Genetic variants associated with susceptibility to late-onset Alzheimer disease are known for individuals of European ancestry, but whether the same or different variants account for the genetic risk of Alzheimer disease in African American individuals is unknown. Identification of disease-associated variants helps identify targets for genetic testing, prevention, and treatment.
To identify genetic loci associated with late-onset Alzheimer disease in African Americans.
Design, Setting, and Participants
The Alzheimer Disease Genetics Consortium (ADGC) assembled multiple data sets representing a total of 5896 African Americans (1968 case participants, 3928 control participants) 60 years or older that were collected between 1989 and 2011 at multiple sites. The association of Alzheimer disease with genotyped and imputed single-nucleotide polymorphisms (SNPs) was assessed in case-control and in family-based data sets. Results from individual data sets were combined to perform an inverse variance–weighted meta-analysis, first with genome-wide analyses and subsequently with gene-based tests for previously reported loci.
Main Outcomes and Measures
Presence of Alzheimer disease according to standardized criteria.
Genome-wide significance in fully adjusted models (sex, age, APOE genotype, population stratification) was observed for a SNP in ABCA7 (rs115550680, allele = G; frequency, 0.09 cases and 0.06 controls; odds ratio [OR], 1.79 [95% CI, 1.47-2.12]; P = 2.2 × 10–9), which is in linkage disequilibrium with SNPs previously associated with Alzheimer disease in Europeans (0.8
Conclusions and Relevance
In this meta-analysis of data from African American participants, Alzheimer disease was significantly associated with variants in ABCA7 and with other genes that have been associated with Alzheimer disease in individuals of European ancestry. Replication and functional validation of this finding is needed before this information is used in clinical settings.
Background and purpose
Magnitude, geographic and ethnic variation in trends in stroke within the US require updating for health services and health disparities research.
Data for stroke were analyzed from the US mortality files for 1999–2007. Age-adjusted death rates were computed for non-Hispanic African Americans (AA) and European Americans (EA) aged 45 years and over.
Between 1999 and 2007 the age-adjusted death rate per 100,000 for stroke declined both in AA and in EA of both genders. Among AA females, EA females and EA males, rates declined by at least 2% annually in every division. Among AA males, rates declined little in the East and West South Central Divisions where disparities in trends by urbanization level were found.
Between 1999 and 2007, the rate of decline in stroke mortality varied by geographic region and ethnic group.
African Americans; Aging; Cerebrovascular disorders; Mortality; geography
Geographic variation in racial differences in occurrence of dementia within the US has received little attention despite its importance for generation of new etiologic hypotheses and health disparities research. We test the hypothesis that the geographic pattern of mortality with dementia coded on the death certificate varies by race and racial differences vary by geography in the US.
Analysis of the US multiple cause of death files for 1999–2004.
United States of America.
Decedents with dementia coded as underlying or contributing cause of death on the death certificate.
Age-adjusted death rates for US Census geographic divisions for blacks and whites aged 65 years and over.
In 1999–2004 the US age-adjusted annual death rate per 100,000 for dementia was 628 in blacks and 647 in whites. The difference between rates in blacks and whites ranged from −130 deaths per 100,000 (−36%) in the Middle Atlantic to +55 (+8%) in the South Atlantic division. Blacks had higher rates in three divisions and whites in five. In the Middle Atlantic and US, blacks were relatively more likely to receive a diagnosis of unspecified dementia/senility (66%) than Alzheimer’s disease (30%) compared to whites (58% versus 41%).
Although overall rates were similar, geographic variation in racial differences in rates of death with dementia occurred among US regions. Further research is needed to assess geographic and racial variation in artifacts of certification versus biological variation as possible causes of variation to enhance utility of mortality data for disease monitoring and health disparities research.
Blacks; Aging; Dementia; Mortality; Geography; Alzheimer's Disease
Magnitudes, geographic and racial variation in trends in coronary heart disease (CHD) mortality within the US require updating for health services and health disparities research. Therefore the aim of this study is to present data on these trends through 2007.
Data for CHD were analyzed using the US mortality files for 1999–2007 obtained from the US Centers for Disease Control and Prevention. Age-adjusted annual death rates were computed for non-Hispanic African Americans (AA) and European Americans (EA) aged 35–84 years. The direct method was used to standardize rates by age, using the 2000 US standard population. Joinpoint regression models were used to evaluate trends, expressed as annual percent change (APC).
For both AA men and women the magnitude in CHD mortality is higher compared to EA men and women, respectively. Between 1999 and 2007 the rate declined both in AA and in EA of both sexes in every geographic division; however, relative declines varied. For example, among men, relative average annual declines ranged from 3.2% to 4.7% in AA and from 4.4% to 5.5% in EA among geographic divisions. In women, rates declined more in later years of the decade and in women over 54 years. In 2007, age-adjusted death rate per 100,000 for CHD ranged from 93 in EA women in New England to 345 in AA men in the East North Central division. In EA, areas near the Ohio and lower Mississippi Rivers had above average rates. Disparities in trends by urbanization level were also found. For AA in the East North Central division, the APC was similar in large central metro (−4.2), large fringe metro (−4.3), medium metro urbanization strata (−4.4), and small metro (−3.9). APC was somewhat higher in the micropolitan/non-metro (−5.3), and especially the non-core/non-metro (−6.5). For EA in the East South Central division, the APC was higher in large central metro (−5.3), large fringe metro (−4.3) and medium metro urbanization strata (−5.1) than in small metro (−3.8), micropolitan/non-metro (−4.0), and non-core/non-metro (−3.3) urbanization strata.
Between 1999 and 2007, the level and rate of decline in CHD mortality displayed persistent disparities. Declines were greater in EA than AA racial groups. Rates were greater in the Ohio and Mississippi River than other geographic regions.
Coronary heart disease; African Americans; Mortality
Genetic susceptibility testing for common diseases is expanding, but little is known about race group differences in test perceptions. The purpose of this study was to examine differences between African Americans and Whites in knowledge, attitudes, and motivations regarding genetic susceptibility testing for Alzheimer’s disease (AD). Before enrolling in an AD genetic testing research trial, 313 first-degree relatives of AD patients (20% African American; 71% female; mean age = 58 years) were surveyed regarding: (1) knowledge about genetics and AD risk; (2) concerns about developing AD; and (3) reasons for seeking testing. In comparison to Whites, African Americans were less knowledgeable about genetics and AD risk (p<.01) and less concerned about developing AD (p<.05), with lower levels of perceived disease risk (p=.04). The results suggest that African Americans and Whites differ notably in their knowledge, beliefs, and attitudes regarding genetic testing for AD. Additional research with more representative samples is needed to better understand these differences.
Genetic testing; African Americans; Alzheimer’s disease; APOE; Risk assessment; Susceptibility testing; Health beliefs; Health literacy; Health disparities
To evaluate the association of genetic variation with late-onset Alzheimer disease (AD) in African Americans, including genes implicated in recent genome-wide association studies of whites.
We analyzed a genome-wide set of 2.5 million imputed markers to evaluate the genetic basis of AD in an African American population.
Five hundred thirteen well-characterized African American AD cases and 496 cognitively normal African American control subjects.
Data were collected from multiple sites as part of the Multi-Institutional Research on Alzheimer Genetic Epidemiology (MIRAGE) Study and the Henry Ford Health System as part of the Genetic and Environmental Risk Factors for Alzheimer Disease Among African Americans (GenerAAtions) Study.
Several significant single-nucleotide polymorphisms (SNPs) were observed in the region of the apolipoprotein E gene (APOE). After adjusting for the confounding effects of APOE genotype, one of these SNPs, rs6859 in PVRL2, remained significantly associated with AD (P=.0087). Association was also observed with SNPs in CLU, PICALM, BIN1, EPHA1, MS4A, ABCA7, and CD33, although the effect direction for some SNPs and the most significant SNPs differed from findings in data sets consisting of whites. Finally, using the African American genome-wide association study data set as a discovery sample, we obtained suggestive evidence of association with SNPs for several novel candidate genes.
Some genes contribute to AD pathogenesis in both white and African American cohorts, although it is unclear whether the causal variants are the same. A larger African American sample will be needed to confirm novel gene associations, which may be population specific.
Genetic and environmental hypotheses may explain why normotensive persons at high risk of developing hypertension often exhibit greater cardiovascular reactivity to stressors than those at low risk.
Pearson’s correlation was used to evaluate reproducibility and independent t test to compare the cardiovascular responses to 30 W of exercise of normotensive young adult African-American women with positive and negative parental histories (PH) of hypertension (PH+, n = 23; PH−, n = 20).
Correlations were significant for duplicate measurements. The effects of PH on blood pressure measured at rest and during exercise were not statistically significant (P > 0.1). A nearly significant trend for greater resting V̇O2 (P = 0.08) was detected in the PH− than in the PH+ group (3.67 ± 0.18 versus 3.26 ± 0.14 mL/kg/min).
A hyper-reactive blood pressure response to exercise, characteristic of the evolution of hypertension, may not be present among the normotensive female offspring of hypertensive African Americans. The significance of an 11% intergroup difference in the mean resting V̇O2 observed in this study is unclear.
Hypertension; Exercise; African Americans; Parental history
The aim of our study was to examine whether there is an association between blood pressure reactivity to the cold pressor test in African Americans who engaged in different levels of physical activity. We examined the systolic pressure, diastolic pressure, mean arterial blood pressure, heart rate, cardiac index, total peripheral resistance, and forearm blood flow during a two-minute cold pressor test in 15 aerobic, physically active and 15 physically inactive, normotensive young adult African-American males. Peak oxygen consumption varied as a function of physical activity, and was significantly higher in the physically active than in the physically inactive subjects (54.5 ± 1.5 vs 36.8 ± 0.7 ml · kg−1 · min−1) (P<.05). During the cold pressor test, consisting of immersing the foot in ice water, the change in cardiovascular responses were similar between the physically active and the physically inactive groups. These results suggest that regular physical activity may not contribute to an attenuated blood pressure response to behavioral stress of the cold pressor test in normotensive young adult African-American males.
African Americans; Physical Activity; Blood Pressure Reactivity
An exaggerated exercise blood pressure response (EEBPR) may be associated with an increased risk of hypertension. We hypothesized that aerobic exercise training can decrease EEBPR and the risk for hypertension by decreasing arterial resistance. We studied the effects of aerobic training on the submaximal exercise blood pressure (BP) of eight normotensive young adult African-American men with an EEBPR. Subjects were trained on a stationary bicycle at an intensity of 70% peak oxygen uptake (VO2peak) for 30 min, three times per week, for 8 weeks. BP, heart rate, cardiac output (CO), stroke volume (SV) and total peripheral vascular resistance (TPR) were measured at rest and during submaximal exercise at a work intensity of 50% VO2peak. Significance of the training effects were evaluated by comparing the pre- and post-training measures (t-test, p < 0.05). A 15% post-training increase in VO2peak (34.6 ± 1.4 to 40 ± 1.4 ml/kg/min) and a 9.5 ml post-training increase in mean resting stroke volume were found. A 16.2 mmHg decrement in mean systolic BP, an 11.5 mmHg decrement in mean diastolic BP, a 120 dyne/s/cm5 decrement in TPR and a 1.2 l/min increase in CO were detected during the post-training submaximal exercise tests. These results suggest that reductions in TPR may attenuate the EEBPR of normotensive African-American males following an 8-week training regimen of stationary bicycling at 70% VO2peak. Aerobic exercise training may, therefore, reduce the risk of hypertension in normotensive African-American males by the mechanism of a reduction in TPR. Because of the limited number of subjects, the results of this study should be interpreted cautiously pending confirmation by a larger controlled trial.
blood pressure; exercise training; African-Americans
Previous studies report that low levels cognitive function and history of smoking are associated with increased mortality risk. Elderly smokers may have increased risk of dementia, but risk in former smokers is unclear. We tested the hypotheses that the harmful effect of impaired cognitive function as related to mortality is greater in persons smoking at baseline than in others. Further, we used serum cotinine levels to assess recall bias of smoking history by cognitive function level. Data were analyzed from a longitudinal mortality follow-up study of 4,916 American men and women aged 60 years and over, examined in 1988–1994 with complete data followed an average 8.5 years. Measurements at baseline included smoking history, a short index of cognitive function (SICF), serum cotinine and socio-demographics. Death during follow-up occurred in 1,919 persons. In proportional hazards regression analysis, a significant interaction of current smoking with cognitive function was not found; but there was a significant age-smoking interaction. After adjusting for confounding by age or multiple variables, current smoking associated with over 2-fold increased mortality (hazards ratio and 95% confidence limits current versus never smoking 2.13, 1.75–2.59) and SICF with 32% reduction in mortality; top versus bottom SICF stratum 0.68, 0.53–0.88). Serum cotinine data revealed substantial recall bias of smoking history in persons with cognitive impairment. However analyses correcting for this bias did not alter the main conclusions: In a nationwide cohort of older Americans, analyses demonstrated a lower risk of death independent of confounders among those with high SICF scores and never smokers, without a significant interaction of the two.
smoking; memory; mortality; cotinine
Limited data suggest that physical activity increases postexercise blood pressure in African-American women. The purpose of this study was to evaluate the postexercise blood pressure response to acute exercise in normotensive young adult African-American women.
Eight healthy women (age 22.5±.9 years) performed a cycle ergometer bout of 30 minutes at 60% of peak ventilatory oxygen uptake (VO2 peak). Control arterial blood pressure, heart rate, lower leg blood flow, cardiac output, spectral analysis of blood pressure, heart rate variability, and baroreceptor sensitivity were measured for 5 minutes before exercise and were compared to post-exercise measurements performed at rest intervals of 15–20, 35–40 and 55–60 minutes after exercise.
Exercise performed at 60% VO2 peak produced an arterial pressure of 172±10/70.1±4.0 mm Hg. Postexercise recovery values were not significantly different than the baseline control values.
These results do not support the hypothesis that acute physical activity exerts an adverse effect on postexercise blood pressure in African American women.
Exercise; African-American Women; Blood Pressure
Exercise may contribute to the maintenance of vascular function via enhanced liberation and action of bone-marrow-derived progenitor cells. Activity related changes in oxidative stress may also influence the number and function of these cells. In the present study, we sought to determine (i) whether adaptations in reactive hyperaemic FBF (forearm blood flow) response associated with long-term endurance exercise and short-term detraining were related to resting putative progenitor cell number and function, and (ii) whether oxidative stress affected these factors. Participants included men with a history of more than 30 years of moderate-to-high-intensity exercise (HI group) and healthy low-active age- and BMI (body mass index)-matched control subjects (LO group). Vascular reactive hyperaemic FBF response, resting CD34+ and CD34+/VEGFR2+ (vascular endothelial growth factor receptor 2+] cell number, CFU-EC (colony-forming unit-endothelial cell) count and CFU-EC senescence were evaluated. Oxidative stress measures included OxLDL (oxidized low-density lipoprotein) and TAC (total antioxidant capacity). These measures were assessed following 10 days of detraining in the HI group. The HI group had greater peak reactive hyperaemic FBF responses compared with the LO group, despite no difference in resting CD34+ cell number, CD34+/VEGFR2+ cell number, CFU-EC colonies or CFU-EC senescence. With detraining in the HI group, CD34+ cells declined 44 %, and the percentage change in CD34+/VEGFR2+ cells was positively correlated with the change in FBF response to reactive hyperaemia. The percentage change in CD34+/VEGFR2+ cells and the percentage change in EPC (endothelial progenitor cell) senescence with detraining were related to the percentage change in TAC. These results reveal that changes in reactive hyperaemic FBF are closely related to activity dependent dynamic changes in CD34+/VEGFR2+ cell number, which may be influenced by alterations in oxidative stress.
aging; antioxidant; endothelial progenitor cell; exercise; forearm blood flow; physical inactivity
Increasing physical activity is postulated to slow cognitive decline associated with aging. Low levels of both physical activity and cognitive function are associated with increased risk of mortality. We test the hypothesis that the relative protective effect of high physical activity level as related to mortality is greater in persons with impaired cognitive function than in others.
Data were analyzed from a longitudinal mortality follow-up study of 5903 American men and women aged 60 years and older examined in 1988 to 1994 who were followed an average of 8.5 years. Measurements at baseline included self-reported leisure-time physical activity (LTPA), a short index of cognitive function (SICF), sociodemographic data, health status, and physical and biochemical measurements.
Death during follow-up occurred in 2431 persons. In bivariate cross-sectional analyses, more frequent LTPA was associated with greater cognitive function. In proportional hazards regression analysis, no significant interaction of LTPA with cognitive function was found; however, there was a significant age-LTPA interaction. After adjusting for confounding by baseline sociodemographic data and health status at ages 60 to 74, the hazards ratio (95% confidence intervals) was for LTPA more than 8 times weekly compared with none (0.51; 0.38–0.76, p < .001) and for low SICF score compared with high 1.43 (1.36; 1.00–1.84, p < .05). After controlling for health behaviors, blood pressure, and body mass, C-reactive protein, and high-density lipoprotein cholesterol, the LTPA hazards ratio was 0.52 (0.35–0.78; p = .002), but cognitive function was no longer significant. At ages 75 and older, results were similar for LTPA, but cognitive function remained significant after adjustment.
In a nationwide cohort of older Americans, analyses demonstrated a lower risk of death independent of confounders among those with frequent LTPA. Much of the effect of low cognitive function could be explained by other risk factors at ages 60 to 74 but not 75 years and older.
Aging; Cognitive Function; Dementia; Exercise; Mortality; Physical Activity
Geographic and temporal variation in occurrence of dementia within the US has received little attention despite its importance for generation of new etiologic hypotheses and health services research. We examine methodological problems in the use of vital statistics data for assessing variation over time, among states and within states in the US. We analyzed the US multiple cause of death files for 2005–2006 and 1999–2000 US deaths with Alzheimer’s Disease (International Classification of Disease 10th revision code G30) and other dementias (codes F01, F02, R54) coded as underlying or contributing cause of death based on the death certificate. Age-adjusted death rates were computed by year, state or county for persons aged 65 years and over. In 2005–2006 combined, 555,904 total deaths occurred with any dementia type (212,386 for Alzheimer’s disease) coded as underlying or contributing cause. Among the states, age-adjusted rates per 100,000 per year varied by two fold ranging from 458 in New York to 921 in Oregon. Similar geographic patterns were seen for Alzheimer’s disease. However, between 1999–2000 and 2005–2006 the US death rate for all dementia increased only from 559 to 695 (24%) while that for Alzheimer’s disease doubled from 135 to 266. Use of specific (G30, F01) versus non-specific diagnoses (F02, R54) varied among states and over time, explaining most of the temporal increase in rate of Alzheimer’s disease. Further research is needed to assess artifacts of diagnosis, certification or coding, utilization of health services, versus biological variation as possible causes of temporal and geographic variation to enhance utility of mortality data for dementia monitoring and research.
dementia; mortality; geography
Low levels of both high density lipoprotein cholesterol (HDL) and cognitive function are associated with increased mortality risk. HDL plays an important role in brain metabolism. We test the hypotheses that the relative protective effect of high HDL level as related to mortality is greater in persons with impaired cognitive function than in others. Data were analyzed from a longitudinal mortality follow-up study of 4911 American men and women aged 60 years and over examined in 1988-1994 followed an average 8.5 yr. Measurements at baseline included HDL, a short index of cognitive function (SICF), socio-demographics, health status, and self-reported leisure-time physical activity. In proportional hazards regression analysis, no significant interaction of HDL with cognitive function was found (p = 0.08); there was a significant age-SICF interaction. After stratifying by age and adjusting for confounding by multiple variables, independent associations of HDL and SICF score with survival were strongest among the oldest persons. Consistent with its association with HDL, cognitive function and survival, controlling in addition for physical activity reduced the associations. In a nationwide cohort of older Americans, analyses demonstrated a lower risk of death independent of confounders among those high HDL and SICF scores, strongest among the oldest persons.
Living with a canine companion is postulated to increase physical activity. We test the hypotheses that adults living with a canine companion have a higher level of physical activity and reduced mortality risk compared to those not living with a companion animal. A U.S. national health survey with longitudinal mortality follow-up studied 11,394 American men and women aged 40 years and over examined in 1988–1994 followed an average 8.5 years. Measurements at baseline included self-reported companion animals in the household, socio-demographics, health status, physical and biochemical measurements. Outcome measures were leisure-time physical activity (LTPA), and death from all causes. Death during follow-up occurred in 3,187 persons. In bivariate cross-sectional analyses living with a dog was associated with more frequent LTPA and higher survival. In proportional hazards regression analysis, no significant interaction of age, gender or ethnicity with animals was found. After adjusting for confounding by baseline socio-demographics and health status at ages 40+, the hazards ratio (95% confidence limits) for living with a canine companion compared to no animals was 1.21(1.04–1.41, p < 0.001). After also controlling for health behaviors, blood pressure and body mass, C-reactive protein and HDL-cholesterol, the HR was 1.19 (0.97–1.47, NS). In a nationwide cohort of American adults, analyses demonstrated no lower risk of death independent of confounders among those living with canine or feline companions, despite positive association of canine companions with LTPA.
domestic animals; physical activity; mortality; survival
In order to elucidate cultural correlates of utilization of primary health services by young adult men, we investigated religion in which one was raised and service utilization. Using data from a national survey we tested the hypothesis that religion raised predicts access to and utilization of a regular medical care provider, examinations, HIV and other STD testing and counseling at ages 18–44 years in men born between 1958 and 1984. We also hypothesized that religion raised would be more predictive of utilization for Hispanic Americans and non-Hispanic Black Americans than for non-Hispanic White Americans. The study included a national sample of 4276 men aged 18–44 years. Descriptive and multivariate statistics were used to assess the hypotheses using data on religion raised and responses to 14 items assessing health care access and utilization. Compared to those raised in no religion, those raised mainline Protestant were more likely (p < 0.01) to report a usual source of care (67% vs. 79%), health insurance coverage (66% vs. 80%) and physical examination (43% vs. 48%). Religion raised was not associated with testicular exams, STD counseling or HIV testing. In multivariate analyses controlling for confounders, significant associations of religion raised with insurance coverage, a physician as usual source of care and physical examination remained which varied by race/ethnicity. In conclusion, although religion is a core aspect of culture that deserves further study as a possible determinant of health care utilization, we were not able to document any consistent pattern of significant association even in a population with high rates of religious participation.
access to care; prevention; hispanics; blacks
Aldosterone influences the kidney’s regulation of blood pressure (BP), but aldosterone can contribute to the pathogenesis of hypertension. Blood pressure is reduced with aerobic exercise training (AEX), but the extent to which plasma aldosterone (PA) levels change is unclear. The purpose of this study was to determine whether 6 months of AEX changed PA levels, 24 h sodium (Na+) excretion and BP in prehypertensive and hypertensive subjects and whether these changes differed according to ethnicity. The study was performed in the Kinesiology Department at the University of Maryland, College Park, and 35 (22 Caucasian; 13 African American) sedentary prehypertensive and hypertensive subjects completed 6 months of AEX. Blood samples were collected under fasting and supine conditions, and PA was measured by radioimmunoassay. In total population aerobic exercise training increased maximal oxygen consumption (24 ± 0.8 versus 28 ± 1 ml kg−1 min−1, P < 0.001) and decreased PA levels (97 ± 11 versus 72 ± 6 pg ml−1, P = 0.01), body mass index (28 ± 0.5 versus 28 ± 0.5 kg m−2, P = 0.004) and weight (85 ± 2 versus 83 ± 2 kg, P = 0.003). Aerobic exercise training decreased PA levels (from 119 ± 16 to 81 ± 7 pg ml−1, P = 0.02) in the Caucasians but there was no change in BP or Na+ excretion. African American participants had no significant changes in PA levels, BP and Na+ excretion. Plasma aldosterone levels were 47% lower at baseline (P = 0.01) and 30% lower after AEX (P = 0.04) in African American participants compared with Caucasians. Baseline (P = 0.08) and final PA levels (P = 0.17) did not differ between the two groups after accounting for baseline and final intra-abdominal fat, respectively. The reduction in PA levels with AEX appeared to be driven by the change in PA levels in Caucasian participants. Fat distribution contributed to the ethnic differences in PA levels.
Prior research suggests an interaction between social networks and Alzheimer's disease pathology and cognitive function, all predictors of survival in the elderly. We test the hypotheses that both social integration and cognitive function are independently associated with subsequent mortality and there is an interaction between social integration and cognitive function as related to mortality in a national cohort of older persons.
Data were analyzed from a longitudinal follow-up study of 5,908 American men and women aged 60 years and over examined in 1988–1994 followed an average 8.5 yr. Measurements at baseline included self-reported social integration, socio-demographics, health, body mass index, C-reactive protein and a short index of cognitive function (SICF).
Death during follow-up occurred in 2,431. In bivariate analyses indicators of greater social integration were associated with higher cognitive function. Among persons with SICF score of 17, 22% died compared to 54% of those with SICF score of 0–11 (p < 0.0001). After adjusting for confounding by baseline socio-demographics and health status, the hazards ratio (HR) (95% confidence limits) for low SICF score was 1.43 (1.13–1.80, p < 0.001). After controlling for health behaviors, blood pressure and body mass, C-reactive protein and social integration, the HR was 1.36 (1.06–1.76, p = 0.02). Further low compared to high social integration was also independently associated with increased risk of mortality: HR 1.24 (1.02–1.52, p = 0.02).
In a cohort of older Americans, analyses demonstrated a higher risk of death independent of confounders among those with low cognitive function and low social integration with no significant interaction between them.
Few nationally representative cohort studies have appeared on frequency of attendance at religious services and mortality. We test the hypothesis that > weekly attendance compared with nonattendance at religious services is associated with lower probability of future mortality in such a study.
Data were analyzed from a longitudinal follow-up study of 8450 American men and women age 40 years and older who were examined from 1988 to 1994 and followed an average of 8.5 years. Measurements at baseline included self-reported frequency of attendance at religious services, sociodemographics, and health, physical and biochemical measurements.
Death during follow-up occurred in 2058. After adjusting for confounding by baseline sociodemographics and health status, the hazards ratios (95% confidence limits) were never 1.00 (reference); < weekly 0.89 (0.75–1.04), p = 0.15; weekly 0.82 (0.71–0.94) p = 0.005; and > weekly attenders 0.70 (0.59–0.83), p < 0.001. Mediators, including health behaviors and inflammation, explained part of the association.
In a nationwide cohort of Americans, predominantly Christians, analyses demonstrated a lower risk of death independent of confounders among those reporting religious attendance at least weekly compared to never. The association was substantially mediated by health behaviors and other risk factors.
Aging; Cultural Factors; Epidemiologic Methods; Mortality; Religion; Spirituality