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There is a public health demand to prevent health conditions which lead to increased morbidity and mortality among the rapidly-increasing elderly population. Data for the incidence of such conditions exist in cohort studies worldwide, which, however, differ in various aspects. The Consortium on Health and Ageing: Network of Cohorts in Europe and the United States (CHANCES) project aims at harmonizing data from existing major longitudinal studies for the elderly whilst focussing on cardiovascular diseases, diabetes mellitus, cancer, fractures and cognitive impairment in order to estimate their prevalence, incidence and cause-specific mortality, and identify lifestyle, socioeconomic, and genetic determinants and biomarkers for the incidence of and mortality from these conditions. A survey instrument assessing ageing-related conditions of the elderly will be also developed. Fourteen cohort studies participate in CHANCES with 683,228 elderly (and 150,210 deaths), from 23 European and three non-European countries. So far, 287 variables on health conditions and a variety of exposures, including biomarkers and genetic data have been harmonized. Different research hypotheses are investigated with meta-analyses. The results which will be produced can help international organizations, governments and policy-makers to better understand the broader implications and consequences of ageing and thus make informed decisions.

Making sense of rapidly evolving evidence on genetic associations is crucial to making genuine advances in human genomics and the eventual integration of this information in the practice of medicine and public health. Assessment of the strengths and weaknesses of this evidence, and hence the ability to synthesize it, has been limited by inadequate reporting of results. The STrengthening the REporting of Genetic Association studies (STREGA) initiative builds on the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) Statement and provides additions to 12 of the 22 items on the STROBE checklist. The additions concern population stratification, genotyping errors, modeling haplotype variation, Hardy-Weinberg equilibrium, replication, selection of participants, rationale for choice of genes and variants, treatment effects in studying quantitative traits, statistical methods, relatedness, reporting of descriptive and outcome data, and the volume of data issues that are important to consider in genetic association studies. The STREGA recommendations do not prescribe or dictate how a genetic association study should be designed but seek to enhance the transparency of its reporting, regardless of choices made during design, conduct, or analysis.

Objective: Wide applications for genetic testing in the clinical care of complex diseases have been discussed. However, it has never been quantified to what extent genetic testing could eventually be useful in the clinical care of common disorders. We aimed to quantify the theoretically possible utilization in common ischemic stroke, an example of a complex disease., Methods: We computed the possible impact of genetic testing on risk assessment, secondary prevention and prognosis of ischemic stroke. This was done for hypothetical genotypes with different frequencies and effects., Results: To apply pharmacogenetic secondary prevention based on a genotype with a frequency of 10% and 33% risk reduction, 204 subjects would have to be screened and 110 given genotype specific treatment for 1 year, in order to prevent one recurrent stroke, compared with standard therapy. The application of genetic testing seems to be less promising in risk assessment and the assessment of prognosis of common ischemic stroke., Conclusions: The highest impact of genetic testing on clinical practice of stroke will be in the areas of secondary prevention. Given the weak effects of reported susceptibility genotypes, it is theoretically unlikely that genetic screening will be used for the assessment of risk or prognosis of a complex disorder, except for Mendelian types of disease.

Depression is often accompanied by other disorders including Alzheimer's disease and Parkinson's disease. We studied the familial aggregation of these disorders in order to examine the possibility of a shared genetic origin. In a population-based study of 6596 subjects, we studied the association of self-reported depression, which required treatment by a psychiatrist, to family history of psychiatric disease, dementia, and Parkinson's disease. A family history of psychiatric disease was significantly associated with overall depression as well as with unipolar (n = 303 patients) and bipolar (n = 27 patients) depression. The risk of unipolar depression was associated with the presence of two or more demented individuals among their first degree relatives (e.g. parents, siblings and children). Since there was no evidence for familial aggregation in subjects with only one demented relative, our study suggests that unipolar depression may be associated specifically to a strongly familial, form of dementia. The risk of bipolar depression was increased for those with one or more relatives with dementia and, perhaps, for those with relatives with Parkinson's disease. The familial aggregation of depression with dementia and perhaps Parkinson's disease suggests that there may be shared susceptibility gene(s) underlying these diseases. Our study indicates further that there may be differences in the genetic etiology between unipolar and bipolar depression.

To investigate the association of alcohol intake with mortality from all causes, cardiovascular disease (CVD), cancer and other causes (e.g., accidents, violence, suicide), we performed an analysis of data obtained in a prospective follow-up study conducted in the Netherlands since 1977. Causes of death were defined for a cohort of 1,620 persons (760 men and 860 women) examined in 1977. During the 10-year follow-up period, 123 (7.6%) of the participants died. Frequency of alcohol consumption was obtained separately for wine, beer and liquor by means of a questionnaire. Although no significant association could be established between alcohol consumption and all-cause mortality, all-cause mortality tended to be lower in alcohol consumers compared to abstainers. The age- and sex-adjusted risk estimates of death from CVD were 0.29 (0.11-0.74), 0.46 (0.21-0.96) and 0.32 (0.13-0.77) for subjects with occasional, frequent and daily alcohol use, respectively, compared with those who did not drink at baseline. The mortality risks of never-drinkers and ex-drinkers were similar. A J- or U-shaped relation between alcohol consumption and CVD mortality could not be confirmed in our data but the available information on the amount of alcohol consumed was limited. No significant influence on the risk estimates of death from cancer or other causes was found. However, mortality tended to be higher for those who consumed more alcohol. The protective effect of alcohol intake on CVD mortality found in our data persisted after excluding subjects with cardiovascular or other major diseases at baseline from the analysis.