RLS is a frequent syndrome in the elderly with considerable impact on self-perceived mental health, affecting women about twice as often as men.

The onset of acute myocardial infarction demonstrates a peak on Monday primarily in the working population. If this finding is confirmed in other communities, it may aid in identifying acute triggering events of myocardial infarction and perhaps in improving prevention of the disease.

In the second World Health Organization MONItoring Trends and Determinants in CArdiovascular Disease (MONICA) Augsburg survey in 1989-1990 (#1=4,940), the association between nephelometric plasma fibrinogen level and lifestyle-related potential determinants was assessed in 4,434 subjects aged 25-74 years (89.8% of participants). Irrespective of pregnancy and the use of oral contraceptives, crude fibrinogen values were consistently higher in women than in men of all ages (age-standardized difference, 12.2 mg/dl; 95% confidence interval, 7.0-17.4 mg/dl). Fibrinogen concentrations were positively correlated (psO.0001) with age, body mass index, and waist-to-hip ratio in both sexes and with cigarette smoking In men and were negatively correlated with alcohol consumption in both sexes. In multiple linear regression analyses using categorized determinants as independent variables, a strongly J-shaped relation for body mass index in women and a linear association for waist-to-hip ratio in men were revealed. Smoking had a dose-dependent effect on fibrinogen concentration in men but a lesser effect in women. For alcohol consumption a U-shaped association was found, particularly in men. The curvilinear relations were confirmed in multiple polynomial regression models using continuous determinant variables. The potential epidemiological impact of a determinant was assessed by calculating differences in adjusted fibrinogen concentrations associated with the 10th and 90th percentile values of the determinant distributions actually observed among the study participants. This impact on the population fibrinogen level was most pronounced for age in both sexes, followed by body mass index, cigarette smoking, and alcohol consumption in women and by smoking, waist-to-bip ratio, and alcohol consumption in men. About 29% of the total variance in female and 26% in male fibrinogen values were explained by the three lifestyle factors plus age. Our findings are consistent with the hypothesis that fibrinogen may be an etiologic link between certain lifestyle characteristics and the course of cardiovascular disease. {Arterio- sclerosis and Thrombosis 1992;12:780-788) KEY WORDS • fibrinogen • cardiovascular disease risk factors • body mass index • waist-to-hip ratio • cigarette smoking • alcohol consumption T he evidence that clotting factors may be important in the evolution of atherosclerotic vascular disease was initially derived from case-control 1 " 3 and angiographic 4^ studies in which men with clinically manifest coronary heart disease showed elevated mean fibrinogen levels. Further evidence came from a number of prospective epidemiological studies indicating that plasma fibrinogen levels were strongly predictive of coronary heart disease and stroke incidence and mortality. 6 -12 An as-yet-undetermined part of the association between traditional risk factors and cardiovascular disease From the GSF-Institute of Epidemiology

The clustering of multiple metabolic abnormalities including obesity, insulin resistance, non-insulin-dependent diabetes mellitus (NIDDM), hypertension, and dyslipidaemias has become known as the insulin resistance syndrome [1,2] or multiple metabolic syndrome (MMS) [3,4]. Genetic as well as shared environmental influences on insulin, insulin resistance, and obesity have been reported in family and twin studies [5][6][7][8][9][10][11]. Familial aggregation of NIDDM [12,13], elevated blood pressure levels [14,15], and lipid disorders [16,17] is well established. Metabolic disorders such as familial hypercholesterolaemia [18,19], familial combined hyperlipidaemia [20][21][22], and familial dyslipidemic hypertension [23] require a positive family history as part of their definition.Particularly within genetic epidemiology, studies on the MMS have frequently had a primary focus on a single, continuously distributed metabolic characteristic such as insulin [8,9]. Others have compared multiple metabolic variables among offspring of affected and unaffected parents [24][25][26][27][28][29][30][31]. Focusing on a single metabolic characteristic, however, limits the Diabetologia (1997) Summary The association of a parental history of diabetes mellitus and hypertension with the multiple metabolic syndrome (MMS) was studied in a population survey of middle-aged adults. The eligible population was drawn from the baseline examination of the Atherosclerosis Risk in Communities Study, a population-based, bi-ethnic, multi-centre cohort study. The MMS was defined as a multivariate, categorical phenotype of co-occurring diabetes, hypertension, and dyslipidaemia. MMS cases (n = 356) were compared to disorder-free control subjects (n = 6797) with respect to their parental history of diabetes and hypertension. MMS cases were more likely to report a history of diabetes in both parents (odds ratio [OR] 4.7, 95 % confidence interval (CI) 1.5-14.7) or a history of hypertension in both parents (OR 1.9, 95 % CI 1.1-3.0) than control subjects, adjusting for BMI, waist-to-hip ratio, age, gender, and ethnicity/centre. A parental history of diabetes and hypertension in both parents was associated with the greatest increase in odds of MMS (OR 8.3,. A dose-response relationship between the number of parental disorders (one; two; three to four) and the odds of MMS was observed (OR 1.2, 95 % CI 0.9-1.7; OR 2.0, 95 % CI 1.4-2.8; OR 4.0, 95 % CI 2.5-6.2). Based on the marked associations observed between a parental history of MMS components and the clustering of these metabolic disorders in the offspring generation, we conclude that genetic and/or non-genetic familial influences play a role in the development of the multiple metabolic syndrome. [Diabetologia (1997) 40: 963-970]