The adjustment of children of Australian Vietnam veterans: is there evidence for the transgenerational transmission of the effects of war-related trauma?

Objective: The presence of posttraumatic stress disorder (PTSD) in trauma survivors has been linked with family dysfunction and symptoms in their children, including lower self-esteem, higher disorder rates and symptoms resembling those of the traumatized parent. This study aims to examine the phenomenon of intergenerational transfer of PTSD in an Australian context.

Method: 50 children (aged 16–30) of 50 male Vietnam veterans, subgrouped according to their fathers' PTSD status, were compared with an age-matched group of 33 civilian peers. Participants completed questionnaires with measures of self-esteem, PTSD symptomatology and family functioning.

Results: Contrary to expectations, no significant differences were found between the self-esteem and PTSD symptomatology scores for any offspring groups. Unhealthy family functioning is the area in which the effect of the veteran's PTSD appears to manifest itself, particularly the inability of the family both to experience appropriate emotional responses and to solve problems effectively within and outside the family unit.

Conclusion: Methodological refinements and further focus on the role of wives/mothers in buffering the impact of veterans' PTSD symptomatology on their children are indicated. Further effort to support families of Veterans with PTSD is also indicated.

Intergenerational effects of the Holocaust : subjective well-being in the offspring of survivors

Offspring of Holocaust survivors have been the subject of much research into how traumatic events affect future generations. This study considers the effects of the Holocaust on the well-being rather than trauma of offspring of Holocaust survivors in Australia. 285 Jewish participants completed a questionnaire to measure components of subjective well-being. Analyses revealed that offspring of Holocaust survivors reported lower general positive mood than non-OHS. This result was limited to offspring of Holocaust survivors with two survivor parents. These findings imply that effects of the Holocaust are transmitted to nonclinical offspring of Holocaust survivors and that the number of survivor parents is a crucial determinant in understanding these transgenerational outcomes.

Effects of early-life environment and epigenetics on cardiovascular disease risk in children: highlighting the role of twin studies

Cardiovascular disease (CVD) is the leading cause of death worldwide and originates in early life. The exact mechanisms of this early-life origin are unclear, but a likely mediator at the molecular level is epigenetic dysregulation of gene expression. Epigenetic factors have thus been posited as the likely drivers of early-life programming of adult-onset diseases. This review summarizes recent advances in epidemiology and epigenetic research of CVD risk in children, with a particular focus on twin studies. Classic twin studies enable partitioning of phenotypic variance within a population into additive genetic, shared, and nonshared environmental variances, and are invaluable in research in this area. Longitudinal cohort twin studies, in particular, may provide important insights into the role of epigenetics in the pathogenesis of CVD. We describe candidate gene and epigenome-wide association studies (EWASs) and transgenerational epigenetic inheritance of CVD, and discuss the potential for evidence-based interventions. Identifying epigenetic changes associated with CVD-risk biomarkers in children will provide new opportunities to unravel the underlying biological mechanism of the origins of CVD and enable identification of those at risk for early-life interventions to alter the risk trajectory and potentially reduce CVD incidence later in life.

Early origins of mental disorder - risk factors in the perinatal and infant period

BACKGROUND: There is increasing understanding of the significance of early neurodevelopment in establishing risk for the range of mental disorders. Models of the early aetiology of mental disorders are complex with a range of potential factors from genetic and epigenetic to environmental influencing neurological and psychological development. Whilst the mechanisms are not fully understood, this paper provides an overview of potential biological and neurobiological factors that might be involved. METHOD: An aetiological model is presented and discussed. The discussion includes a range of risk factors for mental disorder. Maternal anxiety disorder is presented and reviewed as an example of the interaction of placental, epigenetic and early parenting factors elevating risk of poor neonatal outcome. RESULTS: Available evidence points to the importance of in-utero influences as well as the role of early attachment and emotional care. Transgenerational mechanisms such as the impact of maternal mental disorder on foetal development are important models for examination of early risk. Maternal anxiety, as an example, is a significant risk factor for compromised mental health. CONCLUSIONS: Development of models for understanding the early origins of mental disorder is an important step in elaborating risk reduction strategies. Comprehensive early identification of risk raises the possibility of preventive interventions.

Cancer and life-history traits: lessons from host-parasite interactions

Despite important differences between infectious diseases and cancers, tumour development (neoplasia) can nonetheless be closely compared to infectious disease because of the similarity of their effects on the body. On this basis, we predict that many of the life-history (LH) responses observed in the context of host-parasite interactions should also be relevant in the context of cancer. Parasites are thought to affect LH traits of their hosts because of strong selective pressures like direct and indirect mortality effects favouring, for example, early maturation and reproduction. Cancer can similarly also affect LH traits by imposing direct costs and/or indirectly by triggering plastic adjustments and evolutionary responses. Here, we discuss how and why a LH focus is a potentially productive but under-exploited research direction for cancer research, by focusing our attention on similarities between infectious disease and cancer with respect to their effects on LH traits and their evolution. We raise the possibility that LH adjustments can occur in response to cancer via maternal/paternal effects and that these changes can be heritable to (adaptively) modify the LH traits of their offspring. We conclude that LH adjustments can potentially influence the transgenerational persistence of inherited oncogenic mutations in populations.