Age at menopause is an important epidemiologic characteristic whose reliability of reporting in the US population is not known. The authors examined four hypotheses about the reliability of reported age at menopause in the United States: 1) women with hysterectomy-induced menopause more reliably report their age at menopause than women who have undergone natural menopause; 2) reliability declines with time since menopause; 3) reliability declines with age; and 4) women with higher educational levels report their age at menopause more reliably than women with less education. The authors used linear regression models among 2,545 women in the First National Health and Nutrition Examination Survey and Followup Study (1971-1984) and compared responses at first and follow-up interviews. Among women who had undergone a natural menopause, 44% reported their age. at menopause within one year from the first to second interviews; among women who had undergone a hysterectomy-induced menopause, 59% reported their age at menopause within one year from first to follow-up interviews. Only hysterectomy status and years from menopause to follow-up interview were significantly associated with the absolute difference between age at menopause reported at first and follow-up interviews. The authors conclude that caution in studies involving age at menopause may enhance our understanding of this critical event in the lives of women.

The authors conducted a survival analysis to determine the effect of poverty on mortality in a national sample of blacks and whites, 25 to 74 years of age (the first National Health and Nutrition Examination Survey (NHANES-1) and NHANES-I Epidemiologic Follow-up Study). They estimated the proportion of mortality associated with poverty during 1971–1984 and in 1991 by calculating population attributable risk and assessed confounding by major known risk factors (e.g., smoking, cholesterol levels, and physical inactivity). In 1973, 6.0 percent of U.S. mortality among black and white persons 25 to 74 years of age was attributable to poverty; in 1991, the proportion was 5.9 percent. In 1991, rates of mortality attributable to poverty were lowest for white women, 2.2 times as high for white men, 8.6 times as high for black men, and 3.6 times as high for black women. Adjustment for all these potential confounders combined had little effect on the hazard ratio among men, but reduced the effect of poverty on mortality among women by 42 percent. The proportion of mortality attributable to poverty among U.S. black and white adults has changed only minimally in recent decades. The effect of poverty on mortality must be largely explained by conditions other than commonly recognized risk factors.

Results of several studies suggest that either a reduction in the serum level of total cholesterol level or a persistently low cholesterol level may be associated with an increase in violent deaths. Although there are several possible explanations for these observations, it has been suggested that the cholesterol level could influence various behaviors. We therefore examined the cross-sectional relation of several psychologic characteristics, assessed by the Diagnostic Interview Schedule and the Minnesota Multiphasic Personality Inventory, to levels of total cholesterol, high-density lipoprotein cholesterol, and triglycerides among 3,490 men aged 31-45 years who were examined in 1985-1986. (All men had served in the US Army between 1965 and 1971). Compared with that of other men, the mean total cholesterol level was 5 mg/dl higher among 697 men diagnosed with generalized anxiety disorder (possibly because of increased catecholamine levels) and 7 mg/dl lower among 325 men with antisocial personality disorder (p < 0.01 for each association). These differences could not be attributed to education, relative weight, cigarette smoking, use of various medications, or other potential confounders. In contrast, cholesterol levels were not significantly associated with major depression or hostility; levels of high-density lipoprotein cholesterol and triglycerides were not related to any diagnosis. If the serum level of total cholesterol is found to be predictive of antisocial personality disorder in longitudinal analyses, this association may have implications for cholesterol-lowering recommendations.

Major depression has been associated with mortality from ischemic heart disease (IHD). In addition, a symptom of depression--hopelessness--has been suggested as a determinant of health status. We studied the relation of both depressed affect and hopelessness to IHD incidence using data from a cohort of 2,832 U.S. adults age 45-77 years who participated in the National Health Examination Follow-up Study (mean follow-up = 12.4 years) and had no history of IHD or serious illness at baseline. We used the depression subscale of the General Well-Being Schedule to define depressed affect and a single item from the scale to define hopelessness. At baseline, 11.1% of the cohort had depressed affect; 10.8% reported moderate hopelessness, and 2.9% reported severe hopelessness. Depressed affect and hopelessness were more common among women, blacks, and persons who were less educated, unmarried, smokers, or physically inactive. There were 189 cases of fatal IHD during the follow-up period. After we adjusted for demographic and risk factors, depressed affect was related to fatal IHD [relative risk = 1.5; 95% confidence interval (CI) = 1.0-2.3]; the relative risks of fatal IHD for moderate and severe levels of hopelessness were 1.6 (95% CI = 1.0-2.5) and 2.1 (95% CI = 1.1-3.9), respectively. Depressed affect and hopelessness were also associated with an increased risk of nonfatal IHD. These data indicate that depressed affect and hopelessness may play a causal role in the occurrence of both fatal and nonfatal IHD.

ABSTRACT Objective To determine the relative risk of developing a first acute myocardial infarction after treatment with oestrogens alone or oestrogen‐progestogen combinations. Design Prospective cohort study utilizing a prescription‐based and record linkage System for a follow‐up period from 1977 to 1983. Average individual observation time was 5–8 years. Setting The entire female population of the Uppsala Health Care Region (14 million inhabitants), one‐sixth of the total Swedish population. Subjects 23 174 women aged 35 years and older, identified from pharmacy records as having been prescribed non‐contraceptive oestrogens during 1977–1980. Outcomes Admissions to hospitals for first acute myocardial infarctions. Results Overall, 227 cases of a first acute myocardial infarction were observed as against 281–l expected, RR=0.81 (95% confidence limits 0.71 to 0.92). Women who were younger than 60 years at entry into the study and prescribed oestradiol com‐pounds (1–2 mg) or conjugated oestrogens (0.625–1.25 mg) showed a significant 30% reduction of the relative risk ( RR=0.69 ,0.54 to 0.86). Those prescribed a com‐bined oestradiol‐levonorgestrel brand also demonstrated a significantly lowered relative risk ( RR=0.53 , 0.30 to 0.87). The risk estimates were near unity during the first year of follow‐up but decreased during subsequent years. Exposure to the weak oestrogen oestriol did not alter the risk. Conclusion Hormonal replacement therapy with oestrogens alone, and maybe also when cyclically combined with progestogens, can reduce the risk of acute myocardial infarction.

Although socioeconomic status has been positively related to levels of high density lipoprotein (HDL) cholesterol in white Americans, limited evidence suggests that an inverse association may exist among blacks. These associations were further examined using data collected in 1985-1986 from 3,562 white and 500 black men who ranged in age from 31 to 45 years. Overall, mean levels of HDL cholesterol were 8 mg/dl higher among blacks than among whites and, in each group, levels were related positively to alcohol consumption and negatively to Quetelet index and cigarette smoking. A statistically significant interaction, however, was observed between race and educational achievement: no association was seen between educational achievement and levels of HDL cholesterol among white men, but there was an inverse association among blacks. For example, a 13 mg/dl (55 vs. 42 mg/dl) difference in levels of HDL cholesterol was observed between black and white men who did not complete high school, but only a 3 mg/dl black excess (47 vs. 44 mg/dl) was seen among college graduates. About 40 percent of this reduction could be attributed to the effects of cigarette smoking, alcohol consumption, and relative weight. These results indicate that the higher levels of HDL cholesterol frequently found among black men in the United States may not apply to all social strata. Other characteristics, such as physical activity and diet, may account for the differing race-specific associations with educational achievement.

THIS TASK FORCE reviewed an extensive body of evidence dealing with (1) social/environmental factors and (2) personality traits/coping styles or behavior patterns relating to the prevalence and incidence of hypertension. The findings in these areas are often conflicting and controversial. As noted by the task force on Central Nervous System-Behavioral Mechanisms, in animal experiments it has been difficult to induce sustained hypertension among otherwise healthy organisms solely through exposure to stress. Other environmental or biological predisposing factors must be present. However, there are reliable psychosocial correlates of human hypertension, and this working group adopted a strategy of identifying population variations and associations that warrant attention by the scientific and clinical community. The report begins by listing reliable correlates of blood pressure elevations, noting areas of promise and unanswered questions, and concludes with recommendations and a discussion of research needs. Socioeconomic status, race, and elevated blood pressure. Epidemiologic studies conducted in the United States have documented an excess risk for hypertension and its sequelae among blacks compared with whites and among persons of lower socioeconomic status compared with those of higher socioeconomic status.1-4 This impressive association between socioeconomic status and blood pressure has been observed in both blacks and whites. Although these observations are consistent and longstanding, no completely satisfactory explanation exists for the black/white difference or for the difference among social classes.5 The higher rates of hypertension observed in populations of low socioeconomic status may be related to dietary patterns and perhaps to exercise habits, which are determined in part by socioeconomic status. In addition, they may be related to the social and physical characteristics of the environments in which these individuals live and work.6 A growing number of studies have suggested that exposure to environments that require sustained vigilance as well as recurrent mobilization of coping resources to ward off physical or psychosocial harm may raise arterial pressure. at least acutely.7 8 It is well documented in the sociologic literature that individuals of low socioeconomic status

A multidisciplinary working group discussed the conceptual and methodologic issues involved in studying the role of socioeconomic and sociocultural influences in coronary heart disease (CHD) in blacks. Social status was defined as a multidimensional construct with sociostructural and personal, sociopsychological components. A nine-factor conceptual model was developed that affirmed the interplay of sociostructural factors, personal characteristics and behaviors, and health care system attitudes and practices as active contributors to CHD risk, morbidity, and mortality in blacks. Specific recommendations for future research on social status and CHD in blacks were made.

A study was carried out using 616 participants in a randomized clinical trial at the Harvard MRFIT (Multiple Risk Factor Intervention Trial) Clinical Center, to test if there were differences in the psychological dimensions of anxiety, depression, and functional heart symptoms in groups given different levels of treatment in a CHD (Coronary Heart Disease) Intervention Program. A theoretical framework was given to justify a number of hypotheses as to the induction of adverse psychological effects. At the end of two years in the MRFIT Program there were no significant differences between the special intervention group (SI) and the usual care group (UC) in the selected psychological variables.