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Many studies have investigated the role of estrogen during menopause; however, less attention has been paid to the role of androgen. Given the possible opposite effects of estrogen and androgen on cardiovascular disease risk, it is suggested that relative androgen excess may better predict the increased risk of cardiovascular disease in women over the age of 50 years than estrogen levels alone. Three phases of hormonal milieu changes are hypothesized as a better way to identify the hormone-cardiovascular disease risk association. A first phase, prepause, occurs before estrogen levels decline (approximately 2 years before menopause). A second phase, interpause, occurs from the end of prepause until approximately age 55. A third phase, postpause, occurs after interpause. The duration of the interpause phase, characterized by relative androgen excess, may be an independent risk factor of cardiovascular disease. This hypothesis could provide a basis for further clinical and epidemiologic research, and it could have important implications for establishing the initiation and duration of estrogen replacement therapy use as a means to prevent cardiovascular disease.

This analysis describes the association of age with the serum total cholesterol level in 5,010 participants in a geriatric health screening program. Cholesterol levels were measured annually in participants monitored for up to 12 years. The association of age with cholesterol level is described via three approaches: cross-sectional analysis, descriptive longitudinal analysis, and longitudinal analysis using statistical modeling. The results were compared to examine the influence of cohort, period, and survivorship effects on the association between age and cholesterol. In cross-sectional analysis, the cholesterol level was fairly constant for the ages of 65 to 75 years, but decreased by 21% over the age range from 75 to 95 years. Descriptive longitudinal analysis suggested that both cohort and period effects were influencing the cross-sectional findings. In longitudinal analysis adjusting for both cohort and period effects, the findings were similar to those from cross-sectional analysis for the ages of 65 to 75 years, but from the ages of 75 to 95 years, cholesterol decreased by only 9%--half as great a decline as that estimated from cross-sectional analysis. When longitudinal data were limited to those with complete follow-up, the predicted decline for the age range from 75 to 95 years was only 6%. Although this flattening of the age trend was suggestive, there was no conclusive evidence that it reflected an association between baseline cholesterol and loss to follow-up.

Case-control differences in prediagnostic serum levels of retinol, beta-carotene, vitamin E, and selenium are compared for 10 cancer sites in 10 study populations. For all four nutrients, the majority of results showed lower levels among persons who subsequently became cases than among controls. Low levels of beta-carotene were most likely to be associated with subsequent cancer, but there were marked differences by cancer site. The results indicate that it is unlikely that any of these serum micronutrients are associated with protection against carcinogenesis at all sites. A plea is made for greater emphasis on replication of results, for reporting findings for all sites no matter how small the number of cases may be, and for keeping constantly in mind the fact that observational associations are not necessarily causal in nature.

The associations of serum lipid and lipoprotein levels with the risk of cancer mortality were assessed in 2,753 men and 2,476 women aged 40-79 years at baseline (1972-1976) who participated in the Lipid Research Clinics Program Mortality Follow-up Study through 1984. Seventy-nine cancer deaths occurred in men and 65 occurred in women during an average follow-up time of 8.4 years. Total cholesterol and low-density lipoprotein (LDL) cholesterol were significantly inversely associated with overall cancer mortality in men, but no relation was observed in women. Neither high-density lipoprotein (HDL) cholesterol nor triglycerides were significantly related to total cancer mortality in either sex, although in women. HDL cholesterol was positively associated with risk of death from gynecologic cancers. Compared with men with higher cholesterol levels, the relative risk of death from colon cancer, adjusted for age, body mass, cigarette smoking, and alcohol consumption, was 5.20 (95 percent confidence interval (Cl) 1.61-16.8) in men with total cholesterol levels less than or equal to 187 mg/dl and 4.79 (95 percent CI 1.37-16.8) in those with LDL cholesterol levels less than or equal to 119 mg/dl. Death from smoking-related cancers was inversely related to baseline total cholesterol but not to LDL cholesterol. The absence of an association with HDL cholesterol, which has been shown to be lower in persons with clinically manifest malignancy, and evidence from survival curves suggest that the inverse relation in men is not due to preexisting disease.

Smoking status and sociodemographic characteristics were recorded for 23,572 white women 25-74 years of age in a private census of Washington County, Maryland, done in 1963. Deaths from all causes, from total and sudden arteriosclerotic heart disease, and with stroke were recorded for the next 12 years. Smoking-specific mortality rates for women aged 25-44, 45-64, and 65-74 years at entry were calculated after adjustment for the effects of marital status, education, housing quality, and frequency of church attendance. Among women in the 65-74-year age group, smoking was not related to mortality. Among women in the two younger age groups, the risks of dying from any cause and from arteriosclerotic heart disease (total and sudden) were positively associated with cigarette smoking. For all arteriosclerotic heart disease deaths, the relative risks associated with smoking more than 20 cigarettes a day were 3.6 and 2.2 for women aged 25-44 and 45-64, respectively; for sudden deaths from arteriosclerotic heart disease, the relative risks were 6.5 and 2.7. The risk of dying with stroke was not associated with cigarette smoking.