Social Impact of Stress
In general, social support functions as an important stress buffer. The more social support people have, the less stress will have an opportunity to affect them in a negative way.
Social support seems to affect our balance of hormones. Adequate amounts of social support are associated with increases in levels of a hormone called oxytocin, which functions to decrease anxiety levels and stimulate the parasympathetic nervous system calming down responses. Oxytocin also stimulates our desire to seek out social contact and increases our sense of attachment to people who are important to us. Stressed people who have adequate levels of social support receive an oxytocin boost which helps them feel less anxious, more confident in their ability to cope, and more drawn to other people (thus perpetuating the positive cycle of social support).
Oxytocin helps balance out other stress hormones such as vasopressin, which is associated with fight-or-flight behaviors such as enhanced arousal, focused attention, increased aggressive behavior, and a general increase in sympathetic nervous system functioning. People who are stressed and who withdraw from others (rather than seeking out support) become more exposed to hormones like vasopressin than to oxytocin, with predictable negative effects. They may end up having difficulty negotiating smooth interpersonal relationships with spouses, children, friends, and co-workers, and end up becoming more isolated, frustrated and stressed than when they started.
Many people experiencing negative stress simply do not have adequate forms of social support available. They may not have the assertiveness skills necessary to feel comfortable asking for help from others. They may feel depressed enough to start to withdraw from others (a normal symptom of depression), further decreasing the amount of social support available. This social support deficit is both a vulnerability factor for further stress problems, and also a self-fulfilling prophecy (where isolation begets further isolation). We talk more about how to cope with stress by building up levels of social support in a later section on Socialization.
Diathesis-Stress: Why Stress Makes Certain People Sick
The popular diathesis-stress model is a medical and psychological model that explains the cause of illnesses as an interaction between pre-existing vulnerabilities (such as genetic problems, and old traumas or infections), and stressful causal factors (such as new virus or bacteria infections, new traumas, or other stressful insults to the body). In this widely accepted way of thinking, our genetic and other pre-existing vulnerabilities or predispositions (e.g., our diatheses) interact with the environment and various stressors to trigger the onset of illnesses.
A diathesis is a weakness or predisposition; by itself it is not sufficient to cause an illness. Some additional stressor must be added to a diathesis before an illness occurs. All people who have a diathesis for a given illness will be more vulnerable to getting that illness (it will require less stress for them to get the illness) than will other people who do not have that diathesis. However, if a person who has a particular diathesis never experiences the necessary additional stress, that person will not get the illness. The model also predicts that people with smaller diatheses for a given problem will require much more stress to occur before they may experience that problem.
An intriguing and dramatic example of the diathesis-stress theory comes from a study of Jewish concentration camp survivors. Those people who went into the camps with genetic vulnerabilities (diatheses) for developing stress-related illnesses (such as having a family history of heart disease) were more much more likely to die of heart disease later on in life after experiencing the stress of being held in a concentration camp.
The diathesis-stress theory can also provide an explanation for why different people respond so differently to stressful situations. In most people, the HPA axis (previously described here) is designed to be responsive to threats, allowing the body to mobilize to face a threat and then later to relax when the threat has been resolved. Some people inherit differences in the genes that control the activation of the HPA axis. These small genetic differences create varying levels of stress sensitivity diatheses in any given population of people. Some may inherit the tendency (the diathesis) to have a weak responses to stressors (i.e., an under-responsive HPA axis, or decreased sensitivity to stress), while others inherit a hyper-responsive HPA response to even minor threats.
The ability of the HPA axis to respond appropriately to stress can also be permanently altered by stressors themselves. Exposure to extreme stress or trauma during any time of life (adulthood, adolescence, early childhood, or even in the womb) can cause the HPA loop to become hyper-responsive and hyper-sensitive to future stressors. This sensitization process, which is characteristic of Post Traumatic Stress Disorder, results in individuals who are extremely sensitive to perceived threats, and who have a difficult time not overreacting to minor threats that other people would not give much notice.