Explaining the decline in coronary heart disease mortality rates in Japan: Contributions of changes in risk factors and evidence-based treatments between 1980 and 2012

Background We aimed to quantify contributions of changes in risks and uptake of evidence-based treatment to coronary heart disease (CHD) mortality trends in Japan between 1980 and 2012. Methods We conducted a modelling study for the general population of Japan aged 35 to 84 years using the validated IMPACT model incorporating data sources like Vital Statistics. The main outcome was difference in the number of observed and expected CHD deaths in 2012. Results From 1980 to 2012, age-adjusted CHD mortality rates in Japan fell by 61%, resulting in 75,700 fewer CHD deaths in 2012 than if the age and sex-specific mortality rates had remained unchanged. Approximately 56% (95% uncertainty interval [UI]: 54–59%) of the CHD mortality decrease, corresponding to 42,300 (40,900–44,700) fewer CHD deaths, was attributable to medical and surgical treatments. Approximately 35% (28–41%) of the mortality fall corresponding to 26,300 (21,200–31,000) fewer CHD deaths, was attributable to risk factor changes in the population, 24% (20–29%) corresponding to 18,400 (15,100–21,900) fewer and 11% (8–14%) corresponding to 8400 (60,500–10,600) fewer from decreased systolic blood pressure (8.87 mm Hg) and smoking prevalence (14.0%). However, increased levels of cholesterol (0.28 mmol/L), body mass index (BMI) (0.68 kg/m2), and diabetes prevalence (1.6%) attenuated the decrease in mortality by 2% (1–3%), 3% (2–3%), and 4% (1–6%), respectively. Conclusions Japan should continue their control policies for blood pressure and tobacco, and build a strategy to control BMI, diabetes, and cholesterol levels to prevent further CHD deaths

The Differential Heritability of Social Adjustment by Sex

Sex differences in social adjustment are frequently observed; however, there has been very little research on adaptability in the individual and social domains. The aim of this study was to investigate the sex difference in social abilities, such as high self-appeal, sociability, school adaptation, and home adaptation between school-age males and females. The sample for this study included both same-sex and opposite-sex twin pairs: a total of 467 twin pairs. We classified them into three groups: a group of those in lower classes of elementary school, a group of those in higher classes of elementary school, and a group of those in junior high school. The heritability of school adaptation was estimated to be 95% in males and 54% in females in the junior high school group. The full sex-limitation model showed a better fit in this group, and this means that a qualitative genetic difference exists. For school adaptation, there was no sex difference in lower elementary school classes; however, a quantitative difference appeared in higher classes of elementary school. Moreover, a qualitative difference appeared in junior high school. From this research, it became clear that sex differences in heritability exist for school adaptation, and there was a marked increase from the elementary school children to the junior high school children

The Association between Chronic Widespread Musculoskeletal Pain, Depression and Fatigue Is Genetically Mediated

BACKGROUND Chronic widespread muscoloskeletal pain (CWP) is prevalent in the general population and associated with high health care costs, so understanding the risk factors for chronic pain is important for both those affected and for society. In the present study we investigated the underlying etiological structure of CWP to understand better the association between the major clinical features of fatigue, depression and dihydroepiandrosterone sulphate (DHEAS) using a multivariate twin design. METHODOLOGY/PRINCIPLE FINDINGS Data were available in 463 UK female twin pairs including CWP status and information on depression, chronic fatigue and serum DHEAS levels. High to moderate heritabilities for all phenotypes were obtained (42.58% to 74.24%). The highest phenotypic correlation was observed between fatigue and CWP (r = 0.45), and the highest genetic correlation between CWP and fatigue (rg = 0.78). Structural equation modeling revealed the AE Cholesky model to provide the best model of the observed data. In this model, two additive genetic factors could be detected loading heavily on CWP-A2 explaining 40% of the variance and A3 20%. The factor loading heaviest on DHEAS showed only a small loading on the other phenotypes and none on fatigue at all. Furthermore, one distinct non-shared environmental factor loading specifically on CWP-but not on any of the other phenotypes-could be detected suggesting that the association between CWP and the other phenotypes is due only to genetic factors. CONCLUSIONS/SIGNIFICANCE Our results suggest that CWP and its associated features share a genetic predisposition but that they are relatively distinct in their environmental determinants

Chronic widespread pain: clinical comorbidities and psychological correlates

Recent studies have provided consistent evidence for a genetic influence on chronic widespread musculoskeletal pain (CWP). The aim of this study was to investigate a) the etiological structure underlying CWP by examining the covariation between CWP and psychological comorbidities and psycho-affective correlates, and b) the decomposition of the covariation into genetic and environmental components. A total 3,266 female twins (mean age 56.6 years) were subject to multivariate analyses. Using validated questionnaires to classify twins as having CWP, the prevalence of CWP was 20.8%. In the multivariate analysis, the most suitable model was the common pathway model. This model revealed two underlying latent variables, one common to anxiety, emotional intelligence, and emotional instability (f1) and the other common to depression and CWP (f2), the latter being highly heritable (86%). Both latent variables (f1, f2) shared an additive genetic and a non-shared environmental factor. In addition, a second additive genetic factor loading only on f2 was found. This study reveals the structure of genetic and environmental influences of CWP and its psycho-affective correlates. The results show that the clustering of CWP and depression is due to a common, highly heritable, underlying latent trait. In addition, we found evidence that CWP, anxiety, emotional instability and emotional intelligence are influenced by different underlying latent traits sharing the same genetic and non-shared environmental factors. This is the first study to reveal the structure and relative importance of genetic and environmental influences on complex etiological mechanisms CWP and its correlates

Associations between Depressive State and Impaired Higher-Level Functional Capacity in the Elderly with Long-Term Care Requirements.

Depressive state has been reported to be significantly associated with higher-level functional capacity among community-dwelling elderly. However, few studies have investigated the associations among people with long-term care requirements. We aimed to investigate the associations between depressive state and higher-level functional capacity and obtain marginal odds ratios using propensity score analyses in people with long-term care requirements. We conducted a cross-sectional study based on participants aged ≥ 65 years (n = 545) who were community dwelling and used outpatient care services for long-term preventive care. We measured higher-level functional capacity, depressive state, and possible confounders. Then, we estimated the marginal odds ratios (i.e., the change in odds of impaired higher-level functional capacity if all versus no participants were exposed to depressive state) by logistic models using generalized linear models with the inverse probability of treatment weighting (IPTW) for propensity score and design-based standard errors. Depressive state was used as the exposure variable and higher-level functional capacity as the outcome variable. The all absolute standardized differences after the IPTW using the propensity scores were < 10% which indicated negligible differences in the mean or prevalence of the covariates between non-depressive state and depressive state. The marginal odds ratios were estimated by the logistic models with IPTW using the propensity scores. The marginal odds ratios were 2.17 (95%CI: 1.13-4.19) for men and 2.57 (95%CI: 1.26-5.26) for women. Prevention of depressive state may contribute to not only depressive state but also higher-level functional capacity

Results of the model comparison for pain catastrophizing, neuroticism, anxiety sensitivity, and fear of pain among the full ADE Cholesky model and the sub-models.

<p>Results of the model comparison for pain catastrophizing, neuroticism, anxiety sensitivity, and fear of pain among the full ADE Cholesky model and the sub-models.</p

Results of the model comparison among the full ADE Cholesky model and sub-models.

<p>Sample: MZ (N = 219 pairs) and DZ (N = 244 pairs).</p><p>A = additive genetic factors; C = shared environmental factors; D = non-additive genetic factors; E = non-shared environmental factors; AIC = Akaike information criterion; df = degree of freedom; MZ = monozygotic; DZ = dizygotic.</p><p>The most suitable model is shown in bold, having the lowest AIC</p><p>Results of the model comparison among the full ADE Cholesky model and sub-models.</p

Marginal odds ratios by logistic models with depressive status as the exposure and impaired HLFC as the outcome using IPTW with propensity scores^† in men (n = 233) and women (n = 312).

<p>Abbreviations: CI, confidence interval; HLFC, higher-level functional capacity; IPTW, inverse probability of treatment weighting.</p><p>†Propensity scores were estimated by multiple logistic regression analyses with depressive status as the outcome and the following covariates as the predictors: age, body mass index, marital status, annual income, living alone, staying indoors, falling within a year, skin ulcer, subjective memory complains, and medical histories of diabetic, hypertension, stroke, or Parkinson’s disease.</p><p>Marginal odds ratios by logistic models with depressive status as the exposure and impaired HLFC as the outcome using IPTW with propensity scores<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0127410#t004fn002" target="_blank">^†</a> in men (n = 233) and women (n = 312).</p

Phenotypic correlations between the main study variables (N = 2,401).

<p>Phenotypic correlations between the main study variables (N = 2,401).</p