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Background: Both hostile parenting and parental psychopathology have been shown to predict depression in the offspring. However, whether and how they interact in predicting the longitudinal course of depression from adolescence to adulthood remains unclear., Methods: Participants were from the prospective Cardiovascular Risk in Young Finns study, aged 3-18 years at baseline in 1980. We used multilevel modeling for repeated measurements to examine the associations of hostile parenting (i.e., parental intolerance and emotional distance) and parental history of psychopathology with trajectories of depressive symptoms across five study phases from 1992 to 2012., Results: On average, depressive symptoms decreased in a curvilinear pattern with age. A relatively steep decreasing trend was also observed among offspring of parents with a history of psychopathology but low intolerance. By contrast, among the offspring of parents with a history of psychopathology and high intolerance there was a rising trend in depressive symptoms starting from young adulthood. There was no similar interaction between parental history of psychopathology, emotional distance, and age., Limitations: Non-standardized, parental self-report scales were used to measure hostile parenting. The observed effects were small, and the depressive symptoms scale applied in the study may not be used for measuring clinical depression., Conclusions: Parental psychopathology might render individuals sensitive to the unfavorable characteristics of the caregiving environment. Intolerance towards the child can exacerbate the effects of parental psychopathology and have a long-term significance on the developmental trajectory of depressive symptoms over the life-course., (Copyright © 2016 Elsevier B.V. All rights reserved.)

The serotonin system has been shown to be involved in the regulation of hostility, anger, and aggressive behavior. Previous molecular genetic studies suggest that the serotonin receptor 1B (HTR1B) rs6296 genotype might have a particular role in these types of behaviors. We examined whether HTR1B is related to hostility, anger, and aggressive behavior phenotypes over a lifespan and whether it modifies the connection between childhood aggressive behavior and adulthood hostility and anger. The participants were 967 women and men from a large population based sample (The Young Finns Study) with a 27-year follow-up. Childhood aggressive behavior was reported by the mother twice when the participants were 3 to 12 years of age. Adulthood hostility and anger were self-reported by the participants between ages 24 and 36. Childhood aggressive behavior predicted adulthood hostility over 27 years. HTR1B SNP rs6296 was associated with childhood aggressive behavior but not with adulthood anger or hostility. The HTR1B SNP rs6296 modified the association between childhood aggressive behavior and adulthood hostility. Aggressive behavior and hostility might form a life course pattern, and the HTR1B might contribute to a development of this pattern.

Background: Low socio-economic status (SES), and a conflictive, cold and unsupportive family environment in childhood have been associated with early adulthood hostility. However, it is unknown whether this association changes in magnitude with age from childhood to adulthood. We investigated whether childhood family factors (SES and parental child-rearing style) predicted differential development of offspring hostility and anger from early to middle adulthood., Method: Between 2041 and 2316 participants (age range 3-18 years at baseline) were selected from the longitudinal Young Finns study. The participants were followed for 27 years between 1980 and 2007. Childhood SES and parent's self-reported child-rearing style were measured twice: at baseline and 3 years after baseline. Hostility and anger were assessed with self-report questionnaires at 12, 17, 21 and 27 years after baseline., Results: Low parental SES and hostile child-rearing style at baseline predicted higher mean levels of offspring anger and hostility. Low parental SES and one of the hostile child-rearing style components (strict disciplinary style) became more strongly associated with offspring hostility with age, suggesting an accumulating effect., Conclusions: Childhood family factors predict the development of hostility and anger over 27 years and some of these family factors have a long-term accumulating effect on the development of hostility.

Hostility is a multidimensional personality trait with changing expression over the life course. We performed a genome-wide association study (GWAS) of the components of hostility in a population-based sample of Finnish men and women for whom a total of 2.5 million single-nucleotide polymorphisms (SNPs) were available through direct or in silico genotyping. Hostility dimensions (anger, cynicism and paranoia) were assessed at four time points over a 15-year interval (age range 15-30 years at phase 1 and 30-45 years at phase 4) in 982-1780 participants depending on the hostility measure. Few promising areas from chromosome 14 at 99 cM (top SNPs rs3783337, rs7158754, rs3783332, rs2181102, rs7159195, rs11160570, rs941898, P values <3.9 × 10(-8) with nearest gene Enah/Vasp-like (EVL)) were found suggestively to be related to paranoia and from chromosome 7 at 86 cM (top SNPs rs802047, rs802028, rs802030, rs802026, rs802036, rs802025, rs802024, rs802032, rs802049, rs802051, P values <6.9 × 10(-7) with nearest gene CROT (carnitine O-octanoyltransferase)) to cynicism, respectively. Some shared suggestive genetic influence for both paranoia and cynicism was also found from chromosome 17 at 2.8 cM (SNPs rs12936442, rs894664, rs6502671, rs7216028) and chromosome 22 at 43 cM (SNPs rs7510759, rs7510924, rs7290560), with nearest genes RAP1 GTPase activating protein 2 (RAP1GAP2) and KIAA1644, respectively. These suggestive associations did not replicate across all measurement times, which warrants further study on these SNPs in other populations.

We studied whether there is an association between hostility and cardiovascular heart disease (CHD) risk factors, such as the metabolic syndrome, systemic inflammation and autonomic cardiac control. Participants were 912 women and 712 men aged 15-30 when hostility was measured in 1992. Metabolic syndrome was assessed 9years later in 2001 using 3 definitions: the National Institute of Health Adult Treatment Panel III criteria (NCEP), the European Group for the Study of Insulin Resistance criteria (EGIR), and the International Diabetes Federation criteria (IDF). C-reactive protein (CRP) defined in 2001 was the marker of inflammation. Cardiac control indices were from EGC recording. In women, hostility predicted increased risk of metabolic syndrome (EGIR, and the IDF definitions, ORs = 1.34, 1.35, p < 0.05), and higher levels of inflammation (β = 0.09, p < 0.01). We concluded that hostility is associated with metabolic syndrome and systemic inflammation in women and these conditions may be factors linking hostility to CHD., (Copyright © 2011 Elsevier B.V. All rights reserved.)

We examined a modifying role of 5HT1A and 5HT2A receptors in the relation between childhood difficult temperament and adulthood hostility in 729 subjects derived from a population-based sample. Subjects were 3-12 years when their childhood temperaments consisting of hyperactivity, low sociability and negative emotionality (i.e. the difficult temperament), were assessed by their mothers. Their adulthood hostility comprising anger, cynicism and paranoia, was measured twice, 17 and 21 years later. It was found that the 5HT1A and 5HT2A receptors were not related to childhood temperament or to adult hostility, but they modified the association between childhood hyperactivity and adult hostility in men. Male carriers of T/T genotype of 5HTR2A who were rated hyperactive by their mothers expressed a high level of hostility, especially that of cynicism, in adulthood. For men with other genetic variants, such an association was not seen. This finding was consistent across the two follow-ups 4 years apart. Further research is needed to clarify whether mother-related hyperactivity adequately describes the temperament of the child or is a reflection of mother's hostile child-rearing attitudes.