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Background: Variations in early sexual debut among 16 year olds were investigated by social level variables, parental occupation, gender, ethnicity, family structure, family functioning, and individual level variables, future aspirations, academic and social self-perception, and depressed moods. Methods: The variations in sexual debut were investigated by examining proportions of 16 year olds reporting their first intercourse before age 16. The data were collected by self-reporting questionnaires administered to in-school-youth, in Oslo. Multivariate logistic regression analyses were used to test for associations. Gender interactions with all variables were tested. Results: Overall, 25% reported early debut. Independent effect of social class on differences in proportions in early sexual debut were found. Gender interaction with social class, ethnicity and academic self-perception as they associate to proportions having had early sexual debut, were found. For girls the pattern of social class differences was linear and the highest proportions were found among working classes. For boys the pattern was U-shaped and upper managerial and manual working class youth had similar, higher proportions of early debutants. High scores of parental monitoring, future aspirations and academic self-concept and low scores of depressed moods, are protective factors. While high social self-perception is positively associated with early debut for both genders. Conclusion: Early sexual debut varies according to social class, following gender-specific patterns, among 16 year olds in Oslo. The negative association between early debut and academic self-perception are for boys less influenced by other social and individual level factors, than for girls. [ABSTRACT FROM AUTHOR]

Introduction: Stroke mortality comprises different specific diagnoses as cerebral infarction, different haemorrhagic conditions, and unspecified stroke. The prediction by oral health indicators versus established cardiovascular (CVD) risk factors is assessed in the Oslo II-study 12 ½ year follow-up. Aims: Compare previously published results of 21-years follow-up of the Oslo-study of 1972/73 to the 12 ½-year follow-up of the Oslo II-study with the addition of oral health to known CVD risk factors. Methods: In the Oslo-study of 1972/73, 30,025 men in Oslo were invited and a 21-year follow-up was done of 14,403 men with regard to incidence and mortality for stroke and myocardial infarction. In Oslo II in 2000, 12,764 men aged 58 to 77 years were invited to a health screening which included general medical measurements and questionnaire information. Mortality data were supplied by Statistics Norway for the 12 ½-year follow-up of the attending 6,530 men of whom 364 men with prior stroke were withdrawn from the analyses. Cox proportional hazards analyses were used to establish prediction models for mortality. Results: Published results from the 21-year follow-up concluded that the risk-factor profile differed according to the underlying subtype of stroke. Cerebral infarction clearly shared with myocardial infarction the classical risk factors. Oslo II results for total stroke mortality (n=130) was also given separately for cerebral haemorrhage all combined (n=49), cerebral infarction (n=31), and unspecified stroke (n=50). Results from Cox analyses using the backward elimination procedure showed that oral health by tooth extractions >10 was a predictor for cerebral infarction hazard rate (HR) = 2.92, 95% confidence interval (CI) (1.24-6.89). This was independent of HDL-C (inversely) HR= 0.21, 95% CI (0.06-0.76), frequent alcohol consumption HR= 3.58, 95% CI (1.40-9.13), and diabetes HR= 4.28, 95% CI (1.68-10.89). Predictors for cerebral haemorrhage were age, CRP, and BMI (inversely) and age, total cholesterol (inversely) for unspecified stroke. Overall, stroke mortality was predicted by age, HDL-C, CRP, and diabetes. Conclusions: Oral health measured by more than ten extracted teeth was found to be an independent predictor for cerebral infarction. The pattern of risk factors varied between the specific stroke diagnoses indicting cause-specific differences. [ABSTRACT FROM AUTHOR]