Polymorphisms of the apolipoprotein E gene (ApoE) have been associated with health and longevity. Numerous studies have linked ApoE to health outcomes including cardiovascular disease and mortality, but far fewer studies have examined the relationship of ApoE to other biological markers of health. This study investigates the relationship between ApoE and mortality, as well as ApoE and a set of biomarkers related to cardiovascular and immune function, in a population-based sample of Taiwanese adults ages 54+. ApoE ε2 carriers were less likely to have at-risk levels of high-density lipoprotein (HDL-C) and total cholesterol (total-C) than non-carriers (odds ratio [OR] 0.45, 95% confidence interval [CI] 0.25-0.83 and OR 0.45, 95% CI 0.29-0.71, respectively). ApoE ε4 carriers were less likely to have elevated levels of C-reactive protein (CRP) than non-carriers (OR 0.62, 95% CI 0.39-0.96). ApoE genotype was not, however, associated with mortality after 8-years of follow-up. Our findings confirm the association between ApoE ε2 and cholesterol levels, suggesting a potential protective effect of ApoE ε2 on blood lipids. They also contribute to reports on the relationship between ApoE ε4 carrier status and lower CRP levels.

Identifying how biological parameters change with age can provide insights into the physiological determinants of disease, and ultimately, death. Most prior studies of age-related change in biomarkers are based on cross-sectional data, small or selective samples, or a limited number of biomarkers. We use data from a nationally-representative longitudinal sample of 639 Taiwanese aged 54 and older in 2000 to assess changes over a six-year period in a wide range of biomarkers. Markers that increased most with age were glycoslyated hemoglobin, interleukin-6, and norepinephrine. Markers that decreased most with age were diastolic blood pressure and creatinine clearance. For example, glycoslyated hemoglobin increased by 8-13%, on average, over this six-year period. Several standard clinical risk factors exhibited little evidence of age-related change. Further research is needed to determine whether the observed variation between individuals in biomarker changes represents differences in underlying physiological function that are predictive of future health and survival.

Objectives.

This study assesses whether socioeconomic and demographic differences in reported mobility limitations are attributable to differential perceptions of mobility difficulty that result in the differential use of response categories.

Methods.

Data come from the Social Environment and Biomarkers of Aging Study and its parent study, the Taiwan Longitudinal Study of Aging. Ordered probit models with person-specific cut-points are used to test whether, after controlling for underlying mobility using objective performance measures, cut-points for reporting mobility limitations vary across groups defined by demographic and socioeconomic characteristics.

Results.

Age is the only characteristic that is consistently associated with the location of the cut-points for reporting mobility difficulty: At the same level of underlying mobility difficulty, older adults are more likely than younger adults are to report difficulty with all tasks except short walks. Other variables showed differences but only for one specific activity, for example, urban residents are more likely to report difficulty running than are rural residents with the same underlying level of mobility function.

Discussion.

For most mobility activities, there are no systematic differences in the perception of difficulty by individual characteristics. Thus, for older Taiwanese adults, differences in mobility limitations associated with socioeconomic status are more likely to reflect underlying differences in function than differences in how these groups report the same capacity. The usual loss of mobility with age, however, reflects both a decrease in capacity and a lowering of the threshold for reporting difficulty.

Background Cigarette smoking is responsible for a massive loss of life in both developed and developing countries. This article develops an alternative to the Peto–Lopez method for estimating the number or fraction of smoking-attributable deaths in high-income countries.

Methods We use lung cancer death rates as an indicator of the damage caused by smoking. Using administrative data for the population aged ≥50 years from 20 high-income countries in the period from 1950 to 2006, we estimate a negative binomial regression model that predicts mortality from causes other than lung cancer as a function of lung cancer mortality and other variables. Using this regression model, we estimate smoking-attributable deaths based on the difference between observed death rates from lung cancer and expected rates among non-smokers.

Results Combining the estimated number of excess deaths from lung cancer with those from other causes, we find that among males in 1955 the smoking-attributable fraction was highest in Finland (18%); among women, no country exceeded 1%. By 2003, Hungary had the highest fraction of smoking-attributable deaths among males (32%), whereas the USA held that position among women (24%). Our estimates are remarkably similar to those produced by the Peto–Lopez method, a result that supports the validity of each approach.

Conclusions We provide a simple and straightforward method for estimating the proportion of deaths attributable to smoking in high-income countries. Our results demonstrate that smoking has played a central role in levels, trends and international differences in mortality over the past half century.

Background

We compare the genotype distribution for the serotonin transporter polymorphism (5-HTTLPR) in a sample of older Taiwanese adults with samples of various racial and ethnic groups collected in other studies. We also explore interactions among sex, stressors, and 5-HTTLPR genotype on depressive symptoms in our sample.

Methods

Using a nationally-representative sample of 984 Taiwanese aged 53 and older, we model depressive symptoms as a function of 5-HTTLPR genotype and two classes of stressors: lifetime trauma and recent major life events. We test two- and three-way interactions among stressors, 5 HTTLPR, and sex.

Results

This sample exhibits higher frequency of S/S and lower frequency of L/L genotype than Western samples, but the distribution is comparable to those in East Asian populations. Nearly 9% carry an allele (XL) that has rarely been reported in the literature. Although the gene-environment (GxE) interaction with recent major life events is not significant, our results suggest that trauma has a worse effect on depressive symptoms for those with S/S or S/L genotype than for those who do not carry the S allele (p<0.05). We find no evidence that this GxE interaction varies by sex.

Conclusions

Previous studies of this GxE interaction have been inconclusive, perhaps because interactions between genotype and stressful events are more prominent under extreme stressors. Our findings underscore the need to move beyond a bi-allelic parameterization of the 5-HTTLPR polymorphism and raise questions about why East Asian populations exhibit low rates of depression despite a high frequency of the S allele.

Dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS) have been the focus of considerable publicity because of their demonstrated associations with a broad range of health outcomes. Yet, knowledge about the effects of endogenous DHEA(S) on health in humans is limited and often inconclusive, largely because few of the studies have been based on prospective surveys of population-representative samples. This analysis uses a national longitudinal survey in Taiwan to investigate whether DHEAS is associated with subsequent changes (2000–2003) in functional limitations, cognitive impairment, depressive symptoms, and global self-rated health. Multivariate regression models based on this older Taiwanese sample show that among men, lower levels of DHEAS are related to declines in mobility and self-assessed health status and increases in depressive symptoms, while both low and very high levels of DHEAS are associated with poor cognitive function. There are no significant associations among women. These findings differ from those in a previous cross-sectional analysis based on the Taiwan study and underscore the importance of using prospective data to examine the effects of DHEAS on health. The evidence based on this and other longitudinal studies suggests that endogenous DHEAS is related to health outcomes for men, but not women, in both Western and non-Western populations.

The objective of our study was to investigate whether life satisfaction and depressive symptoms are independent predictors of mortality in a non-Western sample of adults. The sample included 5,131 adults (aged 50 – 95 at baseline) in Taiwan who participated in the Survey of Health and Living Status of the Near Elderly and Elderly. There were 1,815 deaths recorded over a 10-year period. Higher life satisfaction significantly predicted lower risk of mortality after controlling for age, sex, education, marital status and health status. Depressive symptoms significantly predicted higher risk of mortality. A significant interaction with age revealed that the protective effect of life satisfaction weakened with age. The results suggest that life satisfaction and depressive symptoms independently predict mortality risk in adults.

The authors used data from a nationally representative survey of 933 adults aged 54 years or older (mean age = 66.2 years; standard deviation, 8.0) in Taiwan to explore whether mortality prediction at older ages is improved by the use of 3 clusters of biomarkers: 1) standard cardiovascular and metabolic risk factors; 2) markers of disease progression; and 3) nonclinical (neuroendocrine and immune) markers. They also evaluated the extent to which these biomarkers account for the female advantage in survival. Estimates from logistic regression models of the probability of dying between 2000 and 2006 (162 deaths; mean length of follow-up = 5.8 years) showed that inclusion of each of the 3 sets of markers significantly (P = 0.024, P = 0.002, and P = 0.003, respectively) improved discriminatory power in comparison with a base model that adjusted for demographic characteristics, smoking, and baseline health status. The set of disease progression markers and the set of nonclinical markers each provided more discriminatory power than standard risk factors. Most of the excess male mortality resulted from the men being more likely than women to smoke, but each of 3 markers related to disease progression or inflammation (albumin, neutrophils, and interleukin-6) explained more than 10% of excess male mortality.