Social stress is stress that stems from one's relationships with others and from the social environment in general. A person experiences stress when he or she does not have the ability or resources to cope when confronted with an external stimulus (stressor), or when they fear they do not have the ability or resources. An event which exceeds the ability to cope does not necessarily have to occur in order for one to experience stress, as the threat of such an event occurring can be sufficient. This can lead to emotional, behavioral, and physiological changes that can put one under greater risk for developing a mental disorder and physical illness.
Humans are social beings by nature, as they typically have a fundamental need and desire to maintain positive social relationships. Thus, they usually find maintaining positive social ties to be beneficial. Social relationships can offer nurturance, foster feelings of social inclusion, and lead to reproductive success. Anything that disrupts or threatens to disrupt their relationships with others can result in social stress. This can include low social status in society or in particular groups, giving a speech, interviewing with potential employers, caring for a child or spouse with a chronic illness, meeting new people at a party, the threat of or actual death of a loved one, divorce, and discrimination. Social stress can arise from one's micro-environment (e.g., family ties) and macro-environment (e.g., hierarchical societal structure). Social stress is typically the most frequent type of stressor that people experience in their daily lives and affects people more intensely than other types of stressors.
- 1 Measurement
- 2 Mental health
- 3 Physical health
- 4 Physiology
- 5 See also
- 6 References
Social stress is typically studied by asking people about their social experiences and relationships or by inducing social stress in the laboratory.
Questionnaires used to assess stressful social experiences include the Test of Negative Social Exchange, Marital Adjustment Test, and the Risky Families Questionnaire. More detailed information can be gathered by asking open-ended questions. For instance, the UCLA Life Stress Interview includes questions about romantic partners, closest friendships, other friendships, and family relationships.
In rodent models, social disruption and social defeat are two common social stress paradigms. In the social disruption paradigm, an aggressive rodent is introduced into a cage housing male rodents that have already naturally established a social hierarchy. The aggressive "intruder" disrupts the social hierarchy, causing the residents social stress. In the social defeat paradigm, an aggressive "intruder" and another non-aggressive male rodent fight.
In human research, the Trier Social Stress Task (TSST) and conflict discussions are common inductions of social stress. In the TSST, participants have to give an impromptu speech and then perform mental arithmetic as quickly and accurately as possible. Both tasks are completed in front of a judging panel that is trained to provide nonverbal negative feedback. The threat of negative evaluation is the social stressor. In a laboratory conflict discussion between two people, a topic of disagreement is determined and the participants are asked to discuss the topic for a predetermined amount of time.
Research has consistently demonstrated that social stress increases risk for developing negative mental health outcomes. One prospective study asked over fifteen hundred Finnish employees whether they had "considerable difficulties with [their] coworkers/superiors/inferiors during the last 6 months, 5 years, earlier, or never". Information on suicides, hospitalizations due to psychosis, suicidal behavior, alcohol intoxication, depressive symptoms, and medication for chronic psychiatric disorders was then gathered from the national registries of mortality and morbidity. Those who had experienced conflict in the workplace with coworkers or supervisors in the last five years were more likely to be diagnosed with a psychiatric condition.
Risk for developing clinical depression significantly increases after experiencing social stress; depressed individuals often experience interpersonal loss before becoming depressed. One study found that depressed individuals who had been rejected by others had developed depression about three times more quickly than those who had experienced stress not involving social rejection. In non-clinically depressed populations, people with friends and family who make too many demands, criticize, and create tension and conflict tend to have more depressive symptoms. Conflict between spouses also leads to more psychological distress and depressive symptoms, especially for wives. In particular, unhappy married couples are 10–25 times more at risk for developing clinical depression. Similarly, social stress arising from discrimination is related to greater depressive symptoms. In one study, African-Americans and non-Hispanic whites reported on their daily experiences of discrimination and depressive symptoms. Regardless of race, those who perceived more discrimination had higher depressive symptoms.
Social stress occurring early in life can have psychopathological effects that develop or persist in adulthood. One longitudinal study found that children were more likely to have a psychiatric disorder (e.g. anxiety, depressive, disruptive, personality, and substance use disorders) in late adolescence and early adulthood when their parents showed more maladaptive child-rearing behaviors (e.g., loud arguments between parents, verbal abuse, difficulty controlling anger toward the child, lack of parental support or availability, and harsh punishment). Child temperament and parental psychiatric disorders did not explain this association. Other studies have documented the robust relationships between children’s social stress within the family environment and depression, aggression, antisocial behavior, anxiety, suicide, and hostile, oppositional, and delinquent behavior.
Relapse and recurrence
Social stress can also exacerbate current psychopathological conditions and compromise recovery. For instance, patients recovering from depression or bipolar disorder are two times more likely to relapse if there is familial tension. People with eating disorders are also more likely to relapse if their family members make more critical comments, are more hostile, or are over-involved. Similarly, outpatients with schizophrenia or schizoaffective disorder show greater psychotic symptoms if the most influential person in their life is critical and are more likely to relapse if their familial relationships are marked by tension. In regard to substance abuse, cocaine-dependent individuals report greater cravings for cocaine following exposure to a social stressor.
Research has also repeatedly found a robust relationship between various social stressors and aspects of physical health.
Social status, a macro social stressor, is a robust predictor of death. In a study of over 1700 British civil servants, socioeconomic status (SES) was inversely related to mortality. Those with the lowest SES have worse health and greater mortality rats than those with the greatest SES. Other studies have replicated this relationship between SES and mortality in a range of diseases, including infectious, digestive, and respiratory diseases. Similarly, social stressors in the microenvironment are also linked to increased mortality. A seminal longitudinal study of nearly 7,000 people found that socially isolated people had greater risk of dying from any cause.
Social stress also makes people sicker. People who have fewer social contacts are at greater risk for developing illness, including cardiovascular disease. The lower one’s social status, the more likely he or she is to have a cardiovascular, gastrointestinal, musculoskeletal, neoplastic, pulmonary, renal, or other chronic diseases. These links are not explained by other, more traditional risk factors such as race, health behaviors, age, sex, or access to health care. In one laboratory study, researchers interviewed participants to determine whether they had been experiencing social conflicts with spouses, close family members and friends. They then exposed the participants to the common cold virus and found that participants with conflict-ridden relationships were two times more likely to develop a cold than those without such social stress.
Exposure to social stress in childhood can also have long-term effects, increasing risk for developing diseases later in life. In particular, adults who were maltreated (emotionally, physically, sexually abused or neglected) as children report more disease outcomes, such as stroke, heart attack, diabetes, and hypertension or greater severity of those outcomes. The Adverse Childhood Experiences study (ACE), which includes over seventeen thousand adults, also found that there was a 20% increase in likelihood for experiencing heart disease for each kind of chronic familial social stressor experienced in childhood, and this was not due to typical risk factors for heart disease such as demographics, smoking, exercise, adiposity, diabetes, or hypertension.
Social stress has also been tied to worse health outcomes among patients who already have a disease. Patients with end-stage renal disease faced a 46% increased risk for mortality when there was more relationship negativity with their spouse even when controlling for severity of disease and treatment. Similarly, women who had experienced an acute coronary event were three times more likely to experience another coronary event if they experienced moderate to severe marital strain. This finding remained even after controlling for demographics, health behaviors, and disease status.
Social stress leads to a number of physiological changes that mediate its relationship to physical health. In the short term, the physiological changes outlined below are adaptive, as they enable the stressed organism to cope better. However, dysregulation of these systems or repeated activation of them over the long-term can be detrimental to health.
Sympathetic nervous system
The sympathetic nervous system (SNS) becomes activated in response to stress. Sympathetic arousal stimulates the medulla of the medulla to secrete epinephrine and norepinephrine into the blood stream, which facilitates the fight-or-flight response. Blood pressure, heart rate, and sweating increase, veins constrict to allow the heart to beat with more force, arteries leading to muscles dilate, and blood flow to parts of the body not essential for the fight or flight response decreases. If stress persists in the long run, then blood pressure remains elevated, leading to hypertension and atherosclerosis, both precursors to cardiovascular disease.
A number of animal and human studies have confirmed that social stress increases risk for negative health outcomes by increasing SNS activity. Studies of rodents show that social stress causes hypertension and atherosclerosis. Studies of non-human primates also show that social stress clogs arteries.[clarification needed] Although humans cannot be randomized to receive social stress due to ethical concerns, studies have nevertheless shown that negative social interactions characterized by conflict lead to increases in blood pressure and heart rate. Social stress stemming from perceived daily discrimination is also associated with elevated levels of blood pressure during the day and a lack of blood pressure dipping at night.
Hypothalamic-pituitary adrenocortical axis (HPA)
In response to stress, the hypothalamus releases corticotropin-releasing hormone (CRH), stimulating the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal cortex to secrete glucocorticoids, including cortisol. It is thought that social stress can lead to adverse health outcomes by chronically activating the HPA axis or disrupting the HPA system. There are a number of studies that link social stress and indications of a disrupted HPA axis; for instance, monkey infants neglected by their mothers show prolonged cortisol responses following a challenging event. In humans, abused women exhibit a prolonged elevation in cortisol following a standardized psychosocial laboratory stressor compared to those without an abuse history. Maltreated children not only show higher morning cortisol values than non-maltreated children, but their HPA systems also fail to recover after a stressful social interaction with their caregiver. Over time, low-SES children show progressively greater output of cortisol. Although these studies point to a disrupted HPA system accounting for the link between social stress and physical health, they did not include disease outcomes. Nevertheless, a dysfunctional HPA response to stress is thought to increase risk for developing or exacerbating diseases such as diabetes, cancer, cardiovascular disease, and hypertension.
Inflammation is an immune response that is critical to fighting infections and repairing injured tissue. Although acute inflammation is adaptive, chronic inflammatory activity can contribute to adverse health outcomes, such as hypertension, atherosclerosis, coronary heart disease, depression, diabetes, and some cancers.
Research has elucidated a relationship between different social stressors and cytokines (the markers of inflammation). Chronic social stressors, such as caring for a spouse with dementia, lead to greater circulating levels of cytokine interleukin-6 (IL-6), whereas acute social stress tasks in the laboratory have been shown to elicit increases in proinflammatory cytokines. Similarly, when faced with another type of social stress, namely social evaluative threat, participants showed increases in IL-6 and a soluble receptor for tumor necrosis factor-α. Increases in inflammation may persist over time, as studies have shown that chronic relationship stress has been tied to greater IL-6 production 6 months later and children reared in a stressful family environment marked by neglect and conflict tend to show elevated levels of C-reactive protein, a marker of IL-6, in adulthood.
Interactions of physiological systems
There is extensive evidence that the above physiological systems affect one another's functioning. For instance, cortisol tends to have a suppressive effect on inflammatory processes, and proinflammatory cytokines can also activate the HPA system. Sympathetic activity can also upregulate inflammatory activity. Given the relationships among these physiological systems, social stress may also influence health indirectly via affecting a particular physiological system that in turn affects a different physiological system.
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