We studied the cumulative incidence, concordance rate and heritability for diabetes mellitus in a nationwide cohort of 13,888 Finnish twin pairs of the same sex. The twins were born before 1958 and both co-twins were alive in 1967. Data on diabetes were derived through computerized record linkage from death certificates, the National Hospital Discharge Register and the National Drug Register. Records were reviewed in order to assign a diagnostic category to the 738 diabetic patients identified. Of these patients 109 had Type 1 (insulin-dependent) diabetes, 505 Type 2 (non-insulin-dependent) diabetes, 46 gestational diabetes, 24 secondary diabetes, 38 impaired glucose tolerance and 16 remained unclassified. The cumulative incidence of diabetes was 1.4% in men and 1.3% in women aged 28-59 years and 9.3% and 7.0% in men and women aged 60 years and over, respectively. The cumulative incidence did not differ between monozygotic and dizygotic twins. The concordance rate for Type 1 diabetes was higher among monozygotic (23% probandwise and 13% pairwise) than dizygotic twins (5% probandwise and 3% pairwise). The probandwise and pairwise concordance rates for Type 2 diabetes were 34% and 20% among monozygotic twins and 16% and 9% in dizygotic twins, respectively. Heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role.

To evaluate genetic influences on the use and abuse of alcohol, we compared questionnaire measures of the frequency, quantity, and density of social drinking, and the frequency of alcohol-induced passouts self-reported by 879 monozygotic (MZ) and 1940 dizygotic (DZ) pairs of twin brothers, aged 24-49 yr. The measures of frequency, quantity, and density (heavy drinking once or more a month) significantly intercorrelate, and the self-reported alcohol consumption by this sample is satisfactorily stable and consistent with nationwide sales figures. None of the drinking measures was associated with twin type (zygosity), and only density correlated with age. Similarity of drinking habits among twin brothers was evaluated as a function of their genetic resemblance and age, the frequency of their social contact with one another, and the interactions of these terms. The effects were estimated from hierarchical linear regressions of a double-entry data matrix from which each twin's drinking was predicted from that of his twin brother, and that pair's age, zygosity, cohabitation status, and frequency of social contact. Significant genetic variance was found for each of the drinking measures with heritability estimates ranging from 0.36 to 0.40. Co-twins in more frequent social contact with one another reported greater similarity in their use of alcohol, but heritable variance remained after the effects of age and social contact were removed from both mean levels and co-twin resemblance. Reported frequency of passouts yielded significant, but equivalent, correlations in both MZ and DZ twins and no evidence of genetic influence.

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Clinical studies have shown a relationship between allergic disorders and depression, panic disorder, attention deficit/hyperactivity disorder, and social anxiety for a significant subset of patients with these disorders. The nature of the relationship, whether due to shared environmental or biologic vulnerabilities or as a result of the stress of chronic illness, has been less clear. By examining the covariance of atopic disorders and depressive symptoms in a community sample of monozygotic (MZ) and dizygotic (DZ) twins, the contribution of genetic and/or shared environmental etiological factors can be established. A Finnish sample of 1337 MZ and 2506 DZ twin pairs, ages 33-60 years, was sent questionnaires inquiring about history of asthma, eczema, and atopic rhinitis, as well as the Beck Depression Inventory (BDI). The nature of the covariation between twins of these symptoms was investigated by fitting competing genetic and environmental models. Within-person correlation between atopic symptoms and BDI was 0.103 (P < 0.001) for the total sample. Using the Mx statistical modeling program to fit the data to competing quantitative genetic models, the best fitting model estimated that 64% of the association between atopy and BDI was due to shared familial vulnerability, primarily additive genetic influences. Although the measures for allergic disorders and depression are crude, this study supports the hypothesis that there is a small shared genetic risk for atopic and depressive symptoms, and if replicated, may open research for common mechanisms between allergic and depressive disorders. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:146-153, 2000.