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The aim of this study was to assess evidence that genetic factors influence body fat distribution. First-degree relatives of 324 cancer-free females in a population-based prospective study of 41,837 women (99% white) between the ages of 55 and 69 at baseline in 1986 were studied. A total of 396 living sisters (mean age 65.7 years) and 446 living daughters (mean age 41.2 years) were identified through a mailed 'family tree' questionnaire sent to each participant. Family members were mailed a questionnaire to obtain self-reported measures of current height and weight. A paper tape measure and written instructions were enclosed to obtain waist and hip circumferences. The age-adjusted mother-daughters correlations for waist-to-hip ratio and body mass index (kg/m2) were 0.19 and 0.23, respectively (P < 0.05 using Fisher's z-transformation). The corresponding sister-sister correlations were 0.23 and 0.19, respectively (P < 0.05). The sister-sister correlations were not significantly different from the mother-daughter correlations. After adjustment for body mass index the mother-daughter correlation for waist-to-hip ratio increased to 0.20 and the sister-sister correlation increased to 0.26. These familial correlations suggest that genes and common environment may contribute 40 to 50% of the total variance of waist-to-hip ratio in white women in the Midwest.

Tobacco consumption is an established risk factor for cancer at a number of sites: oral cavity, esophagus, nasopharynx, lung, larynx, pancreas, bladder, kidney, and uterine cervix. These sites also demonstrate familial aggregation. To determine if evidence exists for a major gene controlling susceptibility to smoking-associated cancers, maximum likelihood segregation analyses were performed on 337 families (3,276 individuals) ascertained through a deceased lung cancer proband. Models were fitted that allowed for personal tobacco use and variable age of onset. The hypotheses of environmental transmission and no major gene were rejected (P < 0.005), but none of the Mendelian models could be distinguished. According to Akaike's Information Criterion, Mendelian dominant inheritance of an allele that produces cancer at an earlier age of onset provided the best fit to the data. The model suggests that 62% of the population are susceptible, and that the mean age-of-onset differs for men and women: at the mean level of tobacco exposure, female gene carriers are affected, on average, 24 years earlier than non-carriers (77 vs. 101), while in males the difference was 20 years (71 vs. 91). These findings extend our earlier observations on the genetic epidemiology of lung cancer and suggest that Mendelian factors may influence the risk of cancers that are known to be smoking associated.

To test the hypothesis that a high intake of dietary cholesterol and fat is associated with elevated risks of lung cancer, we analyzed data from a population-based, prospective, cohort study conducted among 41,837 postmenopausal Iowa (United States) women who completed, in 1986, a comprehensive mailed questionnaire including information on usual intake of 127 food items. All cohort members were followed for cancer incidence through the statewide cancer registry. By 1991, after six years of follow-up, 272 incident lung-cancer cases were identified. After controlling for total energy intake and other confounding factors, dietary cholesterol, total fat, and animal fat were unrelated to lung cancer risk. Intake in the upper three quartiles of plant-derived fat, however, was related to a 30 to 40 percent lower incidence of lung cancer, comparative with those in the lowest quartile, with more pronounced reduction in risk observed among smokers (relative risk = 0.6, 95 percent confidence interval = 0.4-0.9). This prospective cohort study suggests that high intake of fat of plant origin may be associated with reduced risk of lung cancer, while dietary cholesterol and animal fat intake is unrelated to the etiology of this malignancy in postmenopausal women.

Rationale and Objectives: We asked our nonradiologist colleagues to evaluate and comment on the most desirable format for radiology education., Methods: Questionnaires were distributed to 631 nonradiologist physicians affiliated with the University of Minnesota and representing all medical specialties and academic ranks. Three hundred twenty-seven surveys were returned after one mailing., Results: Residency was retrospectively noted to be indispensable for consolidating knowledge of radiology. The overwhelming majority of clinicians in all specialties believed that formal radiologic instruction should be mandatory for medical students (279 of 322; 87%). Film interpretation was believed to be an indispensable part of a medical student radiology rotation (226 of 321; 70%), but many clinicians indicated a need for additional training. A marked disparity in the perceived level of confidence in interpreting radiologic tests during medical school and residency between those who had and those who had not received formal radiologic instruction during medical school was evident. This difference in perceived level of confidence was present even among the most experienced clinicians., Conclusions: Collectively, the nonradiologist clinicians emphasized the need for a mandatory and clinically oriented radiology curriculum during medical school.

To investigate the relation of dietary intakes of sucrose, meat, and fat, and anthropometric, lifestyle, hormonal, and reproductive factors to colon cancer incidence, data were analyzed from a prospective cohort study of 35,215 Iowa (United States) women, aged 55-69 years and without a history of cancer, who completed mailed dietary and other questionnaires in 1986. Through 1990, 212 incident cases of colon cancer were documented. Proportional hazards regression was used to adjust for age and other risk factors. Risk factors found to be associated significantly with colon cancer included: (i) sucrose-containing foods and beverages other than ice cream/milk; relative risks (RR) across the quintiles = 1.00, 1.73, 1.56, 1.54, and 2.00 (95% confidence intervals [CI] for quintiles two and five exclude 1.0); (ii) sucrose; RR across the quintiles = 1.00, 1.70, 1.81, 1.82, and 1.45 (CI for quintiles two through four exclude 1.0); (iii) height; RR = 1.23 for highest to lowest quintile (P for trend = 0.02); (iv) body mass index; RR = 1.41 for highest to lowest quintile (P for trend = 0.03); and (v) number of livebirths, RR = 1.59 for having had one to two livebirths and 1.80 for having had three or more livebirths compared with having had none (P for trend = 0.04). These data support hypotheses that sucrose intake or being tall or obese increases colon cancer risk; run contrary to the hypothesis that increased parity decreases risk; support previous findings of no association with demographic factors other than age, cigarette smoking, or use of oral contraceptives or estrogen replacement therapy; and raise questions regarding previous associations with meat, fat, protein, and physical activity.

Noninsulin-dependent diabetes mellitus and postmenopausal breast cancer share a number of risk factors, including obesity, increased waist-to-hip ratio, and a positive family history. If risk for these diseases is mediated through a familial tendency for abdominal obesity, then one might expect to see familial clustering of both diseases. We analyzed data from a prospective cohort study of 41,837 Iowa women age 55-69 years. Diabetes was not associated with incidence of breast cancer [relative risk (RR) = 0.97]. The association between family history of breast cancer and breast cancer incidence, however, was slightly modified by individual history of diabetes: a positive family history of breast cancer in the absence of baseline diabetes was associated with a relative risk of 1.36 [95% confidence interval (CI) = 1.08-1.70], whereas the presence of both factors was associated with a RR of 1.87 (95% CI = 0.93-3.76). Adjustment for waist-to-hip ratio greatly diminished this difference. Conversely, a family history of breast cancer was associated with a RR of 5-year diabetes mortality of 1.94 (95% CI = 1.17-3.24) that persisted after stratification by tertile of waist-to-hip ratio. No clear association of family history of breast cancer and waist-to-hip ratio for self-reported diabetes incidence was evident. These data are indicative of a complex interrelation between waist-to-hip ratio, familial predisposition, diabetes, and breast cancer.

Antioxidant micronutrients, including vitamin E, vitamin C, the carotenoids, and selenium, defend the body against free radicals and reactive oxygen molecules, suggesting a potential for these dietary components in cancer prevention. To investigate whether high intakes of antioxidant micronutrients protect against colon cancer in humans, we analyzed data from a prospective cohort study of 35,215 Iowa women aged 55-69 years and without a history of cancer who completed a dietary questionnaire in 1986. Through 1990, 212 incident cases of colon cancer were documented. Adjusted for age, total vitamin E intake was inversely associated with the risk of colon cancer (P for trend < 0.0001); the relative risk for the highest compared to the lowest quintile was 0.32 [95% confidence interval (95% CI) 0.19, 0.54]. Further adjustment for total energy intake and other risk factors in proportional hazards regression had little effect on these estimates. The association was not uniform across age groups: the multivariate relative risk of colon cancer for the highest compared to the lowest quintile of total vitamin E intake was 0.16 (95% CI 0.04, 0.70) for those 55-59 years old, 0.37 (95% CI 0.12, 1.16) for those 60-64 years old, and 0.93 (95% CI 0.27, 3.25) for those 65-69 years old. Multivariate-adjusted relative risks among women with higher total intakes of vitamins A and C and beta-carotene, and among users of selenium supplements, were not significantly different from 1.0. These prospective data provide evidence that a high intake of vitamin E may decrease the risk of colon cancer, especially in persons under 65 years of age.

At least three case-control studies have examined the association between alcohol consumption and endometrial cancer; two studies showed inverse associations, and a third a positive association. To our knowledge, no prospective studies of this association have been reported. The association between alcohol and endometrial cancer was examined in the Iowa Women's Health Study (United States), a prospective study of postmenopausal women. Information on alcohol consumption and other variables was obtained through a mailed questionnaire in January 1986. Through December 1990, 167 incident endometrial cancer cases occurred in the at-risk cohort of 25,170 women. Multivariate-adjusted relative risks (RR) and 95 percent confidence intervals (CI) were computed using Cox proportional hazards regression controlling for age, body mass index (BMI), parity, age at menopause, and noncontraceptive estrogen use, and to determine multiplicative interactions. The RRs of endometrial cancer associated with < 4.0 and > or = 4.0 g of alcohol per day compared with abstainers were 0.7 (CI = 0.5-1.1) and 1.0 (CI = 0.7-1.6), respectively. No statistically significant association between endometrial cancer and consumption of either beer, wine, or liquor was observed. There was no interaction between alcohol and any other endometrial cancer risk factors, including BMI or noncontraceptive estrogen use. These data do not support an association between alcohol and endometrial cancer among postmenopausal women.

Genetic segregation analyses that allowed for variable age of onset of lung cancer and smoking history were performed on 337 families, each ascertained through a lung cancer patient. Results indicated compatibility of the data with Mendelian codominant inheritance of a rare major autosomal gene that acts in concert with smoking to predispose carriers to lung cancer, by producing earlier onset of the cancer when controlling for equivalent smoking levels. Segregation at this locus could account for 69% and 47% of the cumulative incidence of lung cancer in individuals up to ages 50 and 60 respectively, but only 22% of all lung cancers in persons up to age 70. This decrease in the importance of the gene's contribution to overall lung cancer rates at later ages is most likely a reflection of an increasing proportion of noncarriers succumbing to the effects of long-term exposure to tobacco. A significant cohort effect was found, most likely due to differing smoking patterns before and after World War I, but in both cohorts the effect of a major locus could not be rejected.

This study is the result of a cross-sectional survey undertaken in five regions of the Republic of Congo. A sample of 612 women having children under 3 years of age was interviewed to determine the socioeconomic, environmental, demographic and behavioral factors associated with the occurrence of diarrhea in young children. Logistic regression analysis was used to determine which variables predict the occurrence of diarrhea in a multivariable context. Most of the statistically significant variables were those suggesting behaviorally mediated modes of transmission. These include: type of weaning food fed to the child, maternal age, sex of the child, maternal sickness and method of refuse disposal. Male children had a more than two-fold odds of experiencing recent diarrhea than did female children among those greater than 1 year of age. Although breastfeeding status was not statistically significantly associated with diarrheal disease, children under 1 year of age who were already weaned had a greater odds of disease than those who were still breasted. Due to the pattern of extended breastfeeding in this population, this relationship was difficult to assess. Urban residence also was highly associated with diarrheal disease occurrence. Urban residence is likely to reflect a host of socioeconomic, environmental and behavioral factors. These findings underscore the potential impact of educational interventions on the occurrence of diarrheal disease among young children.

Objective: To test the hypothesis that both body mass index (expressed as the ratio of weight in kilograms per height in meters squared) and the ratio of waist circumference to hip circumference are positively associated with mortality risk in older women., Design: Prospective cohort study with a 5-year follow-up period., Setting: General community., Participants: Random sample of 41,837 Iowa women aged 55 to 69 years., Main Outcome Measure: Total mortality (1504 deaths)., Main Results: Body mass index, an index of relative weight, was associated with mortality in a J-shaped fashion: rates were elevated in the leanest as well as in the most obese women. In contrast, waist/hip circumference ratio was strongly and positively associated with mortality in a dose-response manner. Adjusted for age, body mass index, smoking, education level, marital status, estrogen use, and alcohol use, a 0.15-unit increase in waist/hip circumference ratio (eg, a 15-cm [6-in] increase in waist measurement in a woman with 100-cm [40-in] hips) was associated with a 60% greater relative risk of death. The observed associations were not explained to any great degree by bias from weight loss prior to baseline or higher early deaths among lean participants., Conclusions: Waist/hip circumference ratio is a better marker than body mass index of risk of death in older women. Waist/hip circumference ratio should be measured as part of routine surveillance and risk monitoring in medical practice.

We recently provided data from a prospective cohort study of postmenopausal women which suggested that a first livebirth at age 30 or older (cf before age 20) was associated with a twofold increased risk of breast cancer in women without a family history, but a 5.8-fold higher risk in women with a positive family history. To address the question of whether these observations reflect difficulty becoming pregnant or maintaining a pregnancy, we performed additional analyses in which the outcome of each pregnancy was considered. During five years of follow-up, 620 incident cases of breast cancer were identified in the 37,105 women at risk. There was little evidence for an increased risk associated with a history of spontaneous abortion (relative risk [RR] = 1.1; 95 percent confidence interval [CI] = 0.9-1.4), nor was the risk higher among women who reported two or more spontaneous abortions in consecutive pregnancies (RR = 1.0, CI = 0.7-1.4). Although women who reported that they had tried unsuccessfully to become pregnant had only slightly and nonsignificantly elevated risks of breast cancer (RR = 1.1, CI = 0.9-1.3), a more pronounced and statistically significant association was noted in women with a positive family history (RR = 2.1, CI = 1.4-3.2). There was a strong inverse association between failure to become pregnant and parity (P < 0.0001); nearly 50 percent of the nulliparous married women reported having tried and failed to become pregnant, whereas the frequency was only 6.8 percent among married women with five or more livebirths.(ABSTRACT TRUNCATED AT 250 WORDS)

The aggregation of colon, endometrial, ovarian, and possibly breast cancers in families has been described as a "cancer family syndrome" (now called Lynch syndrome II). To determine if the familial clustering of these malignancies was more common in women with cancer than without, we analyzed data from the Iowa Women's Health Study (IWHS), a population-based sample of 41,837 women aged 55-69 years. Self-reported information was collected on history of colon, uterine, ovarian, and breast cancers in female first-degree relatives. A family history of cancer of the breast (odds ratio [OR] = 1.4), colon (OR = 1.3), and uterus (OR = 1.3), but not ovary (OR = 1.2), was significantly more common among women with a personal history of any of these four cancers (all P < 0.05); the pattern of the ORs suggested strongly that the clustering tended to be site-specific. Age-adjusted relative risks (RR) of incident colon cancer over 5 years of follow-up (N = 237) were calculated with regard to family history. Colon cancer incidence was increased among women with a family history of breast (RR = 1.3), uterine (RR = 1.4), colon (RR = 1.5), and ovarian (RR = 1.3) cancers, although none of the risk estimates achieved statistical significance. RR was, however, significantly related to the number of different cancer sites reported among family members (Ptrend = 0.008). These data on a representative sample of postmenopausal women suggest that family histories of colon, breast, uterine, and ovarian cancers are associated with an increased risk of cancer at the same site, but provide little support for the hypothesis that Lynch syndrome II is a non-random occurrence.

There are data to suggest a relationship between alcohol consumption, particularly beer, and lung cancer. This hypothesis was tested on data from a cohort of 41,837 Iowa women aged 55 to 69 years. Women were recruited by mail and provided information on alcohol and tobacco use, physical activity, and education. Compared to a randomly selected group of women without lung cancer (n = 1900), those with lung cancer (n = 109) consumed more alcohol (measured on the Willett food frequency questionnaire) (10.2 versus 3.6 g/d; P = 0.001). The difference was accounted for largely by differences in beer consumption (3.5 versus 0.6 glass/wk; P = 0.003). Liquor consumption by patients was about double that by control subjects (1.7 versus 0.8 glass/wk; P = 0.063). Wine consumption was low and did not differ between those with and those without lung cancer. The relationship between beer consumption and lung cancer risk appeared U-shaped. After adjusting for the other variables (including six categories of pack-years of smoking), beer consumption remained a significant predictor of lung cancer risk. Those drinking 1 or more beers per week had an odds ratio of 2.0 (95% confidence interval, 1.02 to 3.80) compared with those consuming less than 1 glass per week. There was no evidence of interaction with smoking. The association of beer with lung cancer does not appear to be explained solely by confounding with cigarette smoking, although that remains by far the single strongest predictor of risk.

Background: Although the results of animal studies and cross-cultural comparisons generally support a role for dietary fat in the etiology of breast cancer, results of analytic epidemiology studies are equivocal., Purpose: The association between dietary fat and subsequent breast cancer was examined in a cohort of 34,388 postmenopausal women from Iowa., Methods: Dietary habits were assessed by a food-frequency questionnaire mailed in January 1986. Through December 31, 1989, 459 incident cases of breast cancer occurred in this cohort. Proportional hazards regression was used to examine the dietary fat-breast cancer association while adjusting for potential confounders. The effects on this association of four analytic approaches to adjustment for energy intake were also considered., Results: After adjustment for known determinants of breast cancer, a modest positive association of total fat intake with risk of breast cancer was seen. Polyunsaturated fat intake was also positively associated with breast cancer (relative risk from lowest to highest intake, 1.0, 1.25, 1.31, and 1.49; P for trend = .052). Different approaches to adjustment for energy intake, however, provided different impressions of the dietary fat-breast cancer association. One method, involving categorization of crude fat intake and inclusion of total energy intake in regression analysis, gave relative risk estimates from low to high fat intake of 1.0, 1.17, 1.25, and 1.38 (P for trend = .18). Another method, based on categorization of fat intake residuals in which the variation in fat due to total energy intake was removed, gave corresponding estimates of 1.0, 1.24, 1.30, and 1.16 (P for trend = .29). The former suggests increasing breast cancer risk with increasing fat intake; the latter suggests no association., Conclusions: These results are consistent with other cohort studies that have shown a weak association or no association between dietary fat and breast cancer. They are also consistent with studies suggesting that fat intake is a determinant of breast cancer, particularly after accounting for inaccuracies in dietary assessment. The effects of different energy-adjustment methods may account in part for the varying interpretations of four previous cohort studies of dietary fat and breast cancer., Implications: Further work is needed to clarify not only the nature of the dietary fat-breast cancer association, but also the impact of different analytic methods used in the investigation of diet-disease associations.

Background: A family history of breast cancer reflects shared cultural factors, genetic predisposition, or both. There is evidence that the estimated risk associated with a family history of breast cancer increases multiplicatively in combination with other risk factors. We examined the combined effect of family history and anthropometric and reproductive factors on the risk of breast cancer in postmenopausal women., Methods: Using data from a prospective cohort study, we studied 37,105 women 55 to 69 years of age to determine whether known risk factors for breast cancer are modified by a reported family history at the time of entry into the study., Results: During the first 4 years of follow-up, 493 new breast cancers were diagnosed. The association of the waist-to-hip ratio (the circumference of the waist divided by that of the hips) with the risk of breast cancer was limited predominantly to women with a family history of breast cancer; the age-adjusted relative risk of breast cancer for the women above the fourth quintile for waist-to-hip ratio as compared with those below the first quintile was 3.2 in women with a family history of breast cancer and 1.2 for women without such a family history. An interaction was observed between a family history of breast cancer and the number of live-born children; the protective effect of higher parity was observed primarily among women with a family history of breast cancer. Similarly, the age-adjusted relative risk of breast cancer associated with a late age at first pregnancy (i.e., greater than or equal to 30 years) was 5.8 for women with a family history of breast cancer and 2.0 for women without such a family history., Conclusions: The increase in the risk of breast cancer associated with a high waist-to-hip ratio, low parity, or greater age at first pregnancy is more pronounced among women with a family history of breast cancer. These findings suggest etiologic differences between familial breast cancer and the sporadic form.

The initiation and promotion of cancer is thought to result from a series of genetic mutations, some of which may be inherited. Our analysis of 337 lung cancer families suggested that, after allowing for an individual's pack-years of tobacco use, the pattern of disease was best explained by Mendelian codominant inheritance of an allele that produced earlier age of onset. Since lung cancer rarely occurs in the absence of exposure to tobacco, differences in the prevalence of smoking across generations could have a profound influence on the fit of genetic models. In the present study, families were partitioned into two groups, based on the birth cohort of the proband, i.e., born before World War I (age at death, greater than or equal to 60 years) or born after World War I (age at death, less than 60 years). This partition was chosen because the year 1915 signaled the start of the dramatic rise in tobacco use in the United States. In younger proband families, in which parents were more likely to smoke, Mendelian codominant inheritance provided the best fit to the data. In older proband families, for whom smoking among parents was less prevalent, the "no major gene" and "environmental" hypotheses were rejected; however, no Mendelian models could be distinguished. If the results on the families with the most homogeneous exposure to tobacco across generations (born after World War I) reflect the true underlying biology, then the influence of genetic factors in the pathogenesis of lung has been underestimated; the cumulative probability of lung cancer at age 80 for a noncarrier of the gene, at the average level of tobacco consumption, is close to zero, implying that virtually all lung cancer occurs among gene carriers. Identification of this putative genetic factor has profound implications for the detection and prevention of lung cancer.

Background: The relationship of serum lipoprotein lipids and apolipoproteins to obesity was studied in a biracial sample of 2,816 children of ages 5-17 in Bogalusa, Louisiana., Methods: Two measures of obesity were used: fatness (subscapular skinfold thickness) and fat centrality (the ratio of subscapular to triceps skinfold thickness). Plasma insulin and glucose were included as metabolic markers related to obesity., Results: The obesity associations were relatively strong with insulin (rs = 0.29, P less than 0.001, skinfold; rs = 0.15, P less than 0.001, skinfold ratio) and triglycerides (rs = 0.25, P less than 0.001, skinfold; rs = 0.19, P less than 0.001, skinfold ratio). The relationships of serum low-density lipoprotein cholesterol (LDL-C) (rs = 0.17, P less than 0.001, skinfold; rs = 0.13, P less than 0.001, skinfold ratio) and apolipoprotein (apo) B (rs = 0.16, P less than 0.001, skinfold; rs = 0.13, P less than 0.001, skinfold ratio) with the obesity measures were of lesser magnitude, but persisted after adjustment for insulin and triglycerides. The inverse association of obesity to serum high-density lipoprotein cholesterol (HDL-C) (rs = -0.13, P less than 0.001, both skinfold and skinfold ratio) and apo A-I (rs = -0.04, P = 0.03, skinfold; rs = -0.05, P = 0.004, skinfold ratio) was significant only before adjustment for insulin and serum triglycerides. Multiple linear regression of obesity measures showed that, like insulin, serum triglycerides had consistently higher standardized coefficients than LDL-C, HDL-C, apo B, and apo A-I. Apo A-I and apo B added only a small amount (less than 2%) of information to the relationship of serum lipoproteins with obesity measures., Conclusion: These results indicate that serum very-low-density lipoprotein (VLDL) levels are directly and independently related to obesity. The well-known inverse association between obesity and serum HDL-C is not independent, but secondary to the elevated VLDL or triglyceride levels associated with obesity. While associations of obesity and lipoprotein cholesterol are found, far fewer occur with apolipoproteins, especially Apo A-I. Interesting race and sex differences in the relationship of obesity to serum lipoproteins and apoproteins are noted, being greater among white children and more consistent in white males.

Data on 337 lung cancer families were analyzed to determine if known cohort differences in parental cigarette consumption influence parameters from a segregation analysis. Previous results suggested that, after allowing for an individual's pack-years of tobacco exposure, Mendelian codominant inheritance of an allele that produced an earlier age of onset provided a good fit to the data. In the present study, the data were split into two groups of families: probands age 60 and over (born before WWI) and probands younger than age 60. This partition of the data by age of the proband was done to separate families in which there were parents who were less likely to smoke from those with parents more likely to smoke--predicated on the known increase of smoking prevalence after World War I. For the younger proband families (those with parents more likely to smoke), only Mendelian codominant inheritance adequately fit the data. The hypotheses of no major type, environmental transmission, and Mendelian dominant or recessive inheritance were rejected. In contrast to our earlier findings, the estimate of population susceptibility increased from 28% in the total data to 60% in this subset. In the older proband families (those with parents less likely to smoke), the no major type and environmental hypotheses were rejected; further, none of the Mendelian models could be distinguished. Our results demonstrate that cohort differences, probably in exposure to tobacco, can confound parameters of a segregation analysis, and suggest that the genetic component of lung cancer may be greater than previously estimated. It further suggests that susceptibility to lung cancer occurs as a function of susceptibility to the effects of tobacco smoking.

The familial aggregation of certain chronic diseases is well documented [Perkins, 1986; King et al., 1984; Anderson, 1982]. Dietary data on adult brothers living apart were used to examine whether familial clustering of disease could be explained by nature or nutriture. Intakes of nutrients were strikingly more similar among siblings than expected: when correlations were adjusted for country of residence, 21 of 25 (84%) were statistically significant. Thus, dietary patterns among adult siblings are more alike than could be predicted by their sharing a common culture, as alike as has been described for monozygotic twins, and as alike as described for familial correlations of serum cholesterol. Incorporation of dietary measures in co-twin studies or studies of siblings can improve the estimates of the true genetic effect on disease pathogenesis.

A number of studies have documented the familial aggregation of lung cancer; there is at least one report that female reproductive cancers are also increased in these families. To determine if the risk exists for all reproductive cancer sites, we conducted a nested case-control study of lung cancer incidence in a cohort of 41,837 women ages 55-69 years. Women were recruited by mail and asked to provide information on education, occupation, smoking habits, physical activity, and family history of specific cancer sites among female relatives. Four year follow-up for cancer incidence was conducted using a state-wide tumor registry. Compared to random controls (n = 1900), cases (n = 152) were more likely to have reported at baseline a sister affected with cancer of the uterus [crude odds ratio (OR) = 3.4, 95% Cl = 1.7-7.0, P less than 0.01], cervix (OR = 3.2, 95% Cl 1.2-8.6, P less than 0.05), or cancer at any site (OR = 1.6, 95% Cl 1.1-2.4, P less than 0.05). A family history of an affected mother with a female reproductive cancer was also more common among the cases, but not statistically significant. Cases were less educated, more likely to work in a technical/industrial setting, less physically active, more likely to smoke, and to smoke for a longer period of time than the controls (all P less than 0.01). These differences reduced the magnitude of the family history risk indicators; only the combined category of reproductive cancer at all sites among sisters remained statistically significant. Additional family studies should be done to assess environmental factors in the relatives of the cases and controls to disentangle the influence of shared genes and shared environmental factors in these associations.

Segregation analyses that allowed for variable age of onset of lung cancer and smoking history were performed on 337 families, each ascertained through a lung cancer proband. Results indicated compatibility of the data with mendelian codominant inheritance of a rare major autosomal gene that produces earlier age of onset of the cancer. Segregation at this putative locus could account for 69% and 47% of the cumulative incidence of lung cancer in individuals up to ages 50 and 60, respectively. The gene was involved in only 22% of all lung cancers in persons up to age 70, a reflection of an increasing proportion of noncarriers succumbing to the effects of long-term exposure to tobacco.

A stepwise oligogenic method is developed that can be used to adjust the phenotype of a quantitative trait for the effects of a previously identified single-locus component. This method assumes that a single-locus component can be adequately identified through the use of segregation and/or linkage analysis under a 1-locus model and that the variation due to that locus can be removed from the phenotype leaving a residual that can be parameterized in terms of an additional single-locus component. Segregation and/or linkage analysis can then be used in an attempt to identify an additional single-locus component in the residual phenotype. This stepwise process can be repeated until no further single-locus effects are identified. The method is illustrated using family data on the specific activity of dopamine-beta-hydroxylase (DBH), which a number of studies have suggested may be due either to the combined effects of single-locus and multifactorial components or to the combined effects of 2 loci.

A large pedigree (N = 356) with a high prevalence of heart disease and associated adverse lipoprotein phenotype was studied. The adverse lipoprotein phenotype is characterized by both low levels of high-density-lipoprotein cholesterol (HDL-C) alone (16.3%) and in combination with other adverse lipoprotein levels (12.8%). In all, 44.2% of all pedigree members had at least one adverse lipoprotein level. Analysis of mating types showed that all lipids and lipoproteins possess familial clustering with 25-36% of offspring above median levels when both parents had levels below the median, while 67-83% had levels above the median when both parents had levels above the median. Using adjusted lipid and lipoprotein levels, a statistically significant linear trend was found between the degree of relationship to pedigree members with heart disease, and both the low-density-lipoprotein cholesterol/high-density-lipoprotein cholesterol (LDL-C/HDL-C) ratio (P less than .05), and the very-low-density-lipoprotein cholesterol (VLDL-C; P less than .01) level. A similar analysis using the prevalence of adverse lipoprotein levels as the dependent variable and degree of relationship to heart diseased pedigree numbers as the independent variable showed significant (P less than .05) relationships with VLDL-C and the LDL-C/HDL-C ratio. Further genetic analyses of this pedigree may reveal genetic mechanisms responsible for the familiality of lipoprotein levels in this pedigree.

Several investigators have reported that relatives of lung cancer probands have a greater-than-normal likelihood for developing some form of cancer. To evaluate whether this familial risk is general for probands with cancer at any site or limited to lung cancer probands, we did a case-control study in which probands having cancer affecting any body site were identified and their pedigree data were tabulated. Telephone interviews and a mailed questionnaire were used to obtain cancer histories and environmental exposures on the families of 41 lung cancer probands, 105 probands with cancer other than lung, and 127 spouse families. Cumulative tobacco exposure (P less than .05), occupational hazards (P less than .005), and age of the family relatives (P less than .0001) were found to be statistically significant predictors of cancer risk. With consideration given for these variables, we determined that siblings of lung cancer probands were at slightly greater risk of cancer of any kind (odds ratio [OR] = 1.43, P = .06) than siblings in the control group. Much of the elevated risk was attributable to an excess of lung cancer (OR = 2.49, P = .06). Siblings of non-lung/non-breast cancer probands were also determined to be at increased risk of lung cancer as well (OR = 1.61, P = .06). For parents, the risk was lower, although parental information may have been underreported.

Disaster assessment and assistance activities are often hampered by organizational problems which diminish the effect of these efforts on the people they are intended to help. Inefficient targeting of relief causes reduced coverage of needy populations and inflated costs. In order to ensure that the most needy populations receive appropriate types and amounts of assistance, collection of assessment data must be at the lowest possible administrative unit. In addition, it is essential that disaster assessment be a dynamic process in which follow-up activities monitor possible changes in vulnerability and need in the targeted populations. This paper presents a method for post-disaster rapid needs assessment at the community level. Indigenous numerators are used to collect data with which communities are served and ranked according to need. Qualitative and quantitative methods are incorporated to provide rapidly a centralised database with which relief organizations can accurately target specific communities for assistance.