Late and early stressful factors have widely been recognized to play a role in the aetiology of depression. Recent research indicates that such adverse environmental stimuli may alter gene expression in humans via epigenetic modifications. While epigenetic changes such as DNA methylation are likely involved in these processes, it is still unknown what specific genomic loci may be hyper- or hypo-methylated in depression. The association between depressive symptoms during the last 30 days (Brief Symptom Inventory [BSI]) and peripheral-blood DNA methylation levels at genomic loci previously reported as epigenetically altered in saliva and brain of depressive patients was evaluated in a community sample of 34 adult Caucasian MZ twins (17 pairs). Intrapair DNA methylation differences in an intron of DEPDC7 (chr11:33040743) were associated with intrapair differences in current depressive symptoms. Accordingly, a site-specific 10% DNA hypomethylation in a co-twin would correlate with a current depressive symptom score around 3.1 BSI points above the score of his/her less-depressed co-twin. These findings indicate that DEPDC7 hypomethylation in peripheral blood DNA may be associated with recent depressive symptomatology, in line with previous results.

The 20 reported cases of MZ female twins discordant for X-linked diseases are reviewed. In such twins the X-inactivation pattern is opposite skewing (abnormal allele inactivated in most cells of the normal twin, and normal allele inactivated in most cells of the affected twin) or skewing in one twin and random in the cotwin. The diseases involved map in two specific regions: Xq27-28 and Xp21. The only exceptions are Fabry's disease and Aicardi's syndrome, which map in Xq22 and Xp22 respectively. No concordant MZ female carrier twins, either normal or affected, have been described. Three main hypotheses have been proposed to explain such characteristics [2, 5, 14], but none is completely satisfactory. The constant discordance for X-linked diseases in MZ female twins has important consequences for genetic counselling.

White male twins from the NAS-NRC twin sample, who were born in the U.S. between 1917 and 1927 and served in the military, are used to estimate variability in hazard functions for those twins who died during the period 1974-1990. Roughly the same number of MZ and DZ twins died during this period, but their death rates are similar. DZ twins exhibit greater within-pair variation. Using hazard and other analyses, the only statistically significant variables are found to be being a DZ twin (in level equations), date of birth, and, sometimes, wife's religious preference. Variables not significant for level or within-pair equations, include own religion, parental education, working overtime frequently, and number of children. The greater variation in life expectancy of DZ twins is hardly surprising and may say something about the lack of comparability in phenotype variance of DZ twins, which in turn may be worrying.

Many studies of embryogenesis and fate of twin pregnancies are invalidated because zygosity is not determined definitively, or is assumed on the basis of inadequate criteria. This paper briefly reviews methods of zygosity determination. It reports published results and a new series of twins in which zygosity was determined by DNA fingerprinting. Implications for methods of prenatal diagnosis of zygosity are discussed in the context of the occasional need for intervention in twin transfusion syndrome or in twins discordant for major malformations. Definitive zygosity and placental anatomy (number of chorions and amnions) is discussed as the firm substrate for studies of normal and abnormal twin development.

In a sample of monozygotic twins, intrapair differences in reported birthweight were larger in those pairs discordant for later psychosis, compared to pairs concordant for psychosis. A trend towards less family history of psychiatric disorder was also found in the discordant pairs.