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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Suggested Citation:"3 Behavioral Risk Factors." Institute of Medicine. 2001. Health and Behavior: The Interplay of Biological, Behavioral, and Societal Influences. Washington, DC: The National Academies Press. doi: 10.17226/9838.
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Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

3 Behavioral Risk Factors S everal behaviors that exert a strong influence on health are re- viewed 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 vari- ous 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 rela- tionships 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 epide- miologic evidence on the health effects of these behaviors. TOBACCO USE Since the release in 1964 of the surgeon general’s first report on smok- ing, 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, 1990, 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; 87

88 HEALTH AND BEHAVIOR USDHHS, 2000)—but smoking during pregnancy has been linked to ad- verse 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 par- ticularly alarming for several reasons. Evidence shows not only that to- bacco is addictive (USDHHS, 2000) and that only a relatively small per- centage of smokers can stop smoking permanently each year (Centers for Disease Control and Prevention [CDC], 1993, 1996b; USDHHS, 2000), but also that nicotine addiction develops in most smokers during adoles- cence (Institute of Medicine [IOM], 1994; USDHHS, 1988a, 1994, 2000). Curbing or eradicating tobacco use might remain a daunting task. Preven- tion is the primary objective, but many benefits are associated with smok- ing 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 com- munities that cigarette-smoking is the biggest external (nongenetic) con- tributor 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 immuno- deficiency syndrome (AIDS), traffic accidents, alcohol use, suicide, homi- cide, 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, un- safe 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 to- bacco-attributable mortality and morbidity are consequences of smoking that began decades ago. If current U.S. tobacco use patterns persist, it is

BEHAVIORAL RISK FACTORS 89 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 lead- ing cause of death in the United States (USDHHS, 2000); and the sur- geon 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 can- cers 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 (Na- tional Cancer Institute, 1986; NCHS, 1998b). In 1996, lung cancer ac- counted for about 28% of all cancer deaths (NCHS, 1998b; Ries et al., 1996; Ventura et al., 1997). An estimated 172,000 new cases are diag- nosed 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 out- come in the United States. It is estimated that 15–30% of all pregnant women smoke (Chandra, 1995; Ventura et al., 1997). Pregnancy compli- cations associated with maternal smoking include premature detachment of the placenta, development of the placenta in the lower uterine seg- ment, which can cause hemorrhaging in the last trimester; bleeding dur- ing 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

90 HEALTH AND BEHAVIOR 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 preg- nancy. The complex issues associated with the real and perceived risk of to- bacco and tobacco harm-reduction products are explored in an IOM re- port (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). Sec- ond-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 detect- able 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 con- tribute 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

BEHAVIORAL RISK FACTORS 91 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 decreas- ing 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 to- bacco products, perceptions that tobacco use is normative, use and ap- proval of tobacco use by peers and siblings, and lack of parental involve- ment. Personal risk factors include poor self-image and low self-esteem relative to peers, the belief that tobacco use is functional (useful or pro- viding 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 evi- dence 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 gradua- tion. That is important because nicotine addiction occurs in most smok- ers during adolescence (IOM, 1994; USDHHS, 1988a, 1994, 2000).

92 HEALTH AND BEHAVIOR 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 con- tinue 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 be- tween 1965 and 1990, half of all living Americans who had ever smoked had stopped. The 1990 report concluded that smoking cessation has ma- jor and immediate health benefits for men and women of all ages. Former smokers live longer than continuing smokers. For example, on the aver- age, 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 exten- sively 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 devel- oping 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

BEHAVIORAL RISK FACTORS 93 needed to correct this increase in obesity (Hill and Peters, 1998; Taubes, 1998). Although genetic factors are important, physical activity and diet con- tribute significantly to maintenance of appropriate body weight. The com- bination 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 fac- tors are associated with 4 of the 10 leading causes of death, including coronary heart disease, stroke, some forms of cancer, and non-insulin-de- pendent 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 dis- ease, cancer, and musculoskeletal problems. It is not meant to be a com- prehensive 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 “obe- sity” 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 1BMI 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. 2The 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 limita- tion 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.

94 HEALTH AND BEHAVIOR 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 in- creased 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 ac- tivity 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 3Generally 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. Strenu- ous 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.

BEHAVIORAL RISK FACTORS 95 problem (McCrory et al., 2000). One study pointed to an association be- tween 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, in- cluding 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 es- tablish 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 evi- dent throughout the world, although rates differ (Flegal, 1999). In Europe obesity is especially prevalent in Southern and Eastern countries, particu- larly 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 per- centage 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; Ger- many: 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 socio- demographic groups, the prevalence is influenced by specific sociocultural variables, including gender, ethnicity, socioeconomic status, and educa- tion. From 1988 to 1994, about one-third of U.S. adults were overweight,

96 HEALTH AND BEHAVIOR 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). Obe- sity 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 increas- ing income. African American men living in poverty are 3 times more likely to be sedentary than were those with high family incomes. For His- panic 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. Be- cause full adult height generally is attained by age 18, weight gain in adult- hood 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, redistrib- uted 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 activ- ity 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 environ- ment can help people maintain the necessary long-term lifestyle changes

BEHAVIORAL RISK FACTORS 97 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 over- weight people has been shown to ameliorate hyperglycemia, hyperlipi- demia, 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 Guide- lines 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, b; 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.

98 HEALTH AND BEHAVIOR 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 sup- ply 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, com- pared 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 dis- ease (USDHHS, 2000). Although consumption of trans-fatty acids in- creases 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

BEHAVIORAL RISK FACTORS 99 in polyunsaturated fat and monounsaturated fat decreases the risk of coro- nary 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 postmeno- pausal 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 rela- tionship 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 physi- cal activity and colon cancer (Martinez et al., 1997). Physical activity not only increases intestinal motility (Thor et al., 1985) and aids in the sup- pression 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 mu- cosa 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 find- ings 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

100 HEALTH AND BEHAVIOR 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 physi- cal 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 con- tain carotenoids reduce the risk of lung cancer (Ziegler et al., 1996), ran- domized trials of the specific carotenoid, β-carotene, fail to show any ben- efit (Albanes et al., 1996; Hennekens et al., 1996). In fact, the β-Carotene and Retinol Efficacy Trial (Omenn et al., 1996) found an increase in mor- tality in patients taking supplements of β-carotene and vitamin A. Evi- dence 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 dur- ing adulthood (USDHHS, 1996). Increased bone mineral density is posi- tively associated with aerobic exercise (Snow-Harter et al., 1996; USDHHS, 2000). Through its load-bearing effect on the skeleton, physi- cal 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 pro- tein intake and high dairy calcium intake are both related to increased

BEHAVIORAL RISK FACTORS 101 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 deter- mined, it has not been established to what extent increased calcium in- take will prevent osteoporosis. Although most young children meet the dietary requirements for cal- cium, the intake of calcium declines precipitously with age (USDHHS, 2000). In part as a consequence of inadequate calcium in the diet, os- teoporosis 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 strengthen- ing 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 in- creased 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 im- prove functioning among persons who already have osteoarthritis or rheu- matoid 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 asso- ciated with running or bicycling on roads, and various sports are associ-

102 HEALTH AND BEHAVIOR ated 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, al- cohol 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 mil- lion people) meet diagnostic criteria for alcohol dependence, and an addi- tional 7% (more than 5.6 million people) meet diagnostic criteria for al- cohol 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 adoles- cents (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 alcohol- ism 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 alco-

BEHAVIORAL RISK FACTORS 103 hol consumption (NCHS, 1998a). Generally, heavy drinking tends to de- crease with education, and moderate alcohol use increases with education (NCHS, 1998a; Substance Abuse and Mental Health Services Adminis- tration, 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 educa- tion (NCHS, 1998a). White men with high school diplomas were 20% more likely to report heavy alcohol use than were those with more educa- tion. 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 mor- tality and consumption of alcohol (Pearl, 1926). The wide range of alco- hol-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 conse- quences (USDHHS, 1997a; 2000). Long-term excessive drinking in- creases 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 can- cer (Reichman, 1994; USDHHS, 2000).4 The Dietary Guidelines for Ameri- cans (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 4A 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.

104 HEALTH AND BEHAVIOR 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 disor- ders (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 propor- tion 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 relation- ships (Brookoff et al., 1997); it is a factor in homicide, suicide, marital violence, and child abuse (Roizen, 1993; USDHHS, 2000); and it con- tributes to high-risk sexual behavior (Strunin and Hingson, 1992, 1993; USDHHS, 2000). Positive Health Effects In contrast with those harmful effects, however, evidence is over- whelming 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,

BEHAVIORAL RISK FACTORS 105 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 be- cause 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 condi- tional. 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 car- diovascular disease and injuries or trauma varies significantly with age and sex as well as from one society to another. For instance, in Sub-Sa- haran 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 epidemio- logic 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 cardiovas- cular diseases (Schoenborn and Marano, 1988). In another study involv- ing Swedish military recruits in the same age range, a linear increase in

106 HEALTH AND BEHAVIOR risk of death from all causes was found with increasing alcohol consump- tion (Andreasson et al., 1988). Although alcohol consumption is unlikely to reduce total mortality in people under 45 (Doll, 1997), the optimal duration of moderate alco- hol 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 (Jack- son et al., 1992), many of the important effects of ethanol on high-density lipoproteins and clotting components are acute; thus, it is likely that alco- hol 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 (mak- ing them more prone to intoxication than men after drinking the same amount of alcohol) (USDHHS, 2000). Women also have lower age-spe- cific risks of cardiovascular disease and greater susceptibility to liver dam- age 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 con- sume more than 7 drinks per week or more than 3 per occasion (USDHHS, 1995, 2000). The problem of alcohol consumption is frequently one of maldistri- bution, 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 ab- stention and of heavy drinking (Holman and English, 1996). There are risks in promoting a population wide alcohol policy that discourages ab- stention, even if the policy encourages only light-to-moderate regular con- sumption. 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).

BEHAVIORAL RISK FACTORS 107 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 car- diovascular disease. One important consideration is whether physical ac- tivity 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 immunodefi- ciency 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 (Ander- son 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 be- come life threatening.

108 HEALTH AND BEHAVIOR 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 de- cade 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 Ameri- cans 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 part- ners 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 re- ported 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 behav- iors (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 effi- cient 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

BEHAVIORAL RISK FACTORS 109 factors contribute to their rapid spread in a population. Because most sexu- ally transmitted infections are asymptomatic, or produce very mild symp- toms, they often are disregarded, so infected persons do not seek immedi- ate 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 even- tual recognition of a clinically significant health problem; it is sometimes several years before an infection manifests itself. Thus, because the origi- nal infection is often asymptomatic, there is frequently no perceived con- nection 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 contrib- utes both directly and indirectly to the transmission of disease. Directly, women who experience this type of violence are less able to protect them- selves 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 mul- tiple 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, of- ten 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 transmit- ted infections in the United States is the stigma connected with them. Another is the overall discomfort many people have with discussing inti- mate aspects of life, particularly those related to sex (Brandt, 1985;

110 HEALTH AND BEHAVIOR USDHHS, 2000). This is what most significantly separates the United States from industrialized countries that have low rates of sexually trans- mitted infection. (USDHHS, 2000). Even in the most intimate relation- ships, 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 pro- grams for adolescents, and it discourages open discussion between parents and their children and between sex partners regarding sexually transmit- ted 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 approxi- mately 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 hepato- cellular carcinoma (liver cancer) became evident during the 1980s. Hepa- titis 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 sexu- ally transmitted infections, some are disproportionately affected by these diseases and their associated complications. For instance, not only do sexu- ally transmitted diseases occur more frequently in women than in men, but women also suffer more serious complications (USDHHS, 2000), in- cluding pelvic inflammatory disease, ectopic pregnancy, infertility, and

BEHAVIORAL RISK FACTORS 111 chronic pelvic pain (Chandra and Stephen, 1998; USDHHS, 2000). In addition, women are biologically more susceptible to infection when ex- posed to a sexually transmitted disease agent, and sexually transmitted diseases are more difficult to diagnose in women because of female physi- ology and the anatomy of the reproductive tract (USDHHS, 2000). Sexually transmitted diseases pose a risk to unborn children. The dis- eases 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 trans- mitted infection can complicate a pregnancy even without directly reach- ing the fetus or newborn, causing spontaneous abortion, stillbirth, prema- ture 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 bio- logical (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 in- creased almost 5-fold over just 10 years (Fleming et al., 1997; USDHHS, 2000). Several factors contribute these incidences. Because many teenag- ers 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 dis- eases (USDHHS, 2000). Rates of sexually transmitted diseases are higher for minority and eth- nic groups (primarily African American and Hispanic populations) than for whites. For example, although chlamydia is a widely distributed sexu- ally transmitted infection in all racial and ethnic groups, the prevalence is higher in minorities. In 1996, African Americans accounted for approxi- mately 78% of the total number of gonorrhea cases reported—32 times the rate for whites. These high rates also apply to African American ado-

112 HEALTH AND BEHAVIOR lescents 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 Hispan- ics 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 Ameri- cans 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 re- ported 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 popula- tion, 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 part- ners, 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 be- havioral norms. Research conducted in the past decade has shown that sexual behavior and sexual preference exhibit persistent social regulari- ties, which implies that social forces are important in shaping sexual ex- pression (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 infec- tion and ways to prevent it. Because only a small percentage of adoles- cents 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 trans- mitted infections (IOM, 1997). Curricula including information about

BEHAVIORAL RISK FACTORS 113 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 meth- ods: 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 con- dom 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 contracep- tion could help prevent unwanted pregnancies and transmission of infec- tions (Cates and Stone, 1992; USDHHS, 2000). DISEASE SCREENING PRACTICES Screening asymptomatic persons to detect preclinical disease has be- come 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 pri- marily on that person’s age and sex. In addition, consideration of indi- vidual risk factors, such as lifestyle or family history, often is used to deter- mine which tests are appropriate tests and how often testing should be done. In 1984, the U.S. Public Health Service commissioned the U.S. Pre- ventive Services Task Force. This panel was charged with developing rec- ommendations for clinicians on the appropriate use of preventive inter-

114 HEALTH AND BEHAVIOR ventions, including screening for preclinical disease and screening for dis- ease risk, based on a systematic review of evidence of clinical effective- ness. In 1989, the first Guide to Clinical Preventive Services (U.S. Preven- tive 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. Pre- ventive 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 require- ments 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 treat- ing 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 ef- fectiveness 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 short- ening 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

BEHAVIORAL RISK FACTORS 115 major chronic diseases of middle and older ages. For people with unusual family histories of disease, or other medical concerns, screening proce- dures 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 sphyg- momanometry (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 pres- sure elevation and the benefits of treatment. In persons with malignant hypertension, the benefits of treatment are most dramatic: treatment in- creases 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 mor- bidity 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 ob- served in this country since 1972 (Joint National Committee on Detec- tion and Treatment of High Blood Pressure, 1993). The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pres- sure and the American Heart Association recommend blood pressure mea- surement at least once every 2 years for adults with a diastolic blood pres- sure 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 Associa- tion, 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 modi-

116 HEALTH AND BEHAVIOR fiable risk factor for cardiovascular disease. Total cholesterol can be mea- sured 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 ex- perts advise telling people their “cholesterol range,” rather than providing them with a single value (Belsey and Baer, 1990). When a precise esti- mate 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 patho- physiology of coronary heart disease is similar in men and women, and it is likely that reduction of high cholesterol will benefit women as well. How- ever, 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 recom- mended for women aged 45–65 (U.S. Preventive Services Task Force, 1996). According to the U.S. Preventive Services Task Force, there is insuf- ficient 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 per- sons 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 fac- tors, 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.

BEHAVIORAL RISK FACTORS 117 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 cervi- cal cancer has decreased greatly over the past 40 years, due largely to organized screening programs to detect early-stage disease (U.S. Preven- tive 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 Na- tional Cancer Institute, the American College of Obstetricians and Gy- necologists, 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 discre- tion 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 per- sons 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 morbid- ity. Screening for early-stage colorectal cancer as well as its precursor le- sions (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 sigmoidos- copy. There is a large literature on the accuracy and effectiveness of these

118 HEALTH AND BEHAVIOR tests under varying conditions and in different groups of persons. As re- viewed 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 sigmoidos- copy is both a screening and diagnostic tool; any polyps detected can be biopsied and removed during the procedure. Evidence shows that screen- ing 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, pro- duces 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 men- tioned above, FOBT screening should be performed annually to achieve maximum benefit. There is insufficient evidence to determine the opti- mal 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 Ameri- can 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 anti- gen) 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 sub- stantial morbidity as a result of impaired sexual, urinary, and bowel func- tion, and because prostate cancer also carries a nonnegligible mortality risk (estimated 0.7%–2% 30-day mortality risk [Murphy et al., 1994;

BEHAVIORAL RISK FACTORS 119 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 pros- tate 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 ex- tremely 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), sev- eral 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. Al- though 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 scien- tific 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 ran- domized clinical trials enrolled enough women in their forties to study the benefit of screening in this age group with statistical confidence, a sum-

120 HEALTH AND BEHAVIOR mary 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 con- vened by NIH in 1997 to examine the question of whether regular mam- mography screening should be recommended for women in their forties. The group concluded that the decision to screen should be made by indi- vidual 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 Obstetri- cians 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 associ- ated 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 trans- mitted 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 screen- ing 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 indi- cating that chlamydia screening is reducing disease burden and prevent- ing associated complications (USDHHS, 2000). In a randomized, con- trolled 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 popula- tion (Britton et al., 1992; USDHHS, 2000). Testing has been identified, as has counseling, as an effective tool for

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Health and Behavior reviews our improved understanding of the complex interplay among biological, psychological, and social influences and explores findings suggested by recent research—including interventions at multiple levels that we can employ to improve human health.

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