We are continuously learning about the impact relational and social experience have on the developing person, including the CNS, gene expression (epigenetics), etc. Persons could usefully, according to Ernest G. Schachtel in his excellent classic “Metamorphosis,” be viewed as “embedduals,” i.e., embedded in various relational and sociocultural frameworks. There is emergent research demonstrating that fetal cells in the rat could transform into neurons, astrocytes, oligodendrocytes, and macrophages, crossing the maternal blood brain barrier and responding to molecular distress signals if the mother's brain is injured (Choi 2005). In this way, the fetus gives back to the mother as well. The human mother's brain regulates to a significant degree, e.g., through the maternal-placental-fetal neuroendocrine system, the developing fetal brain, creating long-term predispositions towards stress reactivity, e.g., placental corticotropin releasing hormone/factor (Wadhwa 2005).
The neurocircuitry for social pain draws on the neurocircuitry for physical pain. Social pain, e.g., social exclusion, is equivalent neurobiologically, i.e., through activation of the dorsal anterior cingulate cortex (dACC), to actual physical pain: words and social isolation are painful. Social status influences the actual structure of certain neural regions, e.g., “high-status” animals actually have greater degrees of neurogenesis, and more neurons in the hippocampus, a neural region important in learning and memory. Mirror neurons help us to replicate and simulate within our own brains and minds the experience, goals and motivations/intentions of the other. Simulated embodiment, a prereflective (precognitive) grasping of the experience of the other, helps us to be affectively attuned to other persons. Marco Iacoboni, neurologist and mirror neuron researcher, has formulated an “existential neuroscience,” in which the inherent relationality of the human being is highlighted.
Social support and social bonds are negatively correlated with various ‘physical’ and ‘mental’ illnesses from cardiovascular disease to the schizophrenias. Social isolation is tied to a significantly enhanced risk of mortality and a heightened risk of both chronic and acute health disorders. One key pathway mediating these associations may be stress. When people are socially isolated their SNS (sympathetic nervous system) and LHPA (limbic-hypothalamic-pituitary-adrenal axis) response to stress may continue unabated, leading to a state of immunological vulnerability.
Social bonds promote reproduction, survival in the organism and its offspring, healthy development and reduce stress reactivity. The presence of social bonds is most dramatically documented by the intense emotional reactions to separation from or the loss of attachment figures. Oxytocin (OT), a hypothalamic neuropeptide, is released both by loss of social bonds as well as social connection. Its loss during social disconnection can be viewed as a form of social homeostat in which the organism is motivated to seek affiliative connection. It may be that OT initially signals distress and then induces affiliative efforts. If those affiliative contacts are supportive, and not critical or antagonistic, then affiliation would result in positive feelings and less stress. OT has anxiolytic and analgesic properties; it reduces the release of stress hormones, e.g., cortisol, and the reactivity of the autonomic nervous system, including reductions in heart rate and blood pressure.
The biological components of stress/anxiety depends significantly on two interacting stress systems, the sympathetic-adrenomedullary (SAM) system and the hypothalamic-adrenocortical (HPA) axis. OT expression downregulates the activity of the limbic-hypothalamic-pituitary-adrenal axis and the SAM system. There is an affiliative neurocircuitry which promotes affiliation, especially in response to threat and stress. Social contacts protect against the adverse effects of stress through a process which implicates OT-induced suppression of the HPA axis. The OT-opioid-dopaminergic system regulates social approach behavior. OT is released by touch (hence the importance of “keeping in touch”) and during positive social interactions. It is released in breast-feeding mothers and reduces anxiety in the latter compared to bottle-feeding mothers. OT is present in human breast milk and may serve as a anxiolytic for infants.
Dopamine and endogenous opioids play a significant role in social bonding. Dopamine-oxytocin and dopamine-vasopressin interactions and dopamine may be essential in the formation of social bonds. Dopamine antagonists which saturate dopaminergic receptors, therefore, may run interference with social bond formation, e.g., between patients and therapists.
Social relationships and pair bond formation play powerful roles in neural development, especially under conditions of challenge and stress. Evidence supporting intergenerational transmission of social experiences via changes in such neuropeptides as oxytocin also comes from recent research on maternal behavior in rats. The capacity of these neuroendocrine systems, e.g., corticotropin-releasing factor (CRF), to experience long-lasting functional modifications may help to explain the origins of what we call “temperament” and “gender.” Understanding these psychobiological systems and how deeply they are tied to social experience will offer potential insights into the development of what we call pathological or maladaptive behaviors.
Graduate Faculty, New York University
and Long Island University