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This study tested the performance optimality hypothesis of action identification theory in the context of self-presentation. Optimal performance is said to occur when a personally easy action is identified in relatively high level terms (i.e., the action's goals and likely effects) or a personally difficult action is identified in relatively low level terms (i.e., the action's mechanical details). To test this idea with respect to self-presentation, subjects were asked to describe themselves to either a difficult-to-impress or an easy-to-impress stranger in advance of a get-acquainted conversation with him or her. Subjects were induced to think about the self-description task in either high level terms (e.g., demonstrating their personality) or low level terms (e.g., smiling when appropriate). Support for the optimality hypothesis was obtained in subjects' self-reports of their self-presentation effectiveness and in observers' evaluations of subjects. Discussion centered on the manifestation of self-presentation nonoptimality in the early stages of relationship formation.

Data from 12 US case-control studies of ovarian cancer, conducted during the period 1956–1986 and representing some 3, 000 cases and 10,000 controls, were pooled and reanalyzed. Separate analyses were conducted for four subgroups of the pooled data: invasive epithelial ovarian cancers in white women; epithelial ovarian cancers of low malignant potential in white women, epithelial ovarian cancers in black women, and nonepithelial ovarian cancers. This paper gives a brief description of the participating studies and describes the methods used in the collaborative analysis. Am J Epidemiol1992; 136: 1175–83

Data collected from 2,197 white ovarian cancer patients and 8,893 white controls in 12 US case-control studies conducted in the period 1956–1986 were used to evaluate the relation of invasive epithelial ovarian cancer to reproductive and menstrual characteristics, exogenous estrogen use, and prior pelvic surgeries. Clear trends of decreasing risk were evident with increasing number of pregnancies (regardless of outcome) and increasing duration of breast feeding and oral contraceptive use. Ovarian dysfunction leading to both infertility and malignancy is an unlikely explanation for these trends for several reasons: 1) The trends were evident even among the highly parous; 2) risk among nulliparous women did not vary by marital status or gravidity; and 3) risk among ever-married women showed little relation to length of longest pregnancy attempt or history of clinically diagnosed infertility. Risk was increased among women who had used fertility drugs and among women with long total duration of premenopausal sexual activity without birth control; these associations were particularly strong among the nulligravid. No consistent trends in risk were seen with age at menarche, age at menopause, or duration of estrogen replacement therapy. A history of tubal ligation or of hystereclomy with ovarian conservation was associated with reduced ovarian cancer risk. These observations suggest that pregnancy, breast feeding, and oral contraceptive use induce biological changes that protect against ovarian malignancy, that, at most, a small fraction of the excess ovarian cancer risk among nulliparous women is due to infertility, and that any increased risk associated with infertility may be due to the use of fertility drugs. Am J Epidemiol 1992; 136: 1184–1203

Epithelial ovarian neoplasms of low malignant potential, also called borderline ovarian tumors, have various features of malignancy, but they do not invade the ovarian stroma. Women with these tumors usually are younger when diagnosed and have better prognoses than do women with invasive tumors. There have been few epidemiologic studies of borderline tumors, and it is unclear whether there are etiologic differences between the two types of tumor behavior. Combined data from nine case-control studies, conducted from 1974 to 1986 and representing 327 white women with tumors of low malignant potential and 4, 144 white controls, were used to evaluate the relation between these tumors and personal characteristics related to invasive ovarian cancer. The risk profile for tumors of low malignant potential was found to be similar to that for invasive tumors, with two exceptions: Compared with that of invasive tumors, risk of borderline tumors was less clearly reduced among women who had used oral contraceptives and more clearly elevated among women with a history of Infertility. Am J Epidemiol 1992; 136: 1204–11

Two hypotheses have been proposed to explain the reduced risk of epithelial ovarian cancer associated with pregnancy and oral contraceptive use. The first states that some sequelae of ovulation increase the likelihood of malignancy and that pregnancies and oral contraceptives protect by suppressing ovulation. The second hypothesis states that circulating levels of pituitary gonadotropins increase the risk of malignancy and that pregnancies and oral contraceptives protect by suppressing secretion of these hormones. The authors evaluate the two hypotheses in light of combined data from 12 United States case-oxitrol studies of epithelial ovarian cancer in white women conducted from 1956 to 1986. While a number of observations support both hypotheses, there are exceptions. Differential risk reduction associated with pregnancy and oral contraceptive use (pregnancy being the more effective in young women and the less effective in older women) conflicts with the first “ovulation” hypothesis, while reduced risk associated with breast feeding and absence of altered risk associated with estrogen replacement therapy conflicts with the second “gonadotropin” hypothesis. Several findings would not have been predicted by either hypothesis, e.g., only weak trends relate cancer risk to age at menarche, and, among older women, no clear trends relate risk to age at menopause. Odds ratio attenuation due to errors in reporting personal characteristics may be responsible for some of these inconsistencies. Multidisciplinary research is needed to clarify the etkrfogic roles of ovulation and gonadotropin stimulation, both of which may enhance carcinogenesis in the ovarian epithelium. Am J Epidemiol 1992: 136: 1212–20

Background Previous epidemiologic studies of ovarian cancer have focused chiefly on White women, who have a higher incidence of ovarian cancer than Black women. No study has previously examined risk factors for ovarian cancer among Black women. Purpose This study was designed to evaluate the risk of epithelial ovarian cancer in Black women in relation to reproductive characteristics such as pregnancy, oral contraceptive use, and breast-feeding, and to determine whether differences in reproductive factors between Black and White women account for differences in ovarian cancer incidence. Methods Combining interview data from seven case-control studies, we compared reproductive characteristics of 110 Black case subjects with a diagnosis of epithelial ovarian cancer between 1971 and 1986 with characteristics of 251 Black population control subjects and 114 Black hospital control subjects. We also compared the prevalence of reproductive factors in 246 Black population control subjects and 4378 White population control subjects and estimated the fraction of Black-White differences in ovarian cancer incidence attributable to racial differences in prevalence of these characteristics. Results Decreased risks of epithelial ovarian cancer in Black women were associated with parity of four or higher (odds ratio [OR]=0.53; 95% confidence interval [CI]=0.25–1.1), breast-feeding for 6 months or longer (OR=0.85; 95% CI=0.36–2.0), and use of oral contraceptives for 6 years or longer (OR=0.62; 95% CI=0.24–1.6). A greater proportion of Black women (48%) than White women (27%) reported four or more term pregnancies, and Black women (62%) were more likely than White women (53%) to have breast-fed their children. Oral contraceptive use was more common among White women (59%) than Black women (51%). Conclusions Differences in the prevalence of other factors related to ovarian cancer risk or differences in genetic susceptibility must explain most of the Black-White differences in incidence of ovarian cancer. [J Natl Cancer Inst 85:142–147, 1993]