Suchergebnisse

Born to Rebel (Sulloway, 1996) embeds a theory of birth order within an evolutionary perspective that gives a refreshing new twist to theorizing about family structure. Most past birth order "theorizing" is of the type that both begins and ends with "Isn't it interesting that…." In Rodgers and Thompson (1985/86), we documented birth order research on presidents and strippers, artists and assassins, hockey players and cigarette smokers; even the birth order of birth order researchers has been investigated. Sulloway (1996), in contrast, provided explicit mechanisms to explain why he believes that birth order plays an important role in revolutionary behavior. The mechanisms derive from sophisticated thinking about both evolution and family dynamics.

"Correlation matrices (along with their unstandardized counterparts, covariance matrices) underlie much of the statistical machinery in common use today. A correlation matrix is more than a matrix filled with correlation coefficients. The value of one coefficient in the matrix puts constraints on the values of the others, and this is a major theme of the volume. The volume is written accessibly, and key points are illustrated with a wide range of lively examples, including correlations between intelligence measured at different ages through adolescence; correlations between public health expenditures, health life expectancy, adult mortality, and other country characteristics; correlations between wellbeing and state-level vital statistics; correlations between the racial composition of cities and professional sports teams; and correlations between childbearing intentions and childbearing outcomes over the reproductive life course"--

Research designs to study alcohol use and abuse have included twin, adoption and family history/high risk studies. Results have consistently implied a genetic factor in the aetiology of alcohol abuse. However, less research has been conducted in search of environmental factors. This study uses kinship structure in a large national dataset (the National Longitudinal Survey of Youth) to estimate (using DeFries–Fulker analysis) the extent of the shared genetic, non-shared genetic, shared environmental and non-shared environmental influences on alcohol use. The NLSY kinship sample contained 3890 pairs of cousins, half-siblings, full-siblings and twins between the ages of 14 and 21 in the initial year of the survey (1979). Estimates of heritability (h2) and shared environment (c2) were small to moderate for the entire dataset for both light drinking and heavy drinking behaviour, with h2 estimates slightly higher in each case. Non-shared genetic measures of self-esteem and locus of control accounted for a significant portion of the remaining variance in heavy drinking behaviour. Race and gender patterns showed c2 and h2 estimates that were also small to moderate for both light and heavy drinking behaviour. Significant non-shared effects were found for the White group for heavy drinking behaviour, and for male pairs for both heavy and light drinking behaviour. Additionally, implications and future directions are discussed.

Fisher (1930) presented both theoretical and empirical results concerning genetic influences on fertility. Since then, only sparse research has been done on the genetics of fertility, although more sophisticated methodogy and data now exist than were available to Fisher. This paper presents a behavioural genetic analysis of age at first intercourse, accounting for genetic, shared environmental, and selected non-shared environmental influences. The data came from the nationally representative National Longitudinal Survey of Youth (NLSY). A newly developed kinship linking procedure was used that identifies links for cousins, half-siblings, full-siblings and twins in the NLSY. The results suggest a genetic influence in the overall dataset, and also among whites and in male–male and opposite-sex pairs. Genetic influences were extremely small or non-existent for blacks and for female–female pairs. Shared environmental influences were small for most subsets of the data, but moderate for female–female pairs. Two specific non-shared environmental influences – self-esteem and locus of control – were ruled out as accounting for any meaningful variance, although other general sources of non-shared environmental influence appear potentially important. Analysis of selected samples from upper and lower tails suggested that genetic influences are important in accounting for both early and late non-virginity. These findings are consistent with work reported by Miller et al. (1999), who used molecular genetic methods. Generally, these findings support the existence of genetic influences and implicate non-shared environmental influences as being important determinants of the timing of loss of virginity among US adolescents and young adults.

Epidemic Models of the Onset of Social Activities (EMOSA) describe behaviors that spread through social networks. Two social influence methods are represented, social contagion (one‐to‐one spread) and general diffusion (spread through cultural channels). Past models explain problem behaviors—smoking, drinking, sexuality, and delinquency. We provide review, and a tutorial (including examples). Following, we present new EMOSA models explaining changes in adolescent and young adult religious participation. We fit the model to 10 years of data from the 1997 U.S. National Longitudinal Survey of Youth. Innovations include a three‐stage bi‐directional model, Bayesian Markov Chain Monte Carlo (MCMC) estimation, graphical innovations, and empirical validation. General diffusion dominated rapid reduction in church attendance during adolescence; both diffusion and social contagion explained church attendance stability in early adulthood.

AbstractStudies have reported that the age‐adjusted incidence of cognitive impairment and dementia have decreased over the past two decades. Aging is the predominant risk factor for Alzheimer's disease and related dementias and for neurocognitive decline. However, aging alone cannot explain changes in the overall age‐adjusted incidence of dementia. The objective of this position paper was to describe the potential for cohort and period effects in cognitive decline and incidence of dementia. Cohort effects have long been reported in demographic literature, but starting in the early 1980s researchers began reporting large historical cohort trends in cognitive function. At the same time, period effects have emerged in the form of economic factors and stressors in early and midlife that may result in reduced cognitive dysfunction. Recognizing that aging individuals today were once children and adolescents and that research has clearly noted that childhood cognitive performance are associated with old‐age cognitive performance, this review proposes the need to connect these cohort effects with differences in late‐life functioning.