Development and Psychopathology has been a premier resource for understanding stressful childhood experiences and the intergenerational continuity of psychopathology. Building on that tradition, we examined the unique and joint influences of maternal stress on children’s effortful control (age 7) and externalizing behavior (age 11) as transmitted via genetics, the prenatal environment, and the postnatal environment. The sample included N = 561 adopted children and their biological and adoptive parents. Path models identified a direct effect of biological mother life stress on children’s effortful control (β = −.08) and an indirect effect of her life stress on child externalizing behavior via effortful control (β = .52), but no main or indirect effects of biological parent psychopathology, prenatal stress, or adoptive mother adverse childhood experiences (ACES). Adoptive mother ACES amplified the association between biological mother life stress and child effortful control (β = −.08), externalizing behavior (β = 1.41), and the indirect effect via effortful control, strengthening associations when adoptive mothers reported average or high ACES during their own childhoods. Results suggest that novel study designs are needed to enhance the understanding of how life stress gets “under the skin” to affect psychopathology in the offspring of adults who have experienced stress.

The aim of this study was to find potential signs of genetic vulnerability to schizophrenia. The differences between adoptees at high genetic risk for schizophrenia (their biological mother had a schizophrenia spectrum disorder) and control adoptees of non-schizophrenia spectrum biological mothers were assessed. The comparisons between these groups were based on the Minnesota Multiphasic Personality Inventory (MMPI) test's subscale scores adjusted by gender, age at MMPI assessment, age at placement into the adoptive family and social class. The subjects were a subsamples of a total of 182 tested adoptees and 136 mentally healthy adoptees in the Finnish Adoptive Family Study. The high-risk group was found to be distinguishable from the low-risk group based on deviant scores on the Hostility, Hypomania and Lie scales. These scales may measure genetic vulnerability and also possibly be indicative of psychometric deviance predicting future onset of schizophrenia.

The aim of the study was to evaluate whether thought disorders are stable, trait-like features specific to subjects who have a genetic liability to schizophrenia or a psychiatric disorder. The thought disorders of adoptees genetically at high risk (HR) or low risk (LR) for schizophrenia from the Finnish adoptive family study of schizophrenia were evaluated twice at a mean interval of 11 years, using the sum of the Thought Disorder Index (TDI) scores on the Rorschach (TDR). At the initial assessment, the mean TDR scores of women were significantly higher than those of men, while no association between genetic risk and psychiatric status or their interactions with the TDR scores at baseline were found. The main finding was that the initial TDR scores statistically significantly predicted the TDR scores at follow-up, thus indicating the stability of thought disorder over time. However, neither genetic or psychiatric status nor gender or any interaction between these variables associated with TDR at follow-up.

The aim of this study was to investigate whether severe formal thought disorders and mature thinking are stable among adoptees (=187) drawn from the Finnish adoptive family study of schizophrenia. A group of 93 adoptees genetically at high risk (HR) and 94 at low risk (LR) for schizophrenia were assessed blindly and reliably using the Index of Primitive Thought (IPT) and the Index of Integration (IOI). Two assessments of the IPT and the IOI were performed with the mean interval of 11 years. Comparisons of the IPT and the IOI mean scores were conducted both at baseline and at follow-up between adoptees at low and high genetic risk, gender, and psychiatric status. The main result was that the IOI as well as the IPT of the adoptees at the initial assessment predicted the IOI and the IPT estimated at follow-up, thus indicating the stability of severe formal thought disorders and mature thinking over time. The stability of IOI or IPT was not related to genetic risk, gender or psychiatric status or their interactions.

The Minnesota Center for Twin and Family Research (MCTFR) comprises multiple longitudinal, community-representative investigations of twin and adoptive families that focus on psychological adjustment, personality, cognitive ability and brain function, with a special emphasis on substance use and related psychopathology. The MCTFR includes the Minnesota Twin Registry (MTR), a cohort of twins who have completed assessments in middle and older adulthood; the Minnesota Twin Family Study (MTFS) of twins assessed from childhood and adolescence into middle adulthood; the Enrichment Study (ES) of twins oversampled for high risk for substance-use disorders assessed from childhood into young adulthood; the Adolescent Brain (AdBrain) study, a neuroimaging study of adolescent twins; and the Siblings Interaction and Behavior Study (SIBS), a study of adoptive and nonadoptive families assessed from adolescence into young adulthood. Here we provide a brief overview of key features of these established studies and describe new MCTFR investigations that follow up and expand upon existing studies or recruit and assess new samples, including the MTR Study of Relationships, Personality, and Health (MTR-RPH); the Colorado-Minnesota (COMN) Marijuana Study; the Adolescent Brain Cognitive Development (ABCD) study; the Colorado Online Twins (CoTwins) study and the Children of Twins (CoT) study.

Nature and nurture are not separate. Instead it is important to investigate the interplay between genes and environment and how they influence on another. To an important degree, genetic effects on behavior come about because they either influence the extent to which the individual is likely to be exposed to individual differences in environmental risk or they affect how susceptible the individual is to environmental adversities.

The current inability to explain or predict which genetically predisposed individuals will finally become schizophrenic has forced us to confront our ignorance of the precise mechanism and mode of the transmission of this disorder. Zubin's proposal to view the schizophrenic as a vulnerable individual who develops a temporary episode only under certain provocations can help place the controversy in proper perspective. Vulnerability (predisposition, diathesis) to schizophrenia can be defined as the individual's characteristic treshold beyond which stressful events produce decompensation manifest in the clinically diagnosable symptom picture.

Several twin studies of children and adolescents have found significant heritability of depressive symptoms. In contrast, the sole adoption study of biologically related and biologically unrelated adopted siblings found no evidence for genetic influence. The present study attempts to confirm these results in middle childhood using two adoption designs. The sample, from the Colorado Adoption Project, included 180 adopted children (77 with adoptive siblings) and their biological and adoptive mothers, and 227 nonadopted children (93 with biological siblings) and their mothers. Mothers reported their own neuroticism, and children's depressive symptoms were reported by the parents and by the children themselves. For both the sibling adoption and the parent-offspring designs heritability was negligible, shared environment modest, and nonshared environment substantial, irrespective of child gender. Although the power of the sibling data is low, the combined findings from the two designs suggest that genetic effects on depressive symptoms in childhood may be somewhat smaller than previously estimated in twin studies.