This article urges counseling psychology researchers to recognize and report how missing data are handled, because consumers of research cannot accurately interpret findings without knowing the amount and pattern of missing data or the strategies that were used to handle those data. Patterns of missing data are reviewed, and some of the common strategies for dealing with them are described. The authors provide an illustration in which data were simulated and evaluate 3 methods of handling missing data: mean substitution, multiple imputation, and full information maximum likelihood. Results suggest that mean substitution is a poor method for handling missing data, whereas both multiple imputation and full information maximum likelihood are recommended alternatives to this approach. The authors suggest that researchers fully consider and report the amount and pattern of missing data and the strategy for handling those data in counseling psychology research and that editors advise researchers of this expectation.

The current paper synthesizes theory and data from the field of life history (LH) evolution to advance a new developmental theory of variation in human LH strategies. The theory posits that clusters of correlated LH traits (e.g., timing of puberty, age at sexual debut and first birth, parental investment strategies) lie on a slow-to-fast continuum; that harshness (externally caused levels of morbidity-mortality) and unpredictability (spatial-temporal variation in harshness) are the most fundamental environmental influences on the evolution and development of LH strategies; and that these influences depend on population densities and related levels of intraspecific competition and resource scarcity, on age schedules of mortality, on the sensitivity of morbidity-mortality to the organism's resource-allocation decisions, and on the extent to which environmental fluctuations affect individuals versus populations over short versus long timescales. These interrelated factors operate at evolutionary and developmental levels and should be distinguished because they exert distinctive effects on LH traits and are hierarchically operative in terms of primacy of influence. Although converging lines of evidence support core assumptions of the theory, many questions remain unanswered. This review demonstrates the value of applying a multilevel evolutionary-developmental approach to the analysis of a central feature of human phenotypic variation: LH strategy.

Drawing on life history theory, Ellis and associates' (2009) recent across- and within-species analysis of ecological effects on reproductive development highlighted two fundamental dimensions of environmental variation and influence: harshness and unpredictability. To evaluate the unique contributions of these factors, the authors of present article examined data from a national sample 1364 mothers and their children participating in the NICHD Study of Early Child Care and Youth Development. Harshness was operationalized as income-to-needs ratio in the first 5 years of life; unpredictability was indexed by residential changes, paternal transitions, and parental job changes during this same period. Here the proposition was tested that these factors not only uniquely predict accelerated life-history strategy, operationalized in terms of sexual behavior at age 15, but that such effects are mediated by change over the early-childhood years in maternal depression and, thereby, observed maternal sensitivity in the early-elementary-school years. Structural equation modeling provided empirical support for Ellis et al.'s (2009) theorizing, calling attention once again to the contribution of evolutionary analysis to understanding contemporary human parenting and development. Implications of the findings for intervention are discussed.

The current study tested sex-specific pathways to early puberty, sexual debut, and sexual risk taking, as specified by an integrated evolutionary-developmental model of adolescent sexual development and behavior. In a prospective study of 238 adolescents (n = 129 girls and n = 109 boys) followed from approximately 12-18 years of age, we tested for longitudinal relations between ecological stressors, family relationships, pubertal maturation, self-perceived mate value, and sexual risk taking in both boys and girls. Consistent with the theory, (a) higher levels of familial and ecological stress predicted earlier sexual debut and greater sexual risk taking; (b) pubertal maturation partially mediated these relations among girls but not among boys; (c) father absence had unique effects on female sexual outcomes but not on male sexual outcomes; (d) higher self-perceived mate value directly predicted earlier sexual debut and, through it, greater sexual risk taking; and (e) relations between pubertal maturation and early sexual debut were partially mediated by higher self-perceived mate value in boys but not in girls. Discussion focuses on the contribution of an integrated evolutionary-developmental theory to the adolescent sexual health literature.

Girls receiving lower quality paternal investment tend to engage in more risky sexual behavior (RSB) than peers. Whereas paternal investment theory posits that this effect is causal, it could arise from environmental or genetic confounds. To distinguish between these competing explanations, the current authors employed a genetically and environmentally controlled sibling design (N = 101 sister pairs; ages 18-36), which retrospectively examined the effects of differential sibling exposure to family disruption/father absence and quality of fathering. Consistent with a causal explanation, differences between older and younger sisters in the effects of quality of fathering on RSB were greatest in biologically disrupted families when there was a large age gap between the sisters (thus maximizing differential exposure to fathers), with greater exposure within families to higher quality fathering serving as a protective factor against RSB. Further, variation around the lower end of fathering quality appeared to have the most influence on RSB. In contrast, differential sibling exposure to family disruption/father absence (irrespective of quality of fathering) was not associated with RSB. The differential sibling-exposure design affords a new quasi-experimental method for evaluating the causal effects of fathers within families.