Cytokines and vitamin D both have a role in modulating the immune system, and are also potentially useful biomarkers in mental illnesses such as major depressive disorder (MDD) and schizophrenia. Studying the variability of cytokines and vitamin D in a healthy population sample may add to understanding the association between these biomarkers and mental illness. To assess genetic and environmental contributions to variation in circulating levels of cytokines and vitamin D (25-hydroxy vitamin D: 25(OH)D3), we analyzed data from a healthy adolescent twin cohort (mean age 16.2 years; standard deviation 0.25). Plasma cytokine measures were available for 400 individuals (85 MZ, 115 DZ pairs), dried blood spot sample vitamin D measures were available for 378 individuals (70 MZ, 118 DZ pairs). Heritability estimates were moderate but significant for the cytokines transforming growth factor-β1 (TGF-β1), 0.57 (95% CI 0.26–0.80) and tumor necrosis factor-receptor type 1 (TNFR1), 0.50 (95% CI 0.11–0.63) respectively. Measures of 25(OH)D3 were within normal range and heritability was estimated to be high (0.86, 95% CI 0.61–0.94). Assays of other cytokines did not generate meaningful results. These potential biomarkers may be useful in mental illness, with further research warranted in larger sample sizes. They may be particularly important in adolescents with mental illness where diagnostic uncertainty poses a significant clinical challenge.

G × E in psychiatry may explain why environmental risk factors have big impact in some individuals but not in others, and conversely why relatives that are genetically at risk for disease do not all develop disease. Here we discuss two novel methods that use an aggregate genome-wide measure of genetic risk to detect G × E and estimate its effect in the population using data currently available and data we anticipate will be available in the near future. The first method exploits summary statistics from large-scale genome-wide association studies ignorant of the environmental conditions and detects G × E in an out-of-sample risk-profiling framework. The second method relies on larger samples and is based on a mixed linear model framework. It estimates variance explained directly from single nucleotide polymorphisms and environmental measures. Both methods have great potential to improve public health interventions focusing on risk-based screening that is informed by both genetic and environmental risk factors.

Although it is well established that experience seeking behavior (ES) ispositively related to cognitive functioning, the mechanisms underlying thisassociation are not clearly understood. In a large sample of adult twins andsiblings (N = 864, age range 23–75), we studied the causes ofcovariation between ES and general cognitive ability and we studied whether ESmoderates the genetic and environmental causes of variation in general cognitiveability. Results demonstrate a phenotypic correlation of .17 (p <.001)between general cognitive ability and ES, with a common genetic and commonenvironmental background. Moreover, the extent to which genetic andenvironmental factors are shared between general cognitive ability and ES isincreased in individuals with either lower or higher levels of ES. In addition,the extent to which genetic and environmental factors influence individualdifferences in general cognitive ability in adults partly depended on ES.Standardized influences of additive genetic factors on general cognitive abilityranged from 13% to 99%, with lower estimates in higher levels of ES, whilestandardized estimates of environmental factors ranged from almost 1% to 87%,with higher estimates in higher levels of ES. Hence, ES and cognitive abilityare not only associated through common genetic and environmental factors, butalso via moderating effects of genetic and environmental influences on cognitiveability by ES. These findings have implications for future studies on theassociation between ES and general cognitive ability, and for future research onthe genetics of cognitive ability.