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Purpose-The purpose of this study was to examine the prevalence rates for cervical, breast, and colorectal cancer screening among American Indian and Alaska Native people living in Alaska and in the Southwest US, and to investigate predictive factors associated with receiving each of the cancer screening tests. Methods-We used the Education and Research Towards Health (EARTH)Study to measure selfreported cancer screening prevalence rates among 11,358 study participants enrolled in [2004][2005][2006][2007]. We used prevalence odds ratios to examine demographic, lifestyle and medical factors associated with receiving age-and sex-appropriate cancer screening tests.Results-The prevalence rates of all the screening tests were higher in Alaska than in the Southwest. Pap test in the past 3 years was reported by 75.1% of women in Alaska and 64.6% of women in the Southwest. Mammography in the past 2 years was reported by 64.6% of women aged 40 years and older in Alaska and 44.0% of those in the Southwest. Colonoscopy or sigmoidoscopy in the past 5 years was reported by 41.1% of study participants aged 50 years and older in Alaska and by 11.7% of those in the Southwest US. Multivariate analysis found that location (Alaska versus the Southwest), higher educational status, income and the presence of one or more chronic medical condition predicted each of the three screening tests. Additional predictors of Pap test were age (women aged 25-39 years more likely to be screened than older or younger women), marital status (ever married more likely to be screened), and language spoken at home (speakers of American Indian Alaska Native language only less likely to be screened). Additional predictors of mammography were age (women aged 50 years and older were more likely to be screened than those aged 40-49 years), positive family history of breast cancer, use of smokeless tobacco (never users more likely to be screened), and urban/rural residency (urban residents more likely to be screened). Additional predictors of colonoscopy/sigmoidoscopy were age (men and women aged 60 years and older slightly more likely to be screened than those aged 50-59 years), family history of any cancer, family history of colorectal cancer, former smoking, language spoken at home (speakers of American Indian Alaska Native language less likely to be screened), and urban/rural residence (urban residents more likely to be screened).

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An overview of published observations suggests that both genetic predisposition and environment work together to produce hypertension in most persons. High blood pressure before age 55 occurs 3.8 times more often among persons with a strong positive family history of high blood pressure. Much of the total variability in blood pressure in modern populations seems attributable to genetic factors. Estimates of the proportion of the variance attributable to all genetic factors (heritability [H2]) vary from 25% in pedigree studies to 65% in twin studies for sitting diastolic blood pressure. Several biochemical traits associated with high blood pressure are highly genetic (H2, 78-84%) and may help elucidate the pathophysiology of high blood pressure. While pertinent environmental factors such as salt intake, alcohol use, and amount of exercise also correlate significantly among relatives, only 7% of the total variance of diastolic blood pressure seems attributable to all shared environmental factors in family households. Thus most familial aggregation of high blood pressure appears to be due to genes rather than shared family environment. Practical benefit may result from identifying familial predisposition in multiple siblings with high blood pressure before age 55 and lipid abnormalities (labeled "familial dyslipidemic hypertension"). About 12% of high blood pressure patients have familial dyslipidemic hypertension and also have high risk of early coronary heart disease. Hyperinsulinemia and central obesity as well as high triglycerides and low high density lipoprotein cholesterol are prominent features of familial dyslipidemic hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

The genetic and environmental determinants of hypertension, lipid abnormalities, and coronary artery disease (CAD) have been studied for 15 years in Utah in population-based multigenerational pedigrees (2500 subjects among 98 pedigrees), twin pairs (74 monozygous and 78 dizygous), hypertensive siblings (131 sibships), siblings with CAD before age 55 (45 sibships), and anecdotally ascertained pedigrees with type II diabetes (271 subjects among 16 pedigrees), lipoprotein lipase deficiency (106 subjects in a single pedigree), and familial hypercholesterolemia (502 heterozygotes among 50 pedigrees). Estimates of heritability ranged from 20 to 75% for blood pressures and blood lipids. A strong positive family history predicts a future occurrence of hypertension (relative risk [RR] = 3.8) and CAD (RR = 12.7). Segregating single-gene effects were found for several 'intermediate phenotypes' associated with hypertension (erythrocyte sodium-lithium countertransport, intraerythrocytic sodium, a relative fat pattern, total urinary kallikrein excretion, and fasting insulin levels). Strong single-gene effects in segregation analysis were also found for low-density lipoprotein (LDL) cholesterol, lipoprotein (a) (Lp[a]), low high-density lipoprotein (HDL) cholesterol, and high apolipoprotein (apo) B. Deoxyribonucleic acid (DNA) markers of lipid abnormalities or hypertension have included LDL-receptor defects, lipoprotein lipase deficiency, high Lp(a), familial defective apo B, decreased quantitative levels of apo B, apo E phenotype, angiotensinogen, and 'glucocorticoid remediable aldosteronism (GRA) hypertension.' Also tested in Utah studies, but not found to be DNA markers for hypertension, were the genetic loci for the structural genes for renin and angiotensin-converting enzyme, and the sodium antiport system. In addition, important gene-gene interactions (LDL receptor with apo E2) and gene-environment interactions (kallikrein with potassium intake) were found.(ABSTRACT TRUNCATED AT 250 WORDS)

A population-based case-control study was used to assess the relations of physical activity and diet to the development of colon cancer in Utah. Data were obtained for a reference period of two years prior to interview for controls (204 females and 180 males) and two years prior to the date of diagnosis for cases (119 females and 110 males). Both leisure time and occupational activities were ascertained by level of intensity and were converted to calories expended per week for analysis. Dietary data were obtained from a quantitative food frequency questionnaire. Physical activity and dietary data were divided into quartiles based upon the distribution in the study population for analyses. Total physical activity was protective against the development of colon cancer for both males (odds ratio (OR) = 0.70) and females (OR = 0.48) when high and low quartiles of activity were compared. Intense physical activity was the component of activity that had the greatest protective effect for males (OR = 0.27); a similar relation was seen for females (OR = 0.55). The observed relation between physical activity and colon cancer was not confounded by dietary intake of calories, fat, or protein, nor was the diet and colon cancer relation confounded by physical activity (odds ratios for calories, protein, and fat in males were 2.40, 2.57, and 2.18, respectively). Assessment of the interrelations among physical activity, diet, and colon cancer suggests that physical activity modifies colon cancer risk associated with diet.

A death certificate-based case-control study was performed to investigate associations between occupation and non-Hodgkin's lymphoma (NHL) in North Carolina. Cases consisted of 501 men who died of NHL (International Classification of Diseases codes 200 and 202) during the years 1968-1970, 1975-1977, and 1980-1982. Controls were selected from other noncancer deaths, and were frequency matched for age, year of death, and race. Occupation and industry were obtained from the death certificates and coded without knowledge of case-control status. An increased risk for men in professional, technical, and managerial occupations, compared with all others, was detected among whites (OR = 2.69, 1.95-3.72). Black men classified as having "low exposures" by an occupational exposure linkage system had an odds ratio of 1.74 (0.84-3.60). Because of this finding, the occupations were ranked by social class and a statistically significant linear relationship was noted in whites, with risk increasing from lower social class to upper social class. An increased risk was also detected among whites in the rubber, plastics, and synthetics industries (p = .03), and among blacks employed in machine trades occupations (OR = 3.63, 1.32-9.97) and structural work occupations (OR = 2.38, 0.93-6.05). An increased risk was also detected for black painters (p = .02), but not for whites. There was no association found between NHL and employment in the following areas: textile industry; farming; laborers; or occupations with exposures to asbestos or benzene. The association with farming was further examined in counties with high use of pesticides and herbicides, and no increased risk of NHL was detected. Cases were more likely to live in the western part of the state than the eastern. However, NHL mortality rates provided by the North Carolina State Center for Health Statistics did not confirm the relationship.

In four large pedigrees with heterozygous familial hypercholesterolemia (FH) genetically linked to the low density lipoprotein receptor locus, we have observed a strong interaction between the presence of FH and a single apolipoprotein (apo) E2 allele, resulting in a markedly increased prevalence of type III dyslipoproteinemia (DLPIII). DLPIII was denned by chemical criteria. None of the patients with DLPIII had tuberous or palmar xanthomas characteristic of classically denned type HI hyperlipoproteinemia. After exclusion of four persons with apo E 2-2 phenotype, there were 89 FH patients and 110 non-FH subjects. Definite DLPIII (denned as a very low density lipoprotein [VLDL] cholesterol to plasma triglyceride ratio >0.30 with plasma triglycerides >150 mg/dl) was present in 26% of 43 FH patients with a single E2 allele compared with only 3.4% of 29 non-FH subjects with an E2 allele (p=0.003). To further characterize this interaction we performed a two-way analysis of covariance, after adjustment for age, sex, and body mass index, to test for any interaction between FH and the apo E loci. There was a statistically significant interaction between FH and the presence of a single E2 allele for the ratio of VLDL cholesterol to plasma triglycerides and for a newly derived estimate of /3-VLDL cholesterol concentration. Estimated /3-VLDL cholesterol level was strongly correlated with age in the subgroup with FH and an E2 allele but not in other subgroups. There was no difference in estimated /3-VLDL cholesterol between sexes. Correlation between estimated 0-VLDL cholesterol level and body mass index in persons older than 18 years was of only marginal significance and of similar magnitude in persons with or without an apo E2 allele. Present knowledge suggests that /3-VLDLs are highly atherogenic; if so, then a sizable subset of FH patients having at least one apo E2 allele and DLPIII may be at increased risk for premature coronary heart disease. {Arteriosclerosis and Thrombosis 1991;11:1137-1146)