epidemiology and pathophysiology of coronary heart disease is similar in men and women, and it is likely that reduction of high cholesterol will benefit women as well. However, the later onset of coronary heart disease in women, due to protection from estrogen, suggests that routine screening for high cholesterol in women should begin around age 45. Thus, periodic screening is recommended for women aged 45–65 (U.S. Preventive Services Task Force, 1996).

According to the U.S. Preventive Services Task Force, there is insufficient evidence to recommend for or against routine screening of all asymptomatic persons over age 65. Cholesterol appears to plateau by age 65 in women, and earlier in men (U.S. Preventive Services Task Force, 1996). Continued screening, therefore, would be less important in persons who have shown desirable concentrations throughout middle age. However, screening in older persons might be recommended on a case-by-case basis. Older persons with important coronary heart disease risk factors, such as smoking, hypertension, or diabetes, could be more likely to benefit from screening, based on their high risk of coronary heart disease and the proven benefits of lowering cholesterol in older persons with symptomatic coronary heart disease. There is also insufficient evidence to recommend for or against routine screening in children, adolescents, or young adults; again, however, screening could be recommended for people who have a family history of very high cholesterol, premature coronary heart disease in a first-degree relative, or major risk factors for coronary heart disease.

Cervical Cancer Screening

Approximately 16,000 women are diagnosed with cervical cancer each year in the United States, and 4800 women die from the disease annually (NCHS, 1998b). The 5-year survival rate is about 90% for women with localized cervical cancer but is only about 14% for women with advanced disease (NCHS, 1998b). The incidence of invasive cervical cancer has decreased greatly over the past 40 years, due largely to organized screening programs to detect early-stage disease (U.S. Preventive Services Task Force, 1996). Women with a history of multiple sexual partners, early age at onset of sexual intercourse, or both, are at highest risk of cervical cancer. Infection with HIV or some types of the human papilloma virus sharply increases risk.

The Pap smear is the principal screening test for cervical cancer. The U.S. Preventive Services Task Force, American Cancer Society, the National Cancer Institute, the American College of Obstetricians and Gynecologists, and the American Medical Association recommend that all women who are or have been sexually active, or who are 18 years of age or older, should have annual Pap smears. The recommendation permits Pap testing less frequently after 3 or more normal annual smears, at the discretion of individual physicians. There is no consensus on the age at which to discontinue Pap testing.

Colorectal Cancer Screening

Colorectal cancer is the second-most-common form of cancer in the United States, after lung cancer, and is the second-leading cause of cancer death. Each year, about 140,000 new cases are diagnosed, and 55,000 persons die of the disease (NCHS, 1998b). The average patient who dies of colorectal cancer loses 13 years of life, and in addition to the mortality associated with this disease, its treatment can produce significant morbidity. Screening for early-stage colorectal cancer as well as its precursor lesions (adenomatous polyps) thus can significantly reduce morbidity and mortality associated with colorectal cancer.

Colorectal cancer screening can act as both primary and secondary prevention because the tests can detect and (in the case of sigmoidoscopy and colonoscopy) remove precancerous polyps as well as carcinomas. The principal tests for detecting polyps and early malignancy in asymptomatic persons are the fecal occult blood test (FOBT) and flexible sigmoidoscopy. There is a large literature on the accuracy and effectiveness of these tests under varying conditions and in different groups of persons. As reviewed by the Preventive Services Task Force (1996), it is estimated that most positive reactions to FOBT (70–90%) are falsely positive for colorectal cancer. However, despite its low positive predictive value, FOBT is effective in reducing colorectal cancer mortality, especially when done annually (Towler et al., 1998). Unlike FOBT, flexible sigmoidoscopy is both a screening and diagnostic tool; any polyps detected can be biopsied and removed during the procedure. Evidence shows that screening with sigmoidoscopy reduces both incidence of and mortality from colorectal cancer (U.S. Preventive Services Task Force, 1996).

Screening for colorectal cancer is recommended by a variety of groups for all persons aged 50 years and older, although there is no consensus about whether FOBT or sigmoidoscopy, or a combination of the two, produces the greatest benefit. For persons with a family history of colorectal cancer, screening is recommended to begin at an earlier age, particularly if a family member was diagnosed with colorectal cancer at a young age. For persons with a family history of hereditary syndromes associated with very high risk of colorectal cancer, and for those with a previous diagnosis of high-risk adenomatous polyps or colon cancer, regular screening with colonoscopy (at least once a year) is part of routine management. As mentioned above, FOBT screening should be performed annually to achieve maximum benefit. There is insufficient evidence to determine the optimal screening interval for sigmoidoscopy; however, a frequency of 3–5 years has been recommended by some expert groups.

Prostate Cancer Screening

Prostate cancer is the most common non-skin cancer among American men. After lung cancer, it accounts for more cancer deaths in men than any other. Each year about 245,000 men are diagnosed with prostate cancer, and 40,000 die (NCHS, 1998b). The PSA (prostate-specific antigen) test is the principal screening test for prostate cancer. Although this test has adequate sensitivity to detect clinically important cancers at an early stage, it is also likely to detect a large number of cancers of uncertain clinical significance. Because treatment for prostate cancer can cause substantial morbidity as a result of impaired sexual, urinary, and bowel function, and because prostate cancer also carries a nonnegligible mortality risk (estimated 0.7%–2% 30-day mortality risk [Murphy et al., 1994; Wasson et al., 1993]), the question of which cancers should be treated after detection with PSA testing is critical

The absence of proof that screening can reduce mortality from prostate cancer, together with the strong potential that screening will increase treatment-related morbidity, argue against a policy of routine screening in asymptomatic men. Thus, the U.S. Preventive Services Task Force (1996) does not recommend routine screening for prostate cancer. However, the American Cancer Society does recommend yearly PSA testing beginning at age 50 for white men and at age 40 for African American men, in whom risk of the disease is higher.

Breast Cancer Screening

Each year, some 180,000 women are diagnosed with breast cancer in the United States (NCHS, 1998b). This accounts for about 30% of all incident cancers among women. Each year, 44,000 women die of breast cancer (NCHS, 1998b), making it the second-leading cause of cancer deaths among American women, after lung cancer. Breast cancer is extremely rare among women younger than 20, and is uncommon among women under the age of 30. Incidence rates increase sharply with age, however, and become substantial before age 50 years. Rates continue to rise, although less quickly, in postmenopausal women.

As reviewed by the U.S. Preventive Services Task Force (1996), several clinical trials conducted among women aged 40 years and older have shown an overall reduction of breast cancer mortality due to screening. The average reduction is 20–30% (over roughly a 10-year period) for women aged 50–69 who are screened periodically for breast cancer (U.S. Preventive Services Task Force, 1996). However, there is no consensus about the optimal screening interval for women in this age group. Although annual screening has been recommended by many groups, an analysis of data from Sweden revealed little evidence that screening every year provides a greater benefit than does screening every 2 years (Tabar et al., 1987).

Based on data from clinical trials, there is disagreement in the scientific community over whether routine mammographic screening should be recommended for women in their forties. This disagreement has at times been strident and strong (Taubes, 1997). Although none of the randomized clinical trials enrolled enough women in their forties to study the benefit of screening in this age group with statistical confidence, a summary analysis of the trials nonetheless suggested a benefit. The magnitude (10–15% reduction in breast cancer mortality risk over roughly a 10-year period) was smaller than the benefit observed in women aged 50 and older (U.S. Preventive Services Task Force, 1996). A consensus conference convened by NIH in 1997 to examine the question of whether regular mammography screening should be recommended for women in their forties. The group concluded that the decision to screen should be made by individual women in consultation with their physicians (NIH, 1997b). The American College of Physicians, the U.S. Preventive Services Task Force, and the National Cancer Institute agree with that conclusion, but other groups (the American Cancer Society, the American College of Obstetricians and Gynecologists, and the American Medical Association) defer, recommending annual routine mammography for women aged 40–49 (U.S. Preventive Services Task Force, 1996). A detailed review of the literature on behavior change and health communication issues associated with mammography is provided in an IOM report (2001b).

Screening for Sexually Transmitted Diseases

Screening and treatment of sexually transmitted diseases affect both transmission and duration. Studies show that screening for sexually transmitted diseases meets criteria for a successful preventive intervention (USDHHS, 2000; U.S. Preventive Services Task Force, 1996). During the 1990s, for example, significant progress was made toward reducing the burden of disease of the common bacterial sexually transmitted diseases in the United States (i.e., gonorrhea and syphilis) (USDHHS, 2000). For those diseases that often are asymptomatic, research indicates that screening and proper treatment even benefit people who are likely to suffer acute complications if infections are not detected and treated early (Hillis et al., 1995; USDHHS, 2000). For instance, data are becoming available indicating that chlamydia screening is reducing disease burden and preventing associated complications (USDHHS, 2000). In a randomized, controlled trial conducted by a managed care organization, screening for chlamydia was demonstrated to reduce the incidence of subsequent pelvic inflammatory disease by 56% in a screened group (Scholes et al., 1996; USDHHS, 2000). Selective chlamydia screening in the Pacific North-west decreased disease burden by 60% in 5 years in the screened population (Britton et al., 1992; USDHHS, 2000).

Testing has been identified, as has counseling, as an effective tool for assisting HIV-infected individuals both in coping with their infections and in preventing them from infecting other people. The combination of counseling and testing provides the opportunity to guide people with seronegative test results on behaviors and strategies for avoiding infection, in addition to referring them to other needed medical and social services. After the 1994 findings that perinatal HIV transmission rates could be considerably reduced with zidovudine therapy, the Public Health Service issued guidelines suggesting that HIV counseling and voluntary testing be a part of routine prenatal care for pregnant women (USDHHS, 2000). A primary objective of this policy is to ensure that HIV-infected women have access to adequate health care for themselves and have the opportunity to reduce the risk of HIV transmission to their babies.

REFERENCES

  1. Abma J, Chandra A, Mosher W, Peterson L, Piccinino L. Fertility, family planning, and women's health: New data from the 1995 National Survey of Family Growth. National Center for Health Statistics. Vital Health Statistics. 1997;23:1–114. [PubMed: 9201902]
  2. Abma J, Driscoll A, Moore K. Young women's degree of control over first intercourse: An exploratory analysis. Family Planning Perspectives. 1998;30:12–18. [PubMed: 9494810]
  3. Alan Guttmacher Institute. Sex and America's Teenagers. New York: Alan Guttmacher Institute; 1994.
  4. Albanes D, Blair A, Taylor PR. Physical activity and risk of cancer in the NHANES I population. American Journal of Public Health. 1989;79:744–750. [PMC free article: PMC1349635] [PubMed: 2729471]
  5. Albanes D, Heinonen OP, Taylor PR, Virtamo J, Edwards BK, Rautalahti M, Hartman AM, Palmgren J, Freedman LS, Haapakoski J, Barrett MJ, Pietinen P, Malila N, Tala E, Liippo K, Salomaa ER, Tangrea JA, Teppo L, Askin FB, Taskinen E, Erozan Y, Greenwald P, Huttunen JK. Alpha-tocopherol and beta-carotene supplements and lung cancer incidence in the alpha-tocopherol, beta-carotene cancer prevention study: effects of base-line characteristics and study compliance. Journal of the National Cancer Institute. 1996;88:1560–1570. [PubMed: 8901854]
  6. Allison DB, Fontaine KR, Manson JE, Steverns J, VanItallie TB. Annual deaths attributable to obesity in the United States. Journal of the American Medical Association. 1999;282:1530–1538. [PubMed: 10546692]
  7. American Academy of Pediatrics Committee on Substance Abuse and Committee on Children with Disabilities. Fetal alcohol syndrome and fetal alcohol effects. Pediatrics. 1993;91:1004–1006. [PubMed: 8507280]
  8. American Social Health Association. Teenagers know more than adults about STDs, but knowledge among both groups is low. STD News. 1996;3:1–5.
  9. American Social Health Association. Sexually Transmitted Diseases in America: How Many Cases and at What Cost? Menlo Park, CA: Kaiser Family Foundation; 1998.
  10. Anderson R, Kochanek K, Murphy S. Report of Final Mortality Statistics, 1995. Hyattsville, MD: US Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Health Statistics; 1997.
  11. Andreasson S, Allebeck P, Romelsjo A. Alcohol and mortality among young men: Longitudinal study of Swedish conscripts. The British Medical Journal. 1988;296:1021–1025. [PMC free article: PMC2545555] [PubMed: 3130122]
  12. Ascherio A, Hennekens CH, Buring JE, Master C, Stampfer MJ, Willett WC. Trans fatty acids intake and risk of myocardial infarction. Circulation. 1994;89:94–101. [PubMed: 8281700]
  13. Ascherio A, Rimm EB, Giovannucci EL, Colditz GA, Rosner B, Willett WC, Sacks F, Stampfer MJ. A prospective study of nutritional factors and hypertension among US men. Circulation. 1992;86:1475–1484. [PubMed: 1330360]
  14. Bagheri MM, Burd L, Martsolf JT, Klug MG. Fetal alcohol syndrome: Maternal and neonatal characteristics. Journal of Perinatal Medicine. 1998;26:263–269. [PubMed: 9846300]
  15. Barnes-Josiah D, Potter JD, Sellers TA, Himes JH. Early body size and subsequent weight gain as predictors of breast cancer incidence (Iowa, United States) Cancer Causes and Control. 1995;6:112–118. [PubMed: 7749050]
  16. Belsey R, Baer D. Cardiac risk classification based on lipid screening. Journal of the American Medical Association. 1990;263:1250–1252. [PubMed: 2304241]
  17. Berlin J, Colditz G. A meta-analysis of physical activity in the prevention of coronary heart disease. American Journal of Epidemiology. 1990;132:612–628. [PubMed: 2144946]
  18. Bernstein L, Henderson BE, Hanisch R, Sullivan-Halley J, Ross RK. Physical exercise and reduced risk of breast cancer in young women. Journal of the National Cancer Institute. 1994;86:1403–1408. [PubMed: 8072034]
  19. Boushey CJ, Beresford SAA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease: probable benefits of increasing folic acid intakes. Journal of the American Medical Association. 1995;274:1049–1057. [PubMed: 7563456]
  20. Brandt A. No Magic Bullet: A Social History of Venereal Disease in the United States Since 1880. New York: Oxford University Press; 1985.
  21. Britton T, DeLisle S, Fine D. STDs and family planning clinics: A regional program for chlamydia control that works. American Journal of Gynecological Health. 1992;6:80–87. [PubMed: 12319293]
  22. Brookoff D, O'Brien K, Cook C, Thompson T, Williams C. Characteristics of participants in domestic violence. Assessment at the scene of domestic assault. Journal of the American Medical Association. 1997;277:1369–1373. [PubMed: 9134942]
  23. Brown M, Sinacore DR, Host HH. The relationship of strength to function in the older adult. Journal of Gerontology. 1995;50A:55–59. [PubMed: 7493219]
  24. Brunham R, Holmes K, Embree J. Sexually transmitted diseases in pregnancy. In: Holmes K, Mardh P, Sparling P, Weisner P, Cates W, Lemon S, et al., editors. Sexually Transmitted Diseases. 2nd. New York: McGraw-Hill; 1990.
  25. Buchner DM. Preserving mobility in older adults. Western Journal of Medicine. 1997;167:258–264. [PMC free article: PMC1304541] [PubMed: 9348757]
  26. Bureau of the Census. Statistical Abstract of the United States: 1997. 117th. Washington, DC: Department of Commerce; 1997.
  27. Burt V, Whelton P, Roccella E, Brown C, Cutler JA, Higgins M, Horan MJ, Labarthe D. Prevalence of hypertension in the U.S. adult population: Results from the Third National Health and Nutrition Examination Survey, 1988–1991. Hypertension. 1995;25:305–313. [PubMed: 7875754]
  28. Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW. Body-mass index and mortality in a prospective cohort of U.S. adults. The New England Journal of Medicine. 1999;341:1097–1105. [PubMed: 10511607]
  29. Cates W, Stone K. Family planning, sexually transmitted diseases, and contraceptive choice: A literature update. Family Planning Perspectives. 1992;24:75–84. [PubMed: 1612146]
  30. Cates W Jr. Contraception, unintended pregnancies, and sexually transmitted diseases: Why isn't a simple solution possible? American Journal of Epidemiology. 1996;143:311–318. [PubMed: 8633614]
  31. CDC (Centers for Disease Control and Prevention) Smoking cessation during previous year among adults—United States, 1990 and 1991. Morbidity and Mortality Weekly Report. 1993;42:504–507. [PubMed: 8515740]
  32. CDC (Centers for Disease Control and Prevention) Projected smoking-related deaths among youth—United States. Morbidity and Mortality Weekly Report. 1996a;45:971–974. [PubMed: 8965796]
  33. CDC (Centers for Disease Control and Prevention) Cigarette smoking before and after an excise tax increase and an antismoking campaign. Morbidity and Mortality Weekly Report. 1996b;45:966–970. [PubMed: 8965795]
  34. CDC (Centers for Disease Control and Prevention) Guidelines for school health programs to promote lifelong healthy eating. Morbidity and Mortality Weekly Report. 1996c;45 (RR-9):1–42. [PubMed: 8637498]
  35. CDC (Centers for Disease Control and Prevention) Cigarette smoking among adults—United States, 1995. Morbidity and Mortality Weekly Report. 1997a;46:1217–1220. [PubMed: 9427212]
  36. CDC (Centers for Disease Control and Prevention) State-specific prevalence of cigarette smoking among adults, and children's and adolescents' exposure to environmental tobacco smoke—United States. Morbidity and Mortality Weekly Report. 1997b;46:1038–1043. [PubMed: 9370224]
  37. CDC (Centers for Disease Control and Prevention) Monthly Vital Statistics Report. Supplement 2. Vol. 45. Atlanta: National Center for Health Statistics; 1997c. Report of Final Mortality Statistics, 1995.
  38. CDC (Centers for Disease Control and Prevention) Youth risk behavior survey, United States, 1997. Morbidity and Mortality Weekly Report. 1998;47:1–31.
  39. Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men. Diabetes Care. 1994;17:961–969. [PubMed: 7988316]
  40. Chandra A. Health aspects of pregnancy and childbirth: United States, 1982-88. Vital Health Statistics. 1995;23:1–74. [PubMed: 7571475]
  41. Chandra A, Stephen E. Impaired fecundity in the United States: 1982–1995. Family Planning Perspectives. 1998;30:34–42. [PubMed: 9494814]
  42. Chasan-Taber L, Selhub J, Rosenberg IH, Malinow MR, Terry P, Tishler PV, Willett W, Hennekens CH, Stampfer MJ. A prospective study of folate and vitamin B6 and risk of myocardial infarction in US physicians. Journal of the American College of Nutrition. 1996;15:136–143. [PubMed: 8778142]
  43. Chen CL, White E, Malone KE, Daling JR. Leisure-time physical activity in relation to breast cancer among young women (Washington, United States) Cancer Causes and Control. 1997;8:77–84. [PubMed: 9051326]
  44. Chinn S, Rona RJ. Prevalence and trends in overweight and obesity in three corss sectional studies of British children, 1974–94. British Medical Journal. 2001;322:24–26. [PMC free article: PMC26603] [PubMed: 11141148]
  45. Colditz GA, Willett WC, Rotnitzky A, Manson JE. Weight gain as a risk factor for clinical diabetes mellitus in women. Annals of Internal Medicine. 1995;122:481–486. [PubMed: 7872581]
  46. Contento I, Balch GI, Bronner YL, et al. Nutrition education for school-aged children. Journal of Nutrition Education. 1995;27:298–311.
  47. Cooper G, Myers G, Smith S, Schlant R. Blood lipid measurements: Variations and practical utility. Journal of the American Medical Association. 1992;267:3009–3014. [PubMed: 1542176]
  48. Cottingham J, Hunter D. Chlamydia trachomatis and oral contraceptive use: A quantitative review. Genitourinary Medicine. 1992;8:209–216. [PMC free article: PMC1194875] [PubMed: 1398654]
  49. D'Avanzo B, Nanni O, La Vecchia C, Franceschi S, Negri E, Giacosa A, Conti E, Montella M, Talamini R, Decarli A. Physical activity and breast cancer risk. Cancer Epidemiology, Biomarkers and Prevention. 1996;5:155–160. [PubMed: 8833614]
  50. de Leiva A. What are the benefits of moderate weight loss? Experimental And Clinical Endocrinology and Diabetes. 1998;106(Suppl. 2):10–13. [PubMed: 9792475]
  51. DiFranza JR, Lew RA. Effect of maternal cigarette smoking on pregnancy complications and sudden infant death syndrome. Journal of Family Practice. 1995;40:385–394. [PubMed: 7699353]
  52. DiFranza JR, Lew RA. Morbidity and mortality in children associated with the use of tobacco products by other people. Pediatrics. 1996;97:560–568. [PubMed: 8632946]
  53. Doll R. One for the heart. The British Medical Journal. 1997;315:1664–1668. [PMC free article: PMC2128014] [PubMed: 9448535]
  54. Dorgan JF, Brown C, Barrett M, Splansky GL, Kreger BE, D'Agostino RB, Albanes D, Schatzkin A. Physical activity and risk of breast cancer in the Framingham Heart Study. American Journal of Epidemiology. 1994;139:662–669. [PubMed: 8166127]
  55. Dufour MC, Archer L, Gordis E. Alcohol and the elderly: Health promotion and disease prevention. Clinics in Geriatric Medicine. 1992;8:127–141. [PubMed: 1576571]
  56. EDK Associates. The ABCs of STDs. New York: EDK Associates; 1995.
  57. Ettinger WJ Jr, Burns R, Messier SP, Applegate W, Rejeski WJ, Morgan T, Shumaker S, Berry MJ, O'Toole M, Monu J, Craven T. A randomized trial comparing aerobic exercise and resistance exercise with a health education program in older adults with knee osteoarthritis. The Fitness Arthritis and Seniors Trial. Journal of the American Medical Association. 1997;277:25–31. [PubMed: 8980206]
  58. Ettinger WH Jr, Afable R. Physical disability from knee osteoarthritis: The role of exercise as an intervention. Medicine and Science of Sports and Exercise. 1994;26:1435–1440. [PubMed: 7869875]
  59. Evans WJ. Effects of exercise on body composition and functional capacity of the elderly. Journal of Gerontology. 1995;50A:147–150. [PubMed: 7493209]
  60. Expert Panel on Trans Fatty Acids and Coronary Heart Disease. Trans fatty acids and coronary heart disease risk. American Journal of Clinical Nutrition. 1995;62:655S–708S. [PubMed: 7661131]
  61. Farley T, Rosenberg M, Rowe P, Chen J, Meirik O. Intrauterine devices and pelvic inflammatory disease: An international perspective. Lancet. 1992;339:785–788. [PubMed: 1347812]
  62. Feskanich D, Willett WC, Stampfer MJ, Colditz GA. Protein consumption and bone fractures in women. American Journal of Epidemiology. 1996;143:472–479. [PubMed: 8610662]
  63. Feskanich D, Willett WC, Stampfer MJ, Colditz GA. Milk, dietary calcium, bone fractures in women: A 12-year prospective study. American Journal of Public Health. 1997;87:992–997. [PMC free article: PMC1380936] [PubMed: 9224182]
  64. Fish A, Fairweather D, Oriel J, Ridgeway G. Chlamydia trachomatis infection in a gynecology clinic population: Identification of high-risk groups and the value of contact tracing. European Journal of Obstetrics, Gynecology and Reproductive Biology. 1989;31:67–74. [PubMed: 2653896]
  65. Fisher N, Pendergast D. Effects of a muscle exercise program on exercise capacity in subjects with osteoarthritis. Archives of Physical Medicine and Rehabilitation. 1994;75:792–797. [PubMed: 8024427]
  66. Flegal KM. The obesity epidemic in children and adults: Current evidence and research issues. Medical Science in Sports and Exercise. 1999;31 (11 Suppl):S509–S514. [PubMed: 10593520]
  67. Fleming DT, McQuillan GM, Johnson RE, Nahmias AJ, Aral SO, Lee FK, St Louis ME. Herpes simplex virus type 2 in the United States, 1976 to 1994. New England Journal of Medicine. 1997;337:1105–1111. [PubMed: 9329932]
  68. Foreyt JP, Poston WSC II, Goodrick GK. Future directions in obesity and eating disorders. Addictive Behavior. 1996;21:767–778. [PubMed: 8904942]
  69. Freeman L, Prentice R, Clifford C, Harlan W, Henderson M, Roussow J. Dietary fat and breast cancer: Where we are. Journal of the National Cancer Institute. 1993;85:764–765.
  70. Freudenheim JL, Graham S, Marshall JR, Haughey BP, Cholewinski S, Wilkinson G. Folate intake and carcinogenesis of the colon and rectum. International Journal of Epidemiology. 1991;20:368–374. [PubMed: 1917236]
  71. Friedenreich CM, Rohan TE. Physical activity and risk of breast cancer. European Journal of Cancer Prevention. 1995;4:145–151. [PubMed: 7767240]
  72. Gallagher D, Visser M, Sepulveda D, Pierson RN, Harris T, Heymsfield SB. How useful is body mass index for comparison of body fatness across age, sex, and ethnic groups? American Journal of Epidemiology. 1996;143:228–39. [PubMed: 8561156]
  73. Gammon MD, Schoenberg JB, Britton JA, Kelsey JL, Coates RJ, Brogan D, Potischman N, Swanson CA, Daling JR, Stanford JL, Brinton LA. Recreational physical activity and breast cancer risk among women under age 45 years. American Journal of Epidemiology. 1998;147:273–280. [PubMed: 9482502]
  74. Giovannucci E, Ascherio A, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. Physical activity, obesity, and risk for colon cancer and adenoma in men. Annals of Internal Medicine. 1995;122:327–334. [PubMed: 7847643]
  75. Giovannucci E, Stampfer M, Colditz G, Hunter D, Fuchs C, Rosner B, Speizer FE, Willett WC. Multivitamin use, folate, and colon cancer in women in the Nurses' Health Study. Annals of Internal Medicine. 1998;129:517–524. [PubMed: 9758570]
  76. Glantz SA, Parmely WW. Passive smoking and heart disease: Mechanism and risk. Journal of the American Medical Association. 1995;273:1047–1053. [PubMed: 7897790]
  77. Goldenberg RL, Andrews WW, Yuan AC, MacKay HT, St Louis ME. Sexually transmitted diseases and adverse outcomes of pregnancy. Clinics in Perinatology. 1997;24:23–41. [PubMed: 9099500]
  78. Goldstein DJ. Beneficial health effects of modest weight loss. International Journal of Obesity and Related Metabolic Disorders. 1992;16:397–415. [PubMed: 1322866]
  79. Goodman MT, Hankin JH, Wilkens LR, Lyu LC, McDuffie K, Liu LQ, Kolonel LN. Diet, body size, physical activity, and the risk of endometrial cancer. Cancer Research. 1997;57:5077–5085. [PubMed: 9371506]
  80. Grant BF. The impact of a family history of alcoholism on the relationship between age at onset of alcohol use and DSM-IV alcohol dependence. Alcohol Healthand Research World. 1998;22:144–148. [PubMed: 15706789]
  81. Grant BF, Dawson DA. Age at onset of alcohol use and its association with DSM-IV alcohol abuse and dependence: Results from the National Longitudinal Alcohol Epidemiologic Survey. Journal of Substance Abuse. 1997;9:103–110. [PubMed: 9494942]
  82. Gunn R, Montes J, Toomey K, Rolfs R, Greenspan J, Spitters C, Waterman SH. Syphilis in San Diego County 1983–1992: Crack cocaine, prostitution, and the limitations of partner notification. Sexually Transmitted Diseases. 1995;22:60–66. [PubMed: 7709327]
  83. Hagberg J, Montain S, Martin WI, Ehsani A. Effect of exercise training in 60–69-year-old persons with essential hypertension. American Journal of Cardiology. 1989;64:348–353. [PubMed: 2756880]
  84. Hahn R, Teutsch S, Rothenberg R, Marks J. Excess deaths from nine chronic diseases in the United States, 1986. Journal of the American Medical Association. 1990;264:2654–2659. [PubMed: 2232042]
  85. Handsfield H, Jasman L, Roberts P, Hanson VW, Kothenbeutel RL, Stamm WE. Criteria for selective screening for Chlamydia trachomatis infection in women attending family planning clinics. Journal of the American Medical Association. 1986;255:1730–1734. [PubMed: 3081742]
  86. Hansson L. Current and future strategies in the treatment of hypertension. American Journal of Cardiology. 1988;61:2C–7C. [PubMed: 3341223]
  87. Harwood H, Fountain D, Livermore G. The economic costs of alcohol anddrug abuse in the United States 1992. Washington, DC: U.S. Department of Health and Human Services; 1998. (NIH publication number 98-4327)
  88. Hasin D, Grant B, Harford T. Male and female differences in liver cirrhosis mortality in the United States, 1961–1985. Journal of Studies on Alcohol. 1990;51:123–129. [PubMed: 2308349]
  89. Hebel JR, Fox NL, Sexton M. Dose-response of birth weight to various measures of maternal smoking during pregnancy. Journal of Clinical Epidemiology. 1988;41:483–489. [PubMed: 3367179]
  90. Hendriks HF, Veenstra J, Velthuis-te Wierik EJ, Schaafsma G, Kluft C. Effect of moderate dose of alcohol with evening meal on fibrinolytic factors. British Medical Journal. 1994;308:1003–1006. [PMC free article: PMC2539875] [PubMed: 8167511]
  91. Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, LaMotte F, Gaziano JM, Ridker PM, Willett W, Peto R. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. New England Journal of Medicine. 1996;334:1145–1149. [PubMed: 8602179]
  92. Hill JO, Peters JC. Environmental contributions to the obesity epidemic. Science. 1998;280:1371–1374. [PubMed: 9603719]
  93. Hillier S, Nugent R, Eschenbach D, Krohn M, Gibbs R, Martin D, Cotch MF, Edelman R, Pastorek JG 2nd, Rao AV, et al. Association between bacterial vaginosis and preterm delivery of a low birth weight infant. New England Journal of Medicine. 1995;333:1737–1742. [PubMed: 7491137]
  94. Hillis S, Nakashima A, Amsterdam L, Pfister J, Vaughn M, Addiss D, Marchbanks PA, Owens LM, Davis JP. The impact of a comprehensive chlamydia prevention program in Wisconsin. Family Planning Perspectives. 1995;27:108–111. [PubMed: 7672100]
  95. Ho TF, Chay SO, Yip WC, Tay JS, Wong HB. The prevalence of obesity in Singapore primary school children. Australian Paediatric Journal. 1983;19:248–250. [PubMed: 6673725]
  96. Holman C, English D. Ought low alcohol intake to be promoted for health reasons? Journal of the Royal Society of Medicine. 1996;89:123–129. [PMC free article: PMC1295693] [PubMed: 8683513]
  97. Howard G, Wagenknech LE, Burke GE, Diez-Roux A, Evans GW, McGovern P, Nieto FJ, Tell GS. Cigarette smoking and progression of atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Study. Journal of the American Medical Association. 1998;279:119–124. [PubMed: 9440661]
  98. Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA, Hennekens CH, Willett WC. Dietary fat intake and the risk of coronary heart disease in women. New England Journal of Medicine. 1997;337:1491–1499. [PubMed: 9366580]
  99. Huang Z, Hankinson SE, Colditz GA, Stampfer MJ, Hunter DJ, Manson JE, Hennekens CH, Rosner B, Speizer FE, Willett WC. Dual effects of weight and weight gain on breast cancer risk. Journal of the American Medical Association. 1997;278:1407–1411. [PubMed: 9355998]
  100. Huang Z, Willett WC, Manson JE, Rosner B, Stampfer MJ, Speizer FE, Colditz GA. Body weight, weight change, and risk for hypertension in women. Annals of Internal Medicine. 1998;128:81–88. [PubMed: 9441586]
  101. Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: A 26-year follow-up of participants in the Framingham Heart Study. Circulation. 1983;67:968–977. [PubMed: 6219830]
  102. Lynch BS, Bonnie RJ, editors. IOM (Institute of Medicine) Growing Up Tobacco Free: Preventing Nicotine Addiction in Children and Youths. Washington, DC: National Academy Press; 1994.
  103. Stratton K, Howe C, Battaglia F, editors. IOM (Institute of Medicine) Fetal Alcohol Syndrome: Diagnosis, epidemiology, prevention, and treatment. Washington, DC: National Academy Press; 1996.
  104. Eng TR, Butler WT, editors. IOM (Institute of Medicine) The Hidden Epidemic: Confronting Sexually Transmitted Diseases. Washington, DC: National Academy Press; 1997.
  105. Stratton K, Shetty P, Wallace R, Bondurant S, editors. IOM (Institute of Medicine) Clearing the Smoke, Assessing the Science Base for Tobacco Harm Reduction. Washington, DC: National Academy Press; 2001a.
  106. IOM (Institute of Medicine) Speaking of Health: Assessing Health Communication. In: Chrvala C, Scrimshaw S, editors. Strategies for Diverse Populations. Washington, DC: National Academy Press; 2001b.
  107. Ip C, Carroll K, editors. American Journal of Clinical Nutrition. Vol. 65. 1997. Individual fatty acids and cancer; pp. 1505S–1586S. [PubMed: 9417764]
  108. Jackson R, Scragg R, Beaglehole R. Does recent alcohol consumptionreduce the risk of acute myocardial infarction and coronary death in regular drinkers? American Journal of Epidemiology. 1992;136:819–824. [PubMed: 1442747]
  109. Joint National Committee on Detection and Treatment of High Blood Pressure. The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, MD: National Institutes of Health; 1993.
  110. Kaplan G, Seeman T, Cohen R, Knudsen L, Guralnik J. Mortality among the elderly in the Alameda County Study: Behavioral and demographic risk factors. American Journal of Public Health. 1987;77:307–312. [PMC free article: PMC1646902] [PubMed: 3812836]
  111. Kaplan GA, Strawbridge WJ, Cohen RD, Hungerford LR. Natural history of leisure-time physical activity and its correlates: Associations with mortality from all causes and cardiovascular disease over 28 years. American Journal of Epidemiology. 1996;144:793–797. [PubMed: 8857828]
  112. Kawachi I, Troisi R, Rotnitzky A, Coakley E, Colditz G. Can physical activity minimize weight gain in women after smoking cessation? American Journal of Public Health. 1996;86:999–1004. [PMC free article: PMC1380442] [PubMed: 8669525]
  113. Kelder SH, Perry CL, Klepp KI, Lytle LL. Longitudinal tracking of adolescent smoking, physical activity, and food choice behaviors. American Journal of Public Health. 1994;84:1121–1126. [PMC free article: PMC1614729] [PubMed: 8017536]
  114. Kohl HI, Powell K, Gordon N, Blair S, Paffenbarger RJ. Physical activity, physical fitness, and sudden cardiac death. Epidemiologic Reviews. 1992;14:37–58. [PubMed: 1289116]
  115. Kopelman PG. Obesity as a medical problem. Nature. 2000;404:635–643. [PubMed: 10766250]
  116. Kramer MM, Wells CL. Does physical activity reduce risk of estrogen-dependent cancer in women? Medicine and Science in Sports and Exercise. 1996;28:322–334. [PubMed: 8776221]
  117. Kromeyer-Hauschild K, Zellner K, Jaeger U, Hoyer H. Prevalence of overweight and obesity among school children in Jena (Germany) International Journal of Obesity and Related Metabolic Disorders. 1999;23:1143–1150. [PubMed: 10578204]
  118. Kujala UM, Kaprio J, Sarna S, Koskenvuo M. Relationship of leisure-time physical activity and mortality: The Finnish twin cohort. Journal of the American Medical Association. 1998;279:440–444. [PubMed: 9466636]
  119. Kushi L, Fee R, Folsom A, Mink P, Anderson K, Sellers T. Physical activity and mortality in postmenopausal women. Journal of the American Medical Association. 1997;277:1287–1292. [PubMed: 9109466]
  120. LaCroix AZ, Guralnik JM, Berkman LF, Wallace RB, Satterfield S. Maintaining mobility in late life. II. Smoking, alcohol consumption, physical activity, and body mass index. American Journal of Epidemiology. 1993;137:858–869. [PubMed: 8484377]
  121. Lane N. Exercise: a cause of osteoarthritis. Journal of Rheumatology. 1995;22:3–6. [PubMed: 7752130]
  122. Lanyon L. Functional strain in bone tissue as an objective and controlling stimulus for adaptive bone remodelling. Journal of Biomechanics. 1987;20:1083–1093. [PubMed: 3323200]
  123. Lanyon L. Osteocytes, strain detection, bone modeling and remodeling. Calcified Tissue International. 1993;53:S102–S107. [PubMed: 8275362]
  124. Laumann E. The Social Organization of Sexuality. Chicago: University of Chicago Press; 1994.
  125. Le Marchand L, Wilkens LR. Early-age body size, adult weight gain and endometrial cancer risk. International Journal of Cancer. 1991;48:807–811. [PubMed: 1860727]
  126. LeClere FB, Wilson JB. Smoking behavior of recent mothers, 18–44 years of age, before and after pregnancy: United States, 1990. Journal of the American Academy of Nurse Practitioners. 1997;9:323–326.
  127. Lee I-M, Paffenbarger RS. Change in body weight and longevity. The Journal of the American Medical Association. 1992;268:2045–2049. [PubMed: 1404740]
  128. Lee I-M, Paffenbarger RS Jr, Hsieh CC. Physical activity and risk of developing colorectal cancer among college alumni. Journal of the National Cancer Institute. 1991;83:1324–1329. [PubMed: 1886158]
  129. Lee I-M, Bouchard C, Shephard R, Stephens T. Physical Activity, Fitness, and Health: International Proceedings and Consensus Statement. Champaign, IL: Human Kinetics; 1994. Physical activity, fitness, and cancer; pp. 814–831.
  130. Leon A, Connett J, Jacobs D, Rauramaa R. Leisure-time physical activity levels and risk of coronary heart disease and death: The Multiple Risk Factor Intervention Trial. Journal of the Amercian Medical Association. 1987;258:2388–2395. [PubMed: 3669210]
  131. Leong KS, Wilding JP. Obesity and diabetes. Baillieres Best Practices Reseach Clinical Endocrinology Metabolism. 1999;13:221–237. [PubMed: 10761864]
  132. Li CQ, Windsor RA, Perkins L, Goldenberg RL, Lowe JB. The impact on infant birth weight and gestational age of cotinine-validated smoking reduction during pregnancy. Journal of the American Medical Association. 1993;269:1519–1524. [PubMed: 8445814]
  133. Lin BH, Frazao E. Nutritional quality of foods at and away from home. Food Review. 1997;20:33–40.
  134. Lindsted K, Tonstad S, Kuzma J. Self-report of physical activity and patterns of mortality in Seventh-Day Adventist men. Journal of Clinical Epidemiology. 1991;44:355–364. [PubMed: 2010779]
  135. Lissner L, Johansson SE, Qvist J, Rossner S, Wolk A. Social mapping of the obesity epidemic in Sweden. International Journal of Obesity and Related Metabolic Disorders. 2000;24:801–805. [PubMed: 10878690]
  136. Lytle L, Achterberg C. Changing the diet of America's children: What works and why? Journal of Nutrition Education. 1995;27:250–260.
  137. Manson JE, Hu FB, Rich-Edwards JW, Colditz GA, Stampfer MJ, Willett WC, Speizer FE, Hennekens CH. A prospective study of walking compared with vigorous exercise in the prevention of coronary heart disease in women. The New England Journal of Medicine. 1999;341:650–658. [PubMed: 10460816]
  138. Marceau M, Kouame N, Lacourciere Y, Cleroux J. Effects of different training intensities on 24 hour blood pressure in hypertensive subjects. Circulation. 1993;88:2803–2811. [PubMed: 8252694]
  139. Martinez ME, Giovannucci E, Spiegelman D, Hunter DJ, Willett WC, Colditz GA. Leisure-time physical activity, body size, and colon cancer in women. Nurses' Health Study Research Group. Journal of the National Cancer Institute. 1997;89:948–955. [PubMed: 9214674]
  140. Marx R, Aral S, Rolfs R, Sterk C, Kahn J. Crack, sex, and STDs. Sexually Transmitted Diseases. 1991;18:92–101. [PubMed: 1862466]
  141. Mason JB, Levesque T. Folate: effects on carcinogenesis and the potential for cancer chemoprevention. Oncology. 1996;10:1727–1736. 1742–1743. [PubMed: 8953590]
  142. Matsusaki M, Ikeda M, Tashiro E, Koga M, Miura S, Ideishi M. Influence of workload on the antihypertensive effect of exercise. Clinical and Experimental Pharmacology and Physiology. 1992;19:471–479. [PubMed: 1499145]
  143. McCrory MA, Fuss PJ, Hays NP, Vinken AG, Greenberg AS, Roberts SB. Overeating in America: Association between restaurant food consumption and body fatness in healthy adult men and women ages 19 to 80. Obesity Research. 1999;7:564–571. [PubMed: 10574515]
  144. McCrory MA, Fuss PJ, Saltzman E, Roberts SB. Dietary determinants of energy intake and weight regulation in healthy adults. Journal of Nutrition. 2000;130 (2S Suppl):276S–279S. [PubMed: 10721887]
  145. McGinnis JM, Foege WH. Actual causes of death in the United States. Journal of the American Medical Association. 1993;270:2207–2212. [PubMed: 8411605]
  146. McTiernan A, Stanford JL, Weiss NS, Daling JR, Voigt LF. Occurrence of breast cancer in relation to recreational exercise in women age 50–64 years. Epidemiology. 1996;7:598–604. [PubMed: 8899385]
  147. Meade TW, Imeson J, Stirling Y. Effects of changes in smoking and other characteristics on clotting factors and the risk of ischaemic heart disease. Lancet. 1987;2(8566):986–988. [PubMed: 2889958]
  148. Meis PJ, Goldenberg RL, Mercer G, Moawad A, Das A, McNellis D, Johnson F, Iams JD, Thom E, Andrews WW. The preterm prediction study: Significance of vaginal infections. American Journal of Obstetrics and Gynecology. 1995;173:1231–1235. [PubMed: 7485327]
  149. Mertens IL, Van Gaal LF. Overweight, obesity, and blood pressure: The effects of modest weight reduction. Obesity Research. 2000;8:270–278. [PubMed: 10832771]
  150. Miller B, Monson B, Norton M. The effects of forced sexual intercourse on white female adolescents. Child Abuse and Neglect. 1995;19:1289–1301. [PubMed: 8556443]
  151. Minor M. Physical activity and management of arthritis. Annals of Behavioral Medicine. 1991;13:117–124.
  152. Mittendorf R, Longnecker MP, Newcomb PA, Dietz AT, Greenberg ER, Bogdan GF, Clapp RW, Willett WC. Strenuous physical activity in young adulthood and risk of breast cancer (United States) Cancer Causes and Control. 1995;6:347–353. [PubMed: 7548722]
  153. Mokdad A, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The spread of the obesity epidemic in the United States, 1991–1998. Journal of the American Medical Association. 1999;282:1519–1522. [PubMed: 10546690]
  154. Mokdad A, Serdula MK, Dietz WH, Bowman BA, Marks JS, Koplan JP. The continuing epidemic of obesity in the United States. Journal of the American Medical Association. 2000;284:1650–1651. [PubMed: 11015792]
  155. Morrison C, Schwingl P, Cates WJ. Sexual behavior and cancer prevention. Cancer Causes and Control. 1997;8:S21–S25. [PubMed: 9427417]
  156. Murphy GP, Mettlin C, Menck H, Winchester DP, Davidson AM. National patterns of prostate cancer treatment by radical prostatectomy: Results of a survey by the American College of Surgeons Commission on Cancer. Journal of Urology. 1994;152:1817–1819. [PubMed: 7523727]
  157. Murray C, Lopez A. The global burden of disease. Geneva: World Health Organization; 1996.
  158. Must A, Spandano J, Coakley EH, Field AE, Colditz G, Dietz WH. The disease burden associated with overweight and obesity. Journal of the American Medical Association. 1999;282:1523–1529. [PubMed: 10546691]
  159. National Cancer Institute. National Cancer Institute Monographs. Vol. 2. Bethesda, MD: U.S: Department of Health and Human Services; 1986. Cancer Control Objectives for the Nation: 1985–2000.
  160. National Heart Lung Blood Institute Obesity Task Force. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults—the evidence report. Obesity Research. 1998;6 (suppl. 2):51S–209S. [PubMed: 9813653]
  161. National Research Council (NRC) Diet and Health: Implications for ReducingChronic Disease Risk. Washington, DC: National Academy Press; 1989.
  162. National Task Force on the Prevention and Treatment of Obesity. Overweight, obesity, and health risk. Archives of Internal Medicine. 2000;160:898–904. [PubMed: 10761953]
  163. NCHS (National Center for Health Statistics) Health, United States, 1998: With Socioeconomic Status and Health Chartbook. Hyattsville, MD: U.S. Dept. of Health and Human Services; 1998a.
  164. NCHS (National Center for Health Statistics) SEER Cancer Statistics Review, 1973–1995. Bethesda, MD: National Cancer Institute; 1998b.
  165. Nelson ME, Fiatarone MA, Morganti CM, Trice I, Greenberg RA, Evans WJ. Effects of high-intensity strength training on multiple risk factors for osteoporotic fractures. Journal of the American Medical Association. 1994;272:1909–1914. [PubMed: 7990242]
  166. NIAAA (National Institute on Alcohol Abuse and Alcoholism) Alcohol and cancer, (Alcohol Alert no. 21-1993) Bethesda, MD: U.S. Department of Health and Human Services; 1993.
  167. NIH (National Institutes of Health) Methods for voluntary weight loss and control. Annals of Internal Medicine. 1993;119:764–770. [PubMed: 8363212]
  168. NIH (National Institutes of Health) Optimal Calcium Intake. NIH Consensus Statement. 1994;12:1–31. [PubMed: 7599655]
  169. NIH (National Institutes of Health) Management of Hepatitis C. NIH Consensus Statement. 1997a;15:1–41. [PubMed: 9457159]
  170. NIH (National Institutes of Health) Breast Cancer Screening for Women Ages 40–49. NIH Consensus Statement. 1997b;15:1–35. [PubMed: 9267441]
  171. O'Malley PM, Johnston LD, Bachman JF. Alcohol use among adolescents. Alcohol Health and Research World. 1998;22:85–93. [PubMed: 15706782]
  172. Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, Keogh JP, Meyskens FL Jr, Valanis B, Williams JH Jr, Barnhart S, Cherniack MG, Brodkin CA, Hammar S. Risk factors for lung cancer and for intervention effects in CARET, the Beta-Carotene and Retinol Efficacy Trial. Journal of the National Cancer Institute. 1996;88:1550–1559. [PubMed: 8901853]
  173. Oster G, Thompson D, Edelsberg J, Bird AP, Colditz GA. Lifetime health and economic benefits of weight loss among obese persons. American Journal of Public Health. 1999;89:1536–1542. [PMC free article: PMC1508787] [PubMed: 10511836]
  174. Owusu W, Willett WC, Ascherio A, Spiegelman D, Rimm EB, Feskanich D, Colditz G. Body anthropometry and the risk of hip and wrist fractures in men: results from a prospective study. Obesity Research. 1998;6:12–19. [PubMed: 9526965]
  175. Owusu W, Willett WC, Feskanich D, Ascherio A, Spiegelman D, Colditz GA. Calcium intake and the incidence of forearm and hip fractures among men. Journal of Nutrition. 1997;127:1782–1787. [PubMed: 9278560]
  176. Paffenbarger R Jr, Hyde R, Wing A, Lee I-M, Jung D, Kampert J. The association of changes in physical activity level and other lifestyle characteristics with mortality among men. New England Journal of Medicine. 1993;328:538–545. [PubMed: 8426621]
  177. Panush RS, Lane NE. Exercise and the musculoskeletal system. Baillieres Clinical Rheumatology. 1994;8:79–102. [PubMed: 8149452]
  178. Pate RR, Long BJ, Heath G. Descriptive epidemiology of physical activity in adolescents. Pediatric Exercise Science. 1994;6:434–447.
  179. Pearl R. Alcohol and Longevity. New York: Alfred A.Knopf; 1926.
  180. Pirkle JL, Flegal KM, Bernert JT, Brody DJ, Etzel RA, Maurer KR. Exposure of the US population to environmental tobacco smoke: The Third National Health and Nutrition Examination Survey, 1988 to 1991. Journal of the American Medical Association. 1996;275:1233–1240. [PubMed: 8601954]
  181. Pi-Sunyer FX. Medical hazards of obesity. Annals of Internal Medicine. 1993;119:655–660. [PubMed: 8363192]
  182. Popham R, Schmidt W, Israelstam S. Heavy alcohol consumption and physical health problems: A review of epidemiologic evidence. In: Smart RG, Cappell HD, Glaser FB, Israel Y, editors. Recent Advances in Alcohol and Drug Problems, No. 8. New York: Plenum Press; 1984. pp. 149–182.
  183. Potter J. Hazards and benefits of alcohol. New England Journal of Medicine. 1997;337:1763–1764. [PubMed: 9392704]
  184. Ravussin E, Lillioja S, Knowler WC, Christin L, Freymond D, Abbott WG, Boyce V, Howard BV, Bogardus C. Reduced rate of energy expenditure as a risk factor for body-weight gain. New England Journal of Medicine. 1988;318:467–472. [PubMed: 3340128]
  185. Reichman ME. Alcohol and breast cancer. Alcohol Health and Research World. 1994;18:182–184.
  186. Renaud S, Beswick A, Fehily A, Sharp P, Elwood P. Alcohol and platelet aggregation: the Caerphilly prospective heart disease study. American Journal of Clinical Nutrition. 1992;55:1012–1017. [PubMed: 1570795]
  187. Ries LAG, Miller BA, Hankey BF, editors. SEER Cancer Statistics Review, 1973–1993. National Cancer Institute; 1996. (NIH Pub. No. 94-2789)
  188. Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC. Vitamin E consumption and the risk of coronary heart disease in men. New England Journal of Medicine. 1993;328:1450–1456. [PubMed: 8479464]
  189. Rimm EB, Stampfer MJ, Giovannucci E, Ascherio A, Spiegelman D, Colditz GA, Willett WC. Body size and fat distribution as predictors of coronary heart disease among middle-aged and older US men. American Journal of Epidemiology. 1995;141:1117–1127. [PubMed: 7771450]
  190. Rimm EB, Ascherio A, Giovannucci E, Spiegelman D, Stampfer MJ, Willett WC. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. Journal of the American Medical Association. 1996;275:447–451. [PubMed: 8627965]
  191. Rimm E, Williams P, Fosher K, Criqui M, Stampfer M. A biological basis for moderate alcohol consumption and lower coronary heart disease risk: A meta-analysis of effects on lipids and hemostatic factors. British Medical Journal. 1999;319:1523–1528. [PMC free article: PMC28294] [PubMed: 10591709]
  192. Rissanen AM, Heliovaara M, Knekt P, Reunanen A, Aromaa A. Determinants of weight gain and overweight in adult Finns. European Journal of Clinical Nutrition. 1991;45:419–430. [PubMed: 1959514]
  193. Rockhill B, Willett WC, Hunter DJ, Manson JE, Hankinson SE, Spiegelman D, Colditz GA. Physical activity and breast cancer risk in a cohort of young women. Journal of the National Cancer Institute. 1998;90:1155–1160. [PubMed: 9701365]
  194. Roizen J. Issues in the epidemiology of alcohol and violence. In: Martin S, editor. Alcohol and Interpersonal Violence: Fostering Multi-Disciplinary Perspectives, (NIH publication no. 93-3496) U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism; 1993.
  195. Rose G. The Strategy of Preventive Medicine. New York: Oxford University Press; 1992.
  196. Saadatamand F, Stinson FS, Grant BF, Dufour MC. Surveillance Report #45: Liver Cirrhosis Mortality in the United States: 1970–1994. Rockville, MD: NIAAA Division of Biometry and Epidemiology, Alcohol Epidemiological Data System; 1997.
  197. Schatzkin A, Lanze E, Freedman LS, Tangrea J, Cooper MR, Marshall JR, Murphy PA, Selby JV, Shike M, Schade RR, Burt RW, Kikendall JW, Cahill J. The polyp prevention trial. I Rationale, design, recruitment, and baseline participant characteristics. Cancer Epidemiology Biomarkers Prevention. 1996;5:375–383. [PubMed: 9162304]
  198. Scheen AJ. From obesity to diabetes: Why, when and who? Acta Clinica Belgica. 2000;55:9–15. [PubMed: 10783502]
  199. Schmidt W. Effects of alcohol consumption on health. Journal of Public Health Policy. 1980;1:25–40. [PubMed: 7276154]
  200. Schoenborn C, Marano M. Current estimates from the National Health Interview Survey: United States, 1987. Washington, DC: Government Printing Office; 1988.
  201. Scholes D, Stergachis A, Heidrich F, Andrilla H, Holmes K, Stamm W. Prevention of pelvic inflammatory disease by screening for cervical chlamydia infection. New England Journal of Medicine. 1996;334:1362–1366. [PubMed: 8614421]
  202. Seidell JC. Obesity in Europe: Scaling an epidemic. International Journal of Obesity and Related Metabolic Disorders. 1995;19 (Suppl 3):S1–S4. [PubMed: 8581069]
  203. Selhub J, Jacques PF, Bostom AG, D'Agostino RB, Wilson PW, Belanger AJ, O'Leary DH, Wolf PA, Schaefer EJ, Rosenberg IH. Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. New England Journal of Medicine. 1995;332:286–291. [PubMed: 7816063]
  204. Severson RK, Nomura AMY, Grove JS, Stemmermann GN. A prospective analysis of physical activity and cancer. American Journal of Epidemiology. 1989;130:522–529. [PubMed: 2763997]
  205. Shephard R. Exercise in the prevention and treatment of cancer: an update. Sports Medicine. 1993;15:258–280. [PubMed: 8460289]
  206. Shephard R, Verde T, Thomas S, Shek P. Physical activity and the immune system. Canadian Journal of Sport Science. 1991;16:163–185. [PubMed: 1655191]
  207. Sherman SE, D'Agostino RB, Cobb JL, Kannel WB. Physical activity and mortality in women in the Framingham Heart Study. American Heart Journal. 1994;128:879–884. [PubMed: 7942478]
  208. Shetty PS.Obesity and physical activity. 1997. [Accessed on line February 23, 2001]. http://www.nutritionfoundationin.org/ARCHIVES/APR97A.HTM.
  209. Shu XO, Hatch MC, Mills J, Clemens J, Susser M. Maternal smoking, alcohol drinking, caffeine consumption, and fetal growth: results from a prospective study. Epidemiology. 1995;6:115–120. [PubMed: 7742395]
  210. Simmons G, Jackson R, Swinburn B, Yee RL. The increasing prevalence of obesity in New Zealand: Is it related to recent trends in smoking and physical activity? New Zealand Medical Journal. 1996;109:90–92. [PubMed: 8606842]
  211. Slattery M, Jacobs D, Nichaman M. Leisure time physical activity and coronary heart disease death: the US Railroad Study. Circulation. 1989;79:304–311. [PubMed: 2914349]
  212. Slattery ML, Schumacher MC, Smith KR, West DW, Abd-Elghany N. Physical activity, diet, and risk of colon cancer in Utah. American Journal of Epidemiology. 1988;128:989–999. [PubMed: 3189298]
  213. Smith-Warner SA, Spiegelman D, Yaun SS, van den Brandt PA, Folsom AR, Goldbohm RA, Graham S, Holmberg L, Howe GR, Marshall JR, Miller AB, Potter JD, Speizer FE, Willett WC, Wolk A, Hunter DJ. Alcohol and breast cancer in women: A pooled analysis of cohort studies. Journal of the American Medical Association. 1998;279:535–540. [PubMed: 9480365]
  214. Snow-Harter C, Shaw JM, Matkin CC. Physical activity and risk of osteoporosis. In: Marcus R, Feldman D, Kelsey J, editors. Osteoporosis. San Diego, CA: Academic Press; 1996. pp. 511–528.
  215. Sonnenschein E, Toniolo P, Terry MB, Bruning PF, Kato I, Koenig KL, Shore RE. Body fat distribution and obesity in pre- and postmenopausal breast cancer. International Journal of Epidemiology. 1999;28:1026–1031. [PubMed: 10661643]
  216. St Louis ME, Wasserheit JN, Gayle HD. Editorial: Janus considers the HIV pandemic—harnessing recent advances to enhance AIDS prevention. American Journal of Public Health. 1997;87:10–12. [PMC free article: PMC1380755] [PubMed: 9065212]
  217. Stamm W, Holmes K. Chlamydia trachomatis infections in the adult. In: Holmes K, Mardh PA, Sparling P, Weisner P, Cates W, Lemon S, et al., editors. Sexually Transmitted Diseases. 2nd edition. New York: McGraw-Hill, Inc; 1990. pp. 181–193.
  218. Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary disease in women. New England Journal of Medicine. 1993;328:1444–1449. [PubMed: 8479463]
  219. Steinmetz KA, Potter JD. Vegetables, fruit, and cancer. II. Mechanisms. Cancer Causes and Control. 1991;2:427–442. [PubMed: 1764568]
  220. Stock JL, Bell MA, Boyer DK, Connell FA. Adolescent pregnancy and sexual risk-taking among sexually abused girls. Family Planning Perspective. 1997;29:200–203. 227. [PubMed: 9323495]
  221. Strunin L, Hingson R. Alcohol, drugs, and adolescent sexual behavior. International Journal of the Addictions. 1992;27:129–146. [PubMed: 1544720]
  222. Strunin L, Hingson R. Alcohol use and risk for HIV infection. Alcohol Health and Research World. 1993;17:35–38.
  223. Substance Abuse and Mental Health Services Administration. Race/ethnicity,socioeconomic status, and drug abuse (No. (SMA) 93-2062) Washington, DC: U.S. Department of Health and Human Services; 1993.
  224. Tabar L, Faberberg G, Day N, Holmberg L. What is the optimum interval between mammographic screening examinations? An analysis based on the latest results of the Swedish two-county breast cancer screening trial. International Journal of Cancer. 1987;55:547–551. [PMC free article: PMC2001715] [PubMed: 3606947]
  225. Tanne J. US has epidemic of sexually transmitted disease. British Medical Journal. 1998;317:1616.
  226. Taubes G. The breast-screening brawl. Science. 1997;275:1056–1059. [PubMed: 9054004]
  227. Taubes G. As obesity rates rise, experts struggle to explain why. Science. 1998;280:1367–1368. [PubMed: 9634414]
  228. Thor P, Konturek J, Konturek S, Anderson J. Role of prostaglandins in control of intestinal motility. American Journal of Physiology. 1985;248:G353–G359. [PubMed: 3883808]
  229. Thun M, Peto R, Lopez A, Monaco JH, Henley SJ, Heath CW Jr, Doll R. Alcohol consumption and mortality among middle-aged and elderly US adults. New England Journal of Medicine. 1997;337:1705–1714. [PubMed: 9392695]
  230. Thune I, Brenn T, Lund E, Gaard M. Physical activity and the risk of breast cancer. New England Journal of Medicine. 1997;336:1269–1275. [PubMed: 9113929]
  231. Towler B, Irwig L, Glasziou P, Kewenter J, Weller D, Silagy C. A systematic review of the effects of screening for colorectal cancer using the faecal occult blood test, hemoccult. British Medical Journal. 1998;317:559–565. [PMC free article: PMC28648] [PubMed: 9721111]
  232. Troiano RP, Flegal KM. Overweight children and adolescents: Description, epidemiology, and demographics. Pediatrics. 1998;101:497–504. [PubMed: 12224656]
  233. Tseng BS, Marsh DR, Hamilton MT, Booth FW. Strength and aerobic training attenuate muscle wasting and improve resistance to the development of disability with aging. Journal of Gerontology. 1995;50A:113–119. [PubMed: 7493203]
  234. U.S. Preventive Services Task Force. Guide to Clinical Preventive Services. Philadelphia: Williams and Wilkins; 1989.
  235. U.S. Preventive Services Task Force. Guide to Clinical Preventive Services. 2nd edition. Washington, DC: U.S. Department of Health and Human Services; 1996.
  236. USDA (U.S. Department of Agriculture), USDHHS (U. S. Department of Health and Human Services) Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans. Beltsville, MD: U.S. Department of Agriculture, Agricultural Research Service; 1995a.
  237. USDA (U.S. Department of Agriculture), USDHHS (U. S. Department of Health and Human Services) Nutrition and Your Health: Dietary Guidelines for Americans. Washington, DC: U.S. Government Printing Office; 1995b.
  238. USDA (U.S. Department of Agriculture) Dietary Guidelines for Americans. 4th edition. Washington, DC: U.S. Department of Agriculture, Agricultural Research Service; 1995a. (USDA Home and Garden Bulletin No. 232)
  239. USDA (U.S. Department of Agriculture) The Healthy Eating Index (USDA Publication CNPP-1) Washington, DC: U.S. Department of Agriculture, Center for Nutrition Policy and Promotion; 1995b.
  240. USDA (U.S. Department of Agriculture) USDA finds more and more Americanseat out, offers tips for making healthier food choices. 1996. (Press release). Available:http://www.ars.usda.gov/is/pr/eatout1196.htm [1999, November 11]
  241. USDA (U.S. Department of Agriculture) What we eat in America: Results from the1994–96 Continuing Survey of Food Intakes by Individuals. (Fact Sheet) Beltsville, MD: Agricultural Research Service, Human Nutrition Research Center, Food Surveys Research Group; 1997.
  242. Hamburg BA, Lipsett LF, Inoff GE, Drash AL, editors. USDHHS (U.S. Department of Health and Human Services) Behavioral and Psychosocial Issues in Diabetes: Proceedings of the National Conference. 1980. NIH publication no. 80-1993.
  243. USDHHS (U.S. Department of Health and Human Services) The Health Consequences of Smoking: Cardiovascular Disease. A Report of the Surgeon General. Rockville, MD: Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health; 1983.
  244. USDHHS (U.S. Department of Health and Human Services) The Health Consequences of Involuntary Smoking. A Report of the Surgeon General. Rockville, MD: Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health; 1986.
  245. USDHHS (U.S. Department of Health and Human Services) The Health Consequences of Smoking: Nicotine Addiction: A Report of the Surgeon General. Rockville, MD: Centers for Disease Control, Center for Health Promotion and Education, Office on Smoking and Health; 1988a. (DHHS publication no. (CDC) 88-8406)
  246. USDHHS (U.S. Department of Health and Human Services) The Surgeon General's Report on Nutrition and Health. Washington, DC: Public Health Service; 1988b. (DHHS publication no. (PHS) 88-050210)
  247. USDHHS (U.S. Department of Health and Human Services) Reducing the Health Consequences of Smoking: 25 Years of Progress. A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office of Smoking and Health; 1989. (DHHS publication no. (CDC) 89-8411)
  248. USDHHS (U.S. Department of Health and Human Services) The Health Benefits of Smoking Cessation. A Report of the Surgeon General. Rockville, MD: Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1990. (DHHS publication no. (CDC) 90-8416)
  249. USDHHS (U.S. Department of Health and Human Services) Eighth Special Report to Congress on Alcohol And Health. Bethesda, MD: National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism; 1993.
  250. USDHHS (U.S. Department of Health and Human Services) Physical Activity and Health: A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion; 1996.
  251. USDHHS (U.S. Department of Health and Human Services) Ninth Special Report to the U.S. Congress on Alcohol and Health from the Secretary of Human Services (NIH publication no. 97-4017) Bethesda, MD: National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism; 1997a.
  252. USDHHS (U.S. Department of Health and Human Services) Sexually Transmitted Disease Surveillance, 1996. Atlanta, GA: Centers for Disease Control and Prevention, Division of STD Prevention; 1997b.
  253. USDHHS (U.S. Department of Health and Human Services) Healthy People 2010: Understanding and improving health. Washington, DC: U.S. Department of Health and Human Services; 2000.
  254. USDHHS (U.S. Department of Health and Human Services) A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1994. Preventing Tobacco Use Among Young People.
  255. USDHHS (U.S. Department of Health and Human Services) The Physicians Guide to Helping Patients with Alcohol Problems. Bethesda, MD: National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism; 1995. (NIH publication no. 95-3769)
  256. USEPA (U.S. Environmental Protection Agency) Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders. Washington, DC: U.S. Government Printing Office; 1992. (EPA publication no. EPA/600/6-90/006F)
  257. Ventura SJ, Peters KD, Martin JA, Maurer JD. Monthly Vital Statistics Report. Vol. 46. Hyattsville, MD: National Center for Health Statistics; 1997. Births and deaths: United States, 1996.
  258. Walsh RA. Effects of maternal smoking on adverse pregnancy outcomes: examination of the criteria of causation. Human Biology. 1994;66:1059–1092. [PubMed: 7835872]
  259. Wasson J, Cushman C, Bruskewitz R, Littenberg B, Mulley AG Jr, Wennberg JE. A structured literature review of treatment for localized prostate cancer. Archives of Family Medicine. 1993;2:487–493. [PubMed: 8118564]
  260. Whittemore AS, Wu-Williams AH, Lee M, Zheng S, Gallagher RP, Jiao DA, Zhou L, Wang XH, Chen K, Jung D, Teh C-Z, Chengde L, Yao XJ, Paffenbarger RS Jr, Henderson BE. Diet, physical activity and colorectal cancer among Chinese in North America and China. Journal of the National Cancer Institute. 1990;82:915–926. [PubMed: 2342126]
  261. Willett WC. Nutritional Epidemiology. In: Rothman KJ, Greenland S, editors. Modern Epidemiology. Philadelphia: Lippincott-Raven Publishers; 1998. pp. 623–642.
  262. Willett WC, Ascherio A. Trans fatty acids: Are the effects only marginal? American Journal of Public Health. 1994;84:722–724. [PMC free article: PMC1615057] [PubMed: 8179036]
  263. Willett WC, Manson JE, Stampfer MJ, Colditz GA, Rosner B, Speizer FE, Hennekens CH. Weight, weight change, and coronary heart disease in women: Risk within the 'normal' weight range. The Journal of the American Medical Association. 1995;273:461–465. [PubMed: 7654270]
  264. Willett WC, Stampfer MJ, Manson JE, Colditz GA, Speizer FE, Rosner BA, Sampson LA, Hennekens CH. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet. 1993;341:581–585. [PubMed: 8094827]
  265. Wu AH, Paganini-Hill A, Ross RK, Henderson BE. Alcohol, physical activity and other risk factors for colorectal cancer: a prospective study. British Journal of Cancer. 1987;55:687–694. [PMC free article: PMC2002031] [PubMed: 3620314]
  266. Zakhari S. Alcohol and the cardiovascular system: Molecular mechanisms for beneficial and harmful action. Alcohol Health and Research World. 1997;21:21–29. [PubMed: 15706760]
  267. Ziegler RG, Mayne ST, Swanson CA. Nutrition and lung cancer. Cancer Causes and Control. 1996;7:157–177. [PubMed: 8850443]

BMI is used in all these guidelines as a measure of adiposity. It is calculated as weight (in kilograms) divided by height (in meters) squared. Growing evidence suggests that BMI reflects adiposity well through middle age, but might be less clearly related to adiposity at older ages when lean muscle mass can decrease and mass is redistributed to the abdomen.

The correlation between BMI and body fat is both age and sex dependent, and it is valid for comparison across ethnic groups (Gallagher et al., 1996; USDHHS, 2000). A limitation of the BMI measure is that it does not provide information about body fat distribution, which has been identified as an independent predictor of health risk (National Institute of Health, 1993; USDHHS, 2000). However, until a better measure of body fat is developed, BMI will be used as a proxy to screen for overweight and obesity.

Generally terms used to define the intensity of physical activity are light, moderate, hard or vigorous, and very hard or strenuous. A common classification is to use MET (metabolic equivalent task) values. One MET is the number of kilocalories expended in 1 hour of resting. Often, activities with a MET value below 3.0 are considered light activities; easy walking and regular housework are examples. Activities with MET values of at least 3.0 but less than 6.0 are often classified as moderate; examples are brisk walking, heavy gardening, and calisthenics. Activities with MET values of at least 6.0 but less than 12.0 are often called vigorous, and include jogging, running, swimming, aerobics, and bicycling. Strenuous or very hard activities—such as bicycle or foot racing, speed skating, and competitive cross-country skiing—have MET values of 12.0 or higher.

A drink is defined as 0.54 ounces of ethanol, which is the approximately the amount of alcohol in 12 ounces of regular beer, 5 ounces of wine, or 1.5 ounces of 80'proof distilled spirits.

Footnotes

1

BMI is used in all these guidelines as a measure of adiposity. It is calculated as weight (in kilograms) divided by height (in meters) squared. Growing evidence suggests that BMI reflects adiposity well through middle age, but might be less clearly related to adiposity at older ages when lean muscle mass can decrease and mass is redistributed to the abdomen.

2

The correlation between BMI and body fat is both age and sex dependent, and it is valid for comparison across ethnic groups (Gallagher et al., 1996; USDHHS, 2000). A limitation of the BMI measure is that it does not provide information about body fat distribution, which has been identified as an independent predictor of health risk (National Institute of Health, 1993; USDHHS, 2000). However, until a better measure of body fat is developed, BMI will be used as a proxy to screen for overweight and obesity.

3

Generally terms used to define the intensity of physical activity are light, moderate, hard or vigorous, and very hard or strenuous. A common classification is to use MET (metabolic equivalent task) values. One MET is the number of kilocalories expended in 1 hour of resting. Often, activities with a MET value below 3.0 are considered light activities; easy walking and regular housework are examples. Activities with MET values of at least 3.0 but less than 6.0 are often classified as moderate; examples are brisk walking, heavy gardening, and calisthenics. Activities with MET values of at least 6.0 but less than 12.0 are often called vigorous, and include jogging, running, swimming, aerobics, and bicycling. Strenuous or very hard activities—such as bicycle or foot racing, speed skating, and competitive cross-country skiing—have MET values of 12.0 or higher.

4

A drink is defined as 0.54 ounces of ethanol, which is the approximately the amount of alcohol in 12 ounces of regular beer, 5 ounces of wine, or 1.5 ounces of 80'proof distilled spirits.

Copyright © 2001, National Academy of Sciences.
Bookshelf ID: NBK43744
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