A cross-sectional association of obesity with coronary calcium among Japanese, Koreans, Japanese Americans, and U.S. whites.

AIMS: Conflicting evidence exists regarding whether obesity is independently associated with coronary artery calcium (CAC), a measure of coronary atherosclerosis. We examined an independent association of obesity with prevalent CAC among samples of multi-ethnic groups whose background populations have varying levels of obesity and coronary heart disease (CHD). METHODS AND RESULTS: We analysed a population-based sample of 1212 men, aged 40-49 years free of clinical cardiovascular disease recruited in 2002-06; 310 Japanese in Japan (JJ), 294 Koreans in South Korea (KN), 300 Japanese Americans (JA), and 308 Whites in the USA (UW). We defined prevalent CAC as an Agatston score of ≥10. Prevalent CAC was calculated by tertile of the body mass index (BMI) in each ethnic group and was plotted against the corresponding median of tertile BMI. Additionally, logistic regression was conducted to examine whether an association of the BMI was independent of conventional risk factors. The median BMI and crude prevalence of CAC for JJ, KN, JA, and UW were 23.4, 24.4, 27.4, and 27.1 (kg/m2); 12, 11, 32, and 26 (%), respectively. Despite the absolute difference in levels of BMI and CAC across groups, higher BMI was generally associated with higher prevalent CAC in each group. After adjusting for age, smoking, alcohol, hypertension, lipids, and diabetes mellitus, the BMI was positively and independently associated with prevalent CAC in JJ, KN, UW, but not in JA. CONCLUSION: In this multi-ethnic study, obesity was independently associated with subclinical stage of coronary atherosclerosis among men aged 40-49 years regardless of the BMI level.

Serum leptin and total dietary energy intake: the INTERLIPID Study.

PURPOSE: It has been hypothesized that leptin-induced appetite suppression is impaired in obese individuals, but little human evidence is available documenting this. We investigated relations between serum leptin and total energy intake using INTERLIPID/INTERMAP data on Japanese-Americans in Hawaii and Japanese in Japan. METHODS: Serum leptin and nutrient intakes were examined by standardized methods in men and women aged 40-59 years from two population samples, one Japanese-American in Hawaii (88 men, 94 women), the other Japanese in central Japan (123 men, 111 women). Multiple linear regression analyses stratified by BMI category (<25 kg/m(2), 25-29.9 kg/m(2), and ≥ 30 kg/m(2)) with adjustment for possible confounders were used to examine the relation between log-leptin and total dietary energy intake. RESULTS: In multivariate regression analyses, in those with BMI < 25 kg/m(2) and in those with BMI between 25 and 29.9 kg/m(2), log-leptin was not significantly related to total dietary energy intake; in those with BMI ≥ 30 kg/m(2), it was significantly inversely related to total dietary energy intake (P = 0.029), independent of body weight and physical activity. Physical activity score was significantly positively related to total dietary energy intake only in participants with BMI < 25 kg/m(2) (P < 0.001). CONCLUSION: Leptin was significantly inversely associated with dietary energy intake in obese persons, but not in overweight and normal-weight persons.

Arthritis as a risk factor for incident coronary heart disease in elderly Japanese-American males - the Honolulu Heart Program.

BACKGROUND: Arthritis is the most common chronic disease in the elderly. Studies show that rheumatoid arthritis is a risk factor for cardiovascular morbidity and mortality, and osteoarthritis is associated with an unfavorable cardiovascular risk factor profile. METHODS: At the Honolulu Heart Program's fourth examination in 1991 to 1993, arthritis status was assessed among a cohort of 3741 Japanese-American males, ages 71 to 93 years. Arthritis was determined by self-report of physician diagnosis, and subjects were divided into two groups: current arthritis and no current arthritis. Eight years of follow-up data are available for incident coronary heart disease (CHD) in 2777 subjects free of CHD at baseline. Age-adjusted rates of incident CHD and means of cardiovascular risk factors were compared in each group. Cox proportional hazards models were used to calculate relative risks, adjusting for common cardiovascular risk factors, alcohol, and use of aspirin or NSAIDs, or both. RESULTS: There were 279 cases of incident CHD in the cohort over 8 years; in those with arthritis, 11.7% developed incident CHD, compared to 9.8% in those without arthritis (p = 0.24). Age-adjusted rates of incident CHD in those with and without arthritis were 20.5 and 18.0 per 1000 person-years, respectively (p = 0.25). Arthritis was not significantly associated with CHD risk factors. Arthritis was not a significant independent predictor of incident CHD (relative risk, 1.06; 95% CI, 0.74 to 1.51). CONCLUSIONS: Arthritis, and most probably osteoarthritis, may not be associated with most CHD risk factors or 8-year incident CHD in elderly Japanese-American males.

Midlife C-reactive protein and risk of cognitive decline: a 31-year follow-up.

There is evidence for a relationship between raised inflammatory markers, including high sensitivity C-reactive protein (hs-CRP), measured late in life, and an increased risk of cognitive decline and dementia. This study evaluates the association of midlife hs-CRP concentrations with late-life longitudinal trends in cognitive function. Data are from the Honolulu-Asia Aging Study (HAAS), a longitudinal community-based study of Japanese American men. hs-CRP levels were measured on average 25 years before cognitive testing began in 1991. Subjects were followed from up to three follow-up examinations (mean of 6.1 years). At each exam, cognitive function was measured with the Cognitive Abilities Screening Instrument (CASI). This analysis includes a sub-sample of 691 subjects dementia-free in 1991. With incident dementia cases included, those with the highest quartile of hs-CRP had significantly more cognitive decline than those in the lowest quartile, after adjustment for baseline CASI score, demographic and cardiovascular risk factors. When cases were removed, there was no difference in cognitive decline by CRP quartile. This relationship was not modified by the presence of apolipoprotein E varepsilon4. These findings suggest that inflammatory mechanisms during midlife may reflect underlying processes contributing to dementia-related cognitive decline late in life.

Prior hormone therapy and breast cancer risk in the Women's Health Initiative randomized trial of estrogen plus progestin.

OBJECTIVES: To assess the extent to which prior hormone therapy modifies the breast cancer risk found with estrogen plus progestin (E+P) in the Women's Health Initiative (WHI) randomized trial. METHODS: Subgroup analyses of prior hormone use on invasive breast cancer incidence in 16,608 postmenopausal women in the WHI randomized trial of E+P over an average 5.6 years of follow-up. RESULTS: Small but statistically significant differences were found between prior HT users and non-users for most breast cancer risk factors but Gail risk scores were similar. Duration of E+P use within the trial (mean 4.4 years, S.D. 2.0) did not vary by prior use. Among 4311 prior users, the adjusted hazard ratio (HR) for E+P versus placebo was 1.96 (95% confidence interval [CI]: 1.17-3.27), significantly different (p=0.03) from that among 12,297 never users (HR 1.02; 95% CI: 0.77-1.36). The interaction between study arm and follow-up time was significant overall (p=0.01) and among never users (p=0.02) but not among prior users (p=0.10). The cumulative incidence over time for the E+P and placebo groups appeared to cross after about 3 years in prior users, and after about 5 years in women with no prior use. No interaction was found with duration (p=0.08) or recency of prior use (p=0.17). Prior hormone use significantly increased the E+P hazard ratio for larger, more advanced tumors. CONCLUSION: A safe interval for combined hormone use could not be reliably defined with these data. However, the significant increase in breast cancer risk in the trial overall after only 5.6 years of follow-up, initially concentrated in women with prior hormone exposure, but with increasing risk over time in women without prior exposure, suggests that durations only slightly longer than those in the WHI trial are associated with increased risk of breast cancer. Longer-term exposure and follow-up data are needed.