Since 1979, a continuing study of monozygotic and dizygotic twins, separated in infancy and reared apart, has subjected more than 100 sets of reared-apart twins or triplets to a week of intensive psychological and physiological assessment. Like the prior, smaller studies of monozygotic twins reared apart, about 70% of the variance in IQ was found to be associated with genetic variation. On multiple measures of personality and temperament, occupational and leisure-time interests, and social attitudes, monozygotic twins reared apart are about as similar as are monozygotic twins reared together. These findings extend and support those from numerous other twin, family, and adoption studies. It is a plausible hypothesis that genetic differences affect psychological differences largely indirectly, by influencing the effective environment of the developing child. This evidence for the strong heritability of most psychological traits, sensibly construed, does not detract from the value or importance of parenting, education, and other propaedeutic interventions.

A summary of 111 studies identified in a survey of the world literature on familial resemblances in measured intelligence reveals a profile of average correlations consistent with a polygenic mode of inheritance. There is, however, a marked degree of heterogeneity of the correlations within familial groupings, which is not moderated by sex of familial pairing or by type of intelligence test used.

Although common sense suggests that environmental influences increasingly account for individual differences in behavior as experiences accumulate during the course of life, this hypothesis has not previously been tested, in part because of the large sample sizes needed for an adequately powered analysis. Here we show for general cognitive ability that, to the contrary, genetic influence increases with age. The heritability of general cognitive ability increases significantly and linearly from 41% in childhood (9 years) to 55% in adolescence (12 years) and to 66% in young adulthood (17 years) in a sample of 11 000 pairs of twins from four countries, a larger sample than all previous studies combined. In addition to its far-reaching implications for neuroscience and molecular genetics, this finding suggests new ways of thinking about the interface between nature and nurture during the school years. Why, despite life's 'slings and arrows of outrageous fortune', do genetically driven differences increasingly account for differences in general cognitive ability? We suggest that the answer lies with genotype-environment correlation: as children grow up, they increasingly select, modify and even create their own experiences in part based on their genetic propensities.

Late adolescence (ie, 16 -20 years of age) is a period characterized by escalation of drinking and alcohol use problems for many and by the onset of an alcohol use disorder for some. This heightened period of vulnerability is a joint consequence of the continuity of risk from earlier developmental stages and the unique neurologic, cognitive, and social changes that occur in late adolescence. We review the normative neurologic, cognitive, and social changes that typically occur in late adolescence, and we discuss the evidence for the impact of these transitions on individual drinking trajectories. We also describe evidence linking alcohol abuse in late adolescence with neurologic damage and social impairments, and we discuss whether these are the bases for the association of adolescent drinking with increased risks of mental health, substance abuse, and social problems in adulthood. Finally, we discuss both the challenges and successes in the treatment and prevention of adolescent drinking problems. I N THE UNITED States, alcohol involvement sometimes starts but more often escalates between 16 and 20 years of age, when youths are also experiencing dramatic physical, emotional, and social changes. Specifically, a variety of forms of hazardous drinking emerge during middle to late adolescence and, for many youths, these problematic patterns of drinking continue to escalate through 18 to 20 years of age, the period of greatest risk for the onset of an alcohol use disorder (AUD).In seeking to understand youth development and alcohol involvement, it is important to consider all dimensions of functioning, because the interrelated cognitive, biological, social, and affective changes that occur during adolescence not only affect each another but also influence an individual's risk of problem drinking. In particular, the timing, sequence, and synchrony of developmentally specific transitions can affect how well youths master new roles, as well as continuities and discontinuities in their behavior. Therefore, developmental models representing a range of theoretical orientations, including systems theory, behavioral genetics, and developmental psychopathology, hold great promise for advancing our understanding of the processes that underlie adolescent changes, including the emergence of alcohol use and abuse.The need for developmental approaches is underscored by the existence of a consistent body of research showing that the escalation in drinking and the emergence of AUDs in middle and late adolescence have behavioral, social, and biological roots from earlier developmental stages. Moreover, it is becoming increasingly clear that alcohol involvement in adolescence has both short-and long-term effects on health and well-being at later developmental stages. Importantly, the consequences of adolescent drinking seem to differ from those associated with adult drinking, because there is increasing evidence that adolescents are especially vulnerable to the adverse effects of heavy alcohol use on both biological and socia...

The aim of this study was to explore, in a large and non-censored twin cohort, the nature (i.e., additive versus non-additive) and magnitude (i.e., heritability) of genetic influences on inter-individual differences in human longevity. The sample comprised all identified and traced non-emigrant like-sex twin pairs born in Denmark during the period 1870-1900 with a zygosity diagnosis and both members of the pairs surviving the age of 15 years. A total of 2872 pairs were included. Age at death was obtained from the Danish Central Person Register, the Danish Cause-of-Death Register and various other registers. The sample was almost non-censored on the date of the last follow-up (May 1, 1994), all but 0.6% had died, leaving a total of 2872 pairs for analysis. Proportions of variance attributable to genetic and environmental factors were assessed from variance-covariance matrices using the structural equation model approach. The most parsimonious explanation of the data was provided by a model that included genetic dominance (non-additive genetic effects caused by interaction within gene loci) and non-shared environmental factors (environmental factors that are individual-specific and not shared in a family). The heritability of longevity was estimated to be 0.26 for males and 0.23 for females. The small sex-difference was caused by a greater impact of non-shared environmental factors in the females. Heritability was found to be constant over the three 10-year birth cohorts included. Thus, longevity seems to be only moderately heritable. The nature of genetic influences on longevity is probably non-additive and environmental influences non-shared. There is no evidence for an impact of shared (family) environment.