Early life influences on life‐long patterns of behavior and health

Abstract

The stability of a child's early life has profound effects on physical and mental health, and unstable parent-child relationships, as well as abuse, can lead to behavioral disorders and increased mortality and morbidity from a wide variety of common diseases later in life. One common consequence, namely, depressive illness, is associated with chemical imbalances in the brain and hormonal dysregulation, constituting a form of allostatic load that alters interpretations of stimuli and influences, behavioral, and hormonal responses to potentially stressful situations. The brain not only encodes information and controls the behavioral responses but it is also changed structurally by those experiences. Structural changes in the hippocampus and amygdala, which are important brain structures for cognition and emotion, are representative of what may be occurring throughout the brain as a result of allostatic load resulting from the chronic stress of a disorder such as depression. Such structural changes include dendritic debranching and hypertrophy, cell proliferation, and synaptic remodeling; they are produced by the combined overactivity of stress hormones and endogenous neurotransmitters. These mediators are normally involved in adaptation, but can also promote damage when they are dysregulated and over-active. They are very likely to be strongly biased by early life experiences. The findings from animal models thus provide a basis for understanding potential mechanisms of environmental and developmental determinants of individual differences in human stress reactivity, as well as anxiety, depression, and a host of related systemic disorders. There is an increasing amount of translational research that is beginning to tie the basic research to clinical outcomes of individuals exposed to abusive or inconsistent care-giving in early life. A major goal of studies on this important topic is to define times in development and strategies for intervening to prevent or reverse the effects of adverse early life experiences. Although prevention is clearly the preferable route, some degree of reversal of psychopathology and pathophysiology caused by early life adversity appears to be an achievable goal.

Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction

“…Infant experiences result in long-term adaptations that program subsequent behavioral, endocrine, and neural function (3,14,57,61). In addition, infant odors have a powerful modulatory influence on adult behaviors (62,63).…”

Placental programming of anxiety in adulthood revealed by Igf2-null models

“…4a). We focused on the hippocampus (for dissection details, see Supplementary Methods) and the GABAergic and serotoninergic (5-HT) neurotransmitter systems in light of their established key roles in mediating anxiogenic behaviour 37,38 and sensitivity to earlylife manipulations [39][40][41] . Quantitative PCR (see Supplementary Methods) revealed a highly specific pattern of hippocampal gene expression changes, with significant reductions in expression of the GABAAa3 receptor subunit and 5-HT 2A receptor message in the Igf2-P0 KO mice (Fig.…”

Personality traits in rats predict vulnerability and resilience to developing stress-induced depression-like behaviors, HPA axis hyper-reactivity and brain changes in pERK1/2 activity

“…Understanding the sources of such differences in vulnerability to stress is a major challenge for contemporary research. A current view suggests that individual differences are the result of the interactions among genetic factors (de Rijk and de Kloet, 2005), predisposing early life experiences and major life stressors (McEwen, 2003). However, the specific underlying mechanisms that determine an individual's vulnerability to stress are not well understood.…”