Mental health articles

During evolution, processing and performing complex social interaction emerged as a key factor driving the development of larger brains in primates and humans.Social skills that are necessary for profiting from diversification of knowledge, for refining commercial relationships or for building tactical alliances in order to expand power, substantially contributed to the success of the human species. A supportive social environment turned out as one of the most important conditions necessary for mental and physical health. Therefore, acute loss ofgroup support may be perceived as fundamental threat, eliciting astress reaction comparable to acute physical endangerment. But also more chronic forms of socialstress are of interest, as exposure to a socially stressful environmentoften expands over a period of weeks, months or years. Forexample, long-lasting social isolation has a considerable impact onboth physical and mental health, as it is associated with anincreased risk of depression, anxiety, coronary heart disease, anddeath. The impact of social stress as a risk factor forboth mental and physical disease is corroborated by findings thathighlight the beneficial impact of social support. This factoremerged as a powerful resource to mitigate the effects of acutestress. Finally, the presence of this factor isassociated with a reduction of mortality exceeding the influence ofphysical activity, smoking cessation and lower body-mass index.

Stress research, neuroscience and epidemiology have substantiallycontributed to elucidate the role of social stress as a risk factorfor mental disorders. Stress research has identified potent ingredientsof acute social stress. Exposure to tasks that were uncontrollableand included social threat, i.e. failure in front ofsignificant others, were associated with the most profound activationof the endocrine stress response. Pathways through which stress exposure increases the riskof disease manifestation have been investigated in most majormental disorders. They vary according to type of stressor, exposuretime and subject characteristics. In 1997, Walker and Diforio proposed the “neural diathesis-stressmodel”, and suggested that the interaction of specific genetic andenvironmental factors resulted in increased stress system activation,thus facilitating onset, exacerbation and relapse of schizophrenia.According to this model, stressful events are associated with an abnormal activity of the hypothalamic-pituitaryadrenal axis, triggering a cascade of events leading todysfunction of dopaminergic neurotransmission and neural circuitsrelevant for psychosis symptom generation. Significant stress-associated dopamine release in theventral striatum in healthy volunteers andstress-responsive system dysfunction in schizophrenic patientsupon exposure of to an experimental social stressor both support this hypothesis. Furthermore, prolongedexposure to stress seems to be capable of inducing architecturalchanges in specific brain areas such as the prefrontal cortex whichmediates the highest-order cognitive abilities.Chronic stress was also found to be associated with a decrease involume in of the hippocampus, a structure central to memorystorage and retrieval. Interestingly, the hippocampusis also involved in HPA system regulation, as this structureexerts a tonic inhibition on stress system activity, which subsideswith stress exposure. Through this mechanism, hippocampaldamage may result in enduring HPA system overactivity, furtheraggravating damage to brain structures via prolonged cortisolexposure.

Neuroscience has made substantial progress in exploring theneural circuits that support social function and process social stress.Segmentation of social cognition differentiates social perception,attribution and categorization. During these processes, socialstimuli that arise from other group members are detected andanalysed, and behaviour is interpreted as indicating a specificmental state. The emotionaland motivational appraisal of social stimuli is processed in a neuralmutually interacting circuit involving the brain regions amygdala,insulate, subgenual anterior cingulate cortex (ACC) as well as theorbitofrontal cortex. This circuit closely interacts with the brainstructures that direct the stress-responsive systems including theHPA system. The smooth functioning of these neural circuits may beendangered by genetic and environmental factors. Several lines ofevidence indicate that the maturing brain is vulnerable to environmentalstressors especially in genetically predisposed subjects. For example, the action of the hypothalamicneuropeptides oxytocin and vasopressin differs in carriers ofgenetic variants encoding the receptor for these molecules. Exposure to social stressis associated with a profound effect on these receptors, affectingfunction and structure of hypothalamic-limbic circuits. In the caseof schizophrenia, animal data indicate that early life exposure tosocial stress is associated with both increased mesolimbic dopaminereactivity and psychosis related phenotype in adulthood.

Recent work has combined functional magnetic resonance imagingtechniques and stress research tools to identify the brainmechanisms that are involved in translating the effect of city livingon social stress processing. It was shownthat in healthy adults, exposure to an urban environment duringthe first 15 years of life was associated with an increased activationof the ACC, a key structure of the limbic system involved in bothprocessing social information and regulating stress-responsivesystem activation. The association between early-life urbanicity and increased ACC activation during social stress processing followeda doseeresponse relationship and was specific for this brainarea and for stress processing. Furthermore, this neurobiologicalregion is known to be central for exactly those disorder groups(schizophrenia and depression) that are found to be increased incity dwellers, making it plausible that social stress processing is amediator for increased psychiatric risk in the urban environment.Epidemiologic work has described in great detail the magnitudeof mental disorders that follow social isolation, neglect and abuse.Adverse social conditions during childhood showed powerful associationswith many types of mental disorders, including anxiety,mood, disruptive behaviour and substance use disorders. The maladaptive family functioning cluster (parentalmental illness, substance use disorder, and criminality; familyviolence; physical abuse; sexual abuse; and neglect) were thestrongest correlates of disorder onset. Theseepidemiologic data suggest that 45% of childhood-onset disordersand 29% of later-onset disorders are associated with adverse socialconditions during childhood.

Chronic social adversity and discrimination pose also duringadolescence a major social stressor to the individual. These factorshave been identified as a major risk factor for psychotic episodesand schizophrenia  and have been thoroughlystudied in specific minority groups including first and secondgeneration migrants. These cohorts, e.g., individuals who havemigrated from the Caribbean Islands to the United Kingdom andelsewhere, carry a substantially increased risk of schizophrenia. It has been demonstrated that this phenomenondoes not reflect an increased schizophrenia risk in thecountry of origin, but rather depends on the ethnic density of theenvironment where the migrant is actually living (Boydell et al.,2001; Veling et al., 2008). Notably, the presence of a large ethnicgroup to which the migrant belongs to attenuates the increase ofpsychosis risk in migrants. Detailed examination of the sociospatialdistribution of psychosis risk in three neighbouring, ethnicallydiverse and socially deprived inner-city boroughs of East Londondemonstrated that the incidence of non-affective psychoses was independently associated with increased deprivation, income inequality and population density. Ethnicseparation and ethnic density were associated with psychosis riskfor people of black Caribbean and black African origin. These data support the hypothesis that characteristicsthat define individuals as being different from most otherpeople in the local environment may increase psychosis risk. Theobservation that the increase in schizophrenia risk is higher in individualswith dark skin living in a white neighbourhood gives further support to the assumptionthat the feeling of being strange and different from others definesthe core of this form of social stress.

Also during adulthood, social stressors have been recognized asrisk factors for mental disorders. Longitudinal data indicate thatadverse life events are associated with a substantial increase ofpsychotic symptoms in the general population .Repeated exposure to these events seems to exert a cumulativeeffect, as psychosis risk increases with number of adverse lifeevents experienced. Stressful life events arealso associated with a fivefold increase of major depression, identifyingthis factor as one of the most important external causes ofthis affective disorder.

Tags: disorders, mental, mental disorders, social stress