This response system is evolutionarily old and has been shaped by the environmental experiences of thousands of preceding generations. Through millennia of adverse environmental challenges, adaptations and collective evolution, humans have developed a sophisticated stress response system. The physical stress response is a complex network of coordinated physical and behavioral activations from the endocrine and nervous systems: When the initial surge of epinephrine subsides, the hypothalamus activates the Hypothalamic-pituitary-adrenal HPA axis , signaling the release of cortisol to keep the sympathetic nervous system engaged.
The SEM is particularly useful in allowing researchers to study stressors from the micro scale cellular to the macro scale social policy , positioning their work in the larger social ecological context. Policies that affect economic and social determinants top level can decrease access to income and education, and have powerful effects on neighborhood stressors. These policies shape disparities in local environments second level 16 such as poverty, pollution, crime rates and political power.
Daily opportunities third level create or suppress nurturing environments and govern the frequency and intensity of daily hassles discrimination and microaggressions. These layers affect our daily behaviors and patterns fourth level and daily interactions. As these pressures funnel down from the political to the community to the individual, they become observational cues fifth level that the environment is threatening, unpredictable or uncontrollable and thus stressful. Upon activation, the brain sends signals to the body to mount a stress response.
When the brain interprets a threat, it sends a cascading signal through the body that causes a stress response, known casually as "fight or flight" and more formally as an allostatic response. In healthy doses and supportive environments, this response is tempered and can foster learning. These reactions can be exhausting and imprint a strong memory of fear on the brain.
When early-life experiences signal that the environment is unpredictable, threatening or uncontrollable, the stress response system may be reprogrammed, becoming blunted, 26 or may be programmed to be sensitized and thus more responsive. Responsivity is informed by the number of steroid receptors available during stress termination. When there are fewer glucocorticoid receptors in these cells, it takes a higher circulating quantity of cortisol to terminate the stress response. The number of receptors available in the feedback system is dependent on how many proteins are produced in that cell.
This is determined by the availability of the receptor gene to be transcribed into proteins. Stress signals, such as cortisol, circulating in maternal blood during pregnancy, can epigenetically alter the glucocorticoid receptor gene to be permanently downregulated, causing fewer receptor proteins to be produced. How our bodies respond to stress varies across the population, 29 determined by genetic predisposition 30 and previous experiences including exposure to maternal stress signals before birth 31 The typical responsivity can be modified by genetic predisposition 32 but is generally neither amplified nor repressed.
With repeated exposure to stressors, the HPA axis activation is sustained, and stress signals continue to flood the body. This sustained activation delays the onset of restorative repair and pushes the body into pre-disease states.
Over time, stress deteriorates health and resilience. This process is referred to as weathering. The frequency, duration, intensity, source, target and proximity of stressors influence the extent of the stress response.
US life expectancy is below naive expectations mostly because it economically outperforms
Stressors that are higher intensity or longer duration carry a high internal burden allostatic load. In weathering, each body system adapts to this internal pressure through secondary changes: Physiologic shifts following stressful exposures occur in large part through hormone-activated gene expression. Within each cell nucleus, the steroid hormone binds with its receptor, and this complex binds to a stretch of DNA called a hormone response element. In this way, stressful experiences, mediated through the allostatic response, have an epigenetic effect on the body. See our Gene-Environment Interaction page for further explanation.
Through this process, chronic stress responses cause weathering on the body, eroding health status.
Through these mechanisms social structures can get under the skin, alter our bodies and cause disease. The loss of productivity and financial burden of systemic disease further erodes family and community resilience, especially when the chronic stress starts in childhood. Lower social classes experience longer durations of chronic stress, such as lengthy unemployment or institutionalized discrimination.
Those with less power experience barriers to achievement of life goals, such as high costs of educational programs or lack of childcare options, inadequate recognition and rewards for personal qualification such as gender pay differences or for invested effort in the workplace. In the US and other White-majority countries, minorities and women in these environments are exposed to more chronic stressors than their White male counterparts due to differential expectations resulting in role strain and interpersonal conflict.
Both the sources and frequency of stressors are not distributed equally in society, with heavier burdens borne by those with less advantage. A longitudinal study followed 49 children until the age of 24, finding that those in stressful environments resulting from the inequities of poverty experienced changes in brain morphology that impaired cognitive, emotional and learning skills.
The high-stress environments had layering psychosocial child-family separation, violence and family structure unpredictability and physical characteristics noise, crowding and housing quality. These exposures increased amygdala function, which enhances fear, anxiety, and emotional dysfunction, while it decreased prefrontal cortex function, which participates in regulating and terminating the stress response.
Our stress system responds to environmental conditions even before birth 56 and is especially sensitive early in development. Early-life experiences shape our stress response and therefore the impact stress has on our health over the life course. Highly responsive individuals can become hypersensitive to social feedback and psychological manipulation, both capable of detracting individuals from achieving goals.
Stress responsivity shapes the intensity of weathering and has implications for later adult health outcomes. We rely heavily on animal models to understand early-life stress programming because sampling a core of living human brain is not an option. However, we do have direct human associations: the brains of suicide completers show epigenetic changes in the glucocorticoid receptor gene 66 as well as methylation changes in other important genes that inform the intensity of the stress response. Newborns of mothers with depressive symptoms during pregnancy also demonstrated increased methylation of the GR gene in umbilical cord blood cells.
As three-month-old infants, these children had higher levels of salivary cortisol.
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With exposure to chronic stress, the brain changes shape, reducing connections that support nuanced cognitive function, self-regulation and memory; this process is less reversible as a child ages. Through these changes, chronic stress increases the likelihood of aggression, vigilance and anxiety. Through stress biasing, the social determinants can become multigenerational stimulants of chronic disease.
To the individual, there is a cost for high responsivity.
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Chronic early stress impacting social learning may predispose teens to depression and substance abuse, both feeding into adult chronic diseases. Telomeres are structures on the ends of chromosomes that protect and stabilize chromosomes. They are essential for avoiding cellular dysfunction. Telomere length is reduced with age, smoking and stress, and shorter telomeres can impair health.
Telomere length in specific blood cells is viewed as a biomarker for cellular aging that is closely associated with age-related and chronic diseases. For example, a study of nine-year-old boys found that adverse environments shaped by low income, low maternal education, unstable family structure and harsh parenting were associated with a 19 percent shortening of white blood cell telomeres as compared to a cohort in more nurturing environments.
These boys physically aged faster than their chronical age would suggest. Children with the most sensitivity highest responsivity to stress showed the longest telomeres in advantaged environments and the shortest in disadvantaged environments. Resilience, the capacity to recover quickly from difficulties, is a characteristic of both individuals and communities. Parental bonding is a resilience factor, protecting children from the adverse effects of poverty on emotional and cognitive development.
In the context of a natural or manmade disaster, increasing community resilience includes better preparedness and disaster planning, promoting community systems, and reducing threats to health. These are some steps communities and public health can take to build resilience: Research shows impacts of combined stress and toxicants: Psychosocial risk factors for disease include family conflict, neighborhood violence, work stress and social discrimination; these factors can hinder mental and physical health.
Globally, most data available is on intimate partner violence and sexual assault against women. An estimated 35 percent of women worldwide have experienced intimate partner violence over their lifetimes. Worldwide, up to 38 percent of all murders of women are committed by their partners. Domestic violence includes violence from spouses, partners, parents, children, siblings or relatives.
Three-quarters of incidents occur against women. Types of Domestic Violence. Most violence occurs around the home 77 percent , 87 and 19 percent of all violent incidents include the use of a weapon. The National Crime Victimization Survey shows that between and , domestic violence accounted for 21 percent of all violent victimizations in the US, with 70 percent of those from intimate partner violence IPV. Research in high-income areas indicates school-based programs can help prevent relationship violence among young people.
Health outcomes of intimate partner violence. In addition to death and injury bruising, flesh wounds, fractures, brain injury and headaches , the cardiovascular, gastrointestinal, immune, and endocrine systems are impacted from violence-induced stress, as discussed above. Health Consequences of Intimate Partner Violence Cardiovascular disease. Central nervous system disorders.
Any violence—including being a victim, offender or witness—in early childhood extending into young adulthood is considered youth violence. Click to open the Inspire infographic from the WHO website. Risk factors for youth violence: Adverse childhood experiences—ACEs—were first identified in the late s. The risk for violence, victimization, and disease outcomes are heavily impacted by early childhood experiences.
As shown at right, adverse childhood experiences can set children on an arduous path that increases risk for poor health behaviors, disease, disability, social problems and early death outcomes. People who live in neighborhoods with high rates of violence suffer from trauma-related illnesses such as post-traumatic stress disorder PTSD , at higher rates.
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Other health outcomes are associated with negative characteristics of residential settings including fewer cancer screenings, cardiovascular disease , and the outcomes of violence discussed above. The risk or resilience of a community can directly affect the prevalence of child maltreatment.
A review of national and international studies in urban areas found these associations. More research is needed in rural areas to understand if these factors are generalizable: Racism, sexism, and other forms of discrimination exert a negative influence on mental health in a variety of ways. Systematic racism, for example, raises exposure of communities of color to social exclusion and economic adversity, thereby placing them at a higher risk of stress, anxiety and chronic disease.
Factors such as poor work satisfaction, high demand, low job security, harassment and work disorganization can all cause people to feel substantially stressed while on the job. A investigation found 43 percent of working adults said their job negatively affects their stress levels. Others said their job negatively affects their eating habits 28 percent , sleeping habits 27 percent and weight 22 percent.
These mechanisms can be health-supportive, such as mindfulness, meditation, hobbies and the like. Other mechanisms can be health-destructive, such as smoking, alcohol abuse, substance abuse or even violence. Negative coping mechanism can deteriorate health in a way that causes further stress, thus becoming a destructive cycle. For many people with negative coping mechanisms, addressing the underlying stress may be necessary to overcome the negative health behaviors. Stress a powerful risk factor for both developing an addiction and relapsing back into addiction.
CDC offers healthy ways to cope with stress: What we know about stress and addiction: One reason stress is a such a risk factor for substance abuse is that substance abuse can temporarily reduce anxiety caused by stressful events. As stress levels become chronic, the body responds with dysregulated hormonal states and stress-related behaviors that can produce anxiety. This predisposes an individual to seek substances that temporarily alleviate this stress-induced physical state.