Common Stressors
Stress, much like beauty, is in the eye of the beholder. What is stressful for one person may not be for another. However, there are some events and environments which typically cause stress:
- Changes to family: marriage, pregnancy, death, divorce, a new child
- Work environment: job change, job loss, promotion, work overload, conflict at work, business failure, employee strike
- Living environment: new house, relocation to a new community, loss of a home, neighborhood crime
- Physical environment or conditions: noise, pollution, traffic, violence, illness, disability, injury, pain, cold, heat, lack of sleep, hunger, malnutrition, natural disaster, unsafe surroundings, physical abuse or neglect
- Economic environment: poverty, escalating bills, unanticipated expenses, theft
- Social environment: isolation, family or peer demands, forced separation (such as from military service, prison, abandonment or conflict), grief, emotional abuse or neglect, legal entanglements, bullying, difficult roommates or neighbors
Lack of control or the inability to predict situations can add to the stress.
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Our psychosocial environment is the interaction of the various sources of stress in our lives and how we respond to them, both individually and as communities. On this page we describe the impacts of environmental stress on health.
Our "environment" includes both social determinants of health and physical environmental determinants of health. Social impacts on health are embedded in the broader environment in which we live.
Our psychosocial environment includes our responses to stressors in our lives, from temporary ones such as a traffic jam to major stressors such as war, homelessness or major disease. Our relationships with family members, friends, colleagues and other individuals and groups with whom we interact in our communities are an important part of this environment. These can impact our capacity to deal with stressors. Nurturing, supportive relationships allow us to better access all our innate resources to respond to stress in positive ways.
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image from bdinphoenix at Creative Commons
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Conversely, relationships that do not foster growth, learning, resilience and resolution of problems can themselves be a source of stress and can contribute to poor mental and physical health outcomes.
Stress and the Body's Response
Our bodies, families, communities and lives are embedded in a complex network of systems. The degree of support in the environment can shape a person’s resilience. Likewise, an environment that is stressful can foster disease. The conditions of a person’s social and psychological environment—those in which they are born, grow, live, work and age—are known as the social determinants of health. These conditions are shaped by the distribution of money, power and resources at global, national and local levels.
Risks for Stress: Riskscapes
A riskscape, or landscape of risks, captures the overlapping threats to health occurring in a physical location that increase risk for disease. An example of overlapping risks can be seen in impoverished neighborhoods, which often experience many of the stressors listed above simultaneously. We discuss poverty in more detail on our Socioeconomic Environment page.
Minority status, age and gender further interact to increase risk for disease. Individuals experience additional adversity when they live amid wealth and affluence but do not share those resources.
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To better understand how the psychosocial environment impacts health outcomes, one must understand how these conditions interact with the human stress response. The stress response within the psychosocial environment can trigger disease.
Stressful Environments and the Social Ecological Model of Health
The rise of chronic disease is a complex and growing problem for public health in the US. Stress, particularly exposure to long-term chronic stress, is associated with the majority of chronic health conditions.
Social Ecological Model of Health
The Social Ecological Model of Health Promotion (SEM) describes how our psychosocial experiences are nested inside layers that influence health and well-being:
- individual
- interpersonal (familial)
- communal (neighborhood)
- societal
The Human Stress Response System
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 a threat is perceived, the hypothalamus activates the sympathetic nervous system (the "fight or flight" response) by sending signals through the autonomic nerves to the adrenal glands. The adrenal glands pump the hormone epinephrine—also known as adrenaline—into the bloodstream, causing several physiological changes:
- The heart beats faster, pushing blood to the muscles, heart, and other vital organs.
- Pulse rate and blood pressure increase.
- Breathing becomes more rapid, and bronchi—airways in the lungs—open wide to take in more oxygen with each breath.
- Extra oxygen is sent to the brain, increasing alertness.
- Sight, hearing and other senses become sharper.
- Blood sugar (glucose) and fats are released from temporary storage sites in the body, flooding the bloodstream and supplying energy to all parts of the body.
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.
When the threat passes, the parasympathetic nervous system (the "rest and digest" function) calms the body and returns it to a pre-threat state.
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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. Layers are labeled with their corresponding social determinants of health.
graphic by Lorelei Walker; click to zoom
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) 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.
image from Wan Mohd at Creative Commons
Allostasis: The Body’s 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. See The Human Stress Response System at right for more detail.
In healthy doses and supportive environments, this response is tempered and can foster learning. In adversarial environments the allostatic response can manifest as chest pain, heart palpitations, headaches, dysphagia (difficulty swallowing), intestinal cramping, anxiety, panic, immobility, frustration, muscle tension and inflammation.
These reactions can be exhausting and imprint a strong memory of fear on the brain. Fortunately, a feedback system in the brain is capable of stopping the stress response. Terminating the stress response and restoring the body to pre-stress response states is important to protecting the body’s long-term health.
Programming the Stress Response
When early-life experiences signal that the environment is unpredictable, threatening or uncontrollable, the stress response system may be reprogrammed, becoming blunted, or may be programmed to be sensitized and thus more responsive.
Responsivity is informed by the number of steroid receptors available during stress termination. The feedback system in the brain—cells in the hippocampus—have glucocorticoid receptors that, once filled, signal the termination of the stress response. 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.
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How our bodies respond to stress varies across the population, determined by genetic predisposition and previous experiences including exposure to maternal stress signals before birth The typical responsivity can be modified by genetic predisposition but is generally neither amplified nor repressed. This neutral programming is optimal in moderately stressful environment where life is not overly threatening nor consistently safe. Over an individual’s life, neutral programming is optimal in balancing the risk for internal burnout from repetitive stress burden and survival in adverse environments long enough to maximize periods for mating and parenting.
Chronic Stress and Disease: Weathering
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. Chronic stress acts on the cardiovascular, metabolic, neuroendocrine and immune systems:
- Persistent epinephrine surges can damage blood vessels and arteries, increasing blood pressure and raising the risk of heart attacks or strokes.
- Elevated cortisol levels create physiological changes that help to replenish the body's stores of energy that are depleted during the stress response. Cortisol increases appetite and also increases storage of unused nutrients as fat, which can contribute to the accumulation of fat tissue and weight gain.
Over time, stress deteriorates health and resilience. This process is referred to as weathering. Just as a flag that weathers many storms begins to fray, so too does the body when it experiences harsh environments of social inequity. The health outcomes are mental illness, chronic disease morbidity and premature death. In short, stress causes physical changes that impact our health and functioning.
The frequency, duration, intensity, source, target and proximity of stressors influence the extent of the stress response. The duration of response can increase an individual’s risk for physical and mental burnout. Stressors that are higher intensity or longer duration carry a high internal burden (allostatic load). Over time this internal pressure forces body systems to adapt in ways that foster pre-disease states.
In weathering, each body system adapts to this internal pressure through secondary changes:
Dysregulation in these areas |
can cause these secondary changes. |
With chronic stress, such changes increase the risk for these conditions: |
- Cardiopulmonary system
- Metabolism
- Mental functioning
- Autoimmune response
- Aging
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- Increased startle response
- Anxiety and vigilance
- Change in body mass index and visceral fat
- Glucose sensitivity
- Immune suppression
- Changes in HDL cholesterol levels
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Stress-induced Gene Expression
Physiologic shifts following stressful exposures occur in large part through hormone-activated gene expression. When cortisol is released by the adrenal glands into the blood stream, it targets glucocorticoid responsive genes in tissues distributed throughout the body, including the central nervous system, metabolism, immune, cardiovascular, endocrine and renal systems.
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. This binding activates gene expression to shift the physiologic activity of the target cell. 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.
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Through this process, chronic stress responses cause weathering on the body, eroding health status. As years turn into decades, the physiologic changes (such as hypertension, metabolic disorder or anxiety) may become irreversible, often increasing co-morbidities, potentially increasing maladaptive coping mechanisms (such as social aversion, drug and alcohol dependence) and decreasing life expectancy.
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.
Disadvantaged Populations
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. These systems of inequity create differences in health outcomes, known as health disparities.
Stressful Environments and the Developing Child
Stress Effects on Brain Development
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.
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Our stress system responds to environmental conditions even before birth and is especially sensitive early in development. Glucocorticoid receptors are found in most fetal tissue and in the placenta, suggesting they are capable of responding to high maternal cortisol. Early-life experiences shape our stress response and therefore the impact stress has on our health over the life course.
A person’s individual responsiveness to stress signals can shape brain development. Highly responsive individuals demonstrate better learning and health outcomes in supportive environments and worse health outcomes in high adversity environments. Supportive environments foster better mental and social learning, increase memory and improve decision-making; in such environments, children have adequate time for stress response termination and are generally characterized by openness to information.
In negative environments, however, high responsivity magnifies the body’s response to intense or chronic stressors, increasing the risk for weathering over the life span. Highly responsive individuals can become hypersensitive to social feedback and psychological manipulation, both capable of detracting individuals from achieving goals. This increases the risk for future stressful experiences, further increasing the risk for weathering.
Stress responsivity shapes the intensity of weathering and has implications for later adult health outcomes. Responsivity biased toward either under- or over-reactivity can predispose children to adult disease. For example, overexposure to maternal stress hormones before birth can restrict birth weight and predispose the developing child to hypertension later in life. Effects of parental stress, such as reduced opportunities for bonding and distant parent-child relationships, significantly increase the risk up to fourfold for a child to experience anxiety, depression, diabetes and heart disease as an adult. Higher prenatal glucocorticoid exposure is directly associated with higher circulating glucocorticoids in adulthood, and both are associated with increased hypertension and hyperglycemia and changes in adult behaviors.
Investigating Brain Changes
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 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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Brain Changes
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. Because an individual suffering from these changes and conditions is handicapped in becoming a nurturing parent (although many people do overcome adversity and become terrific parents), the effects of stress can be self-perpetuating down generations. Through stress biasing, the social determinants can become multigenerational stimulants of chronic disease.
To the individual, there is a cost for high responsivity. Early life stressors that reshape the brain affect hippocampal and amygdala development that can affect a child’s transition into adolescence. Chronic early stress impacting social learning may predispose teens to depression and substance abuse, both feeding into adult chronic diseases. This is a vicious cycle of early childhood adversity. The stress that parents experience can have direct influences on a child’s biological capacity in responding to future stressful situations. The parent-child relationship, in utero and through development, provides experiential information that programs stress responsivity.
Telomere Changes
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. This biomarker may reflect population-level weathering in communities. 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
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.
Community resilience is difficult to define and measure; the US Department of Health & Human Services defines it as "the ability of a community to use its assets to strengthen public health and healthcare systems and to improve the community’s physical, behavioral, and social health to withstand, adapt to, and recover from adversity". A resilient community is one that is socially connected, takes collective action, and has access to necessary resources.
Substantial risks to community health and well-being lie within community adversities such as climate change, urbanization and disparities. 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:
- Increase access to social services, public health and healthcare
- Promote physical and psychological health
- Build networks of social services, behavioral health services, community organizations, businesses, educational services and faith-based institutions
- Support those at risk by connecting them with services
- Build social connectedness
Interactions between Chronic Psychosocial Stress and Environmental Toxicants
Research shows impacts of combined stress and toxicants:
- Animal models indicate that exposure to air pollution and stress in utero can harm cognitive abilities later in life more than either pollution or stress alone.
- Human evidence points to an association between maternal negative life events, exposure to allergens in mothers and children, and asthma.
- Financial stress after birth has been associated with more wheezing episodes in the first two years of life, a risk factor for asthma.
- Children who are exposed to stress in early development and exposed to air pollution may be at an increased risk for asthma compared to those who are exposed to just one or the other.
- Rodent models demonstrate that lead exposure before birth might affect the stress response system in a way that harms the body and may lead to greater impulsivity.
- Research in Southern California children found that living in a high-stress home is associated with more susceptibility to the negative effects of air pollution on the lungs.
- In a study of children from birth to age seven, children who experienced high levels of air pollution in utero had lower IQ scores than those not exposed, but only when their mothers experienced material hardship.
Selected Sources of Stress and Impacts on Health
Psychosocial risk factors for disease include family conflict, neighborhood violence, work stress and social discrimination; these factors can hinder mental and physical health.
Domestic and Intimate Partner Violence
Global Domestic and Intimate Partner Violence
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. Violence rates range from 71 percent of all women in Ethiopia to 15 percent of all women in Japan. Worldwide, up to 38 percent of all murders of women are committed by their partners.
Domestic and Intimate Partner Violence: United States
Domestic violence includes violence from spouses, partners, parents, children, siblings or relatives. Three-quarters of incidents occur against women. In fact, it is estimated that a US woman is assaulted or beaten every nine seconds.
Types of Domestic Violence.
- Rape
- Sexual assault
- Robbery
- Intimate partner assault
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Most violence occurs around the home (77 percent), and 19 percent of all violent incidents include the use of a weapon.
The National Crime Victimization Survey shows that between 2003 and 2012, domestic violence accounted for 21 percent of all violent victimizations in the US, with 70 percent of those from intimate partner violence (IPV).
data from Truman and Morgan
Preventing Violence in Relationships
Research in high-income areas indicates school-based programs can help prevent relationship violence among young people.
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Costs. Intimate partner violence accounted for $4 billion annually in 1995 in health care services and an additional $900 million in lost productivity. When these amounts are updated to 2003 figures, $8.3 billion in annual expenses are estimated, a combination of higher medical costs ($5.8 billion) and lost productivity ($2.5 billion).
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
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Health conditions |
Asthma
Infections
Circulatory conditions
Cardiovascular disease
Fibromyalgia
Irritable bowel syndrome
Chronic pain
Central nervous system disorders
Gastrointestinal disorders
Joint disease
Migraines
Headaches
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Reproductive conditions |
Gynecological disorders
Pelvic inflammatory disease
Sexual dysfunction
Sexually transmitted infections, including HIV/AIDS
Delayed prenatal care Preterm delivery
Low birth weight babies
Perinatal deaths
Unintended pregnancies
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Psychological conditions |
Anxiety
Depression
PTSD
Antisocial behavior
Suicidal behavior in females
Low self-esteem
Inability to trust
Fear of intimacy
Emotional detachment
Sleep disturbances
Flashbacks
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Social impacts |
Restricted access to services
Strained relationships with health providers and employers
Isolation from social networks
Homelessness
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Health behaviors |
High-risk sexual behaviors
Harmful substance abuse
Unhealthy diet-related behaviors
Overuse of health services
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Child Abuse and Neglect
The CDC provides some 2014 facts on child maltreatment (either abuse or neglect) in the US:
- 700,000 children experienced maltreatment, of which 27 percent were under the age of three
- Estimates exist that up to one in four children experience maltreatment in their lifetime
- 1580 children died from maltreatment
The CDC estimates total lifetime costs of child maltreatment at $124 billion annually.:
Youth Violence
Any violence—including being a victim, offender or witness—in early childhood extending into young adulthood is considered youth violence. The US CDC provides some important US statistics to consider:
- Youth violence is the third leading cause of death for those between the ages of 15 and 24.
- In 2012, an average of 13 people ages 10 to 24 were victims of homicide and 1642 more were treated in emergency departments each day.
- In 2013, 24 percent of high school-aged children were in a physical fight, 18 percent have taken a weapon to school, and up to 20 percent were bullied either at school or electronically.
- Youth homicides and violence-related injuries cost up to $16 billion annually in medical and lost time from work.
World Health Organization with CDC and other global partners created INSPIRE, a technical package of seven evidence-based strategies to end violence against children. Click to open the Inspire infographic from the WHO website.
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Risk factors for youth violence:
- A history of violence
- Substance abuse
- Delinquent behaviors
- Poor family functioning
- Poor grades in school
- Community poverty
Adverse Childhood Experiences
graphic from the CDC; click to zoom
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Adverse childhood experiences—ACEs—were first identified in the late 1990s. 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.
- About two out of every three people have experienced an adverse childhood experience
- About one in five have experienced three or more ACEs
- There is a dose response: having more ACEs increases the risk for poor health and behavior outcomes
Examples of Adverse Childhood Experiences
Abuse
- Emotional
- Physical
- Sexual
Household challenges
- Mother who was treated violently
- Household substance abuse
- Mental illness in the household
- Parental separation or divorce
- Criminal household member
Neglect
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Outcomes associated with adverse childhood experiences:
- Alcoholism / alcohol abuse
- Chronic obstructive pulmonary disease
- Depression
- Fetal death
- Illicit drug use
- Ischemic heart disease
- Liver disease
- Financial stress
- Risk for intimate partner violence
- Sexually transmitted diseases
- Suicide attempts
- Smoking
- Adolescent pregnancy
- Risk for sexual violence
- Poor academic achievement
Neighborhood Violence
Living in a neighborhood that experiences high levels of violence can have a devastating impact on people’s long-term mental and physical health. 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.
Memorial for a child; image from John Perivolaris at Creative Commons
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Exposure to neighborhood violence is especially harmful for children—it has been shown to impair children’s cognitive abilities and academic performance, and potentially contribute to inattentive and compulsive behaviors.
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 2015 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:
- In the US community unemployment rate, per capita income, poverty rate and educational status were associated with intimate partner violence.
- Internationally, though lacking representation from Europe or the Middle East, intimate partner violence was associated with community norms, community attitudes towards women, women’s literacy, education, and murder rates. Women’s empowerment is also shown to be protective against IPV.
- Households with higher proportions of children were also associated with an increased risk of IPV.
- Community characteristics such as lower collective efficacy, social cohesion, higher perceived neighborhood disorder, and general social disorganization are associated with an increase of IPV. Although crime and violence rates themselves have mixed results with association to IPV, higher levels of perceived violence and worry about violence are associated with IPV.
Discrimination
Racism, sexism, and other forms of discrimination exert a negative influence on mental health in a variety of ways. While experiencing discrimination within a person’s community is deeply stressful in and of itself, discrimination can also place certain groups at a higher risk of other adversities (poverty, segregation, unemployment, violence), which can also negatively impact health. Systemic 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.
Work Stress
Many factors in a person’s workplace can have a negative impact on their mental well-being. 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 2016 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).
Behavioral Responses to Stress
People create many mechanisms for coping with stress, or sometimes these mechanisms arise as a product of stressful experiences without deliberate decisions. 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 and Addiction
image from Cabrera Photo at Creative Commons
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Stress a powerful risk factor for both developing an addiction and relapsing back into addiction. Stress affects the reward pathways of the brain, those same pathways involved in stress, in ways that make people especially prone to become addicted to substances such as nicotine, alcohol and drugs.
Health-supporting Mechanisms
CDC offers healthy ways to cope with stress:
- Take a break, even a short one
- Breathe deeply
- Exercise
- Visualize
- Scan your body for tension
- Talk to someone
- Focus on the here and now
- Care for yourself with an adequate diet, amount of water and sleep
- Cut out the caffeine
- Face the problem
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What we know about stress and addiction:
- Those exposed to stress are more likely to use and abuse substances
- Experiencing chronic stress predicts continued drug use
- In research, stressed animals are more likely to self-administer drugs
- Stress increased cravings in abstaining cocaine users
- For smokers, those who received resources on managing stress were more likely to quit smoking
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. After the 9/11 terrorist event in the US, researchers noted a corresponding increase in the sales of various street drugs.
Those who drink alcohol report that doing so makes them feel relaxed and less stressed. However, using alcohol as a coping mechanism for stress, especially on a regular basis, increases alcohol's harm to the body.
Stress and Antisocial or Violent Behavior
Stressors early in life are heavily associated with aggressive tendencies later in adulthood. Universally, childhood maltreatment is a risk factor for conduct disorders, antisocial personality symptoms, and becoming a violent offender. Research has found that abused boys experiencing erratic, coercive and punitive parenting were most at risk of antisocial behaviors later in adulthood, with the earlier the experience the more likely the negative behaviors were. Early child abuse doubles the risk a person will engage in criminal activities later in life.
Environments That Break the Cycle of Violence
- Securing a stable environment
- Engaging in stable relationships
- Psychotherapy
- Promoting positive parenting
- Intervening with preschool for children demonstrating behavior problems
- Intervening with school-aged children who suffer from academic underachievement or absenteeism
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This "cycle of violence" describes the association between experiencing violence during childhood and the increased risk of either becoming violent or being a victim of violence. Although the majority of maltreated do not grow up to abuse others, we do know that one in six maltreated children becomes a violent offender and one in eight sexually abused boys becomes a sex offender. Victims of childhood abuse are at an increased risk of abusing their own children. Researchers also have found that up to one in seven children who experienced maltreatment in childhood also experienced abuse by their spouse. Violent experiences can be collective (gang membership), self-directed (harming oneself) or interpersonal (by a parent or other).
This page's content was created by Lorelei Walker, PhD, and , and last revised in September 2016.
CHE invites our partners to submit corrections and clarifications to this page. Please include links to research to support your submissions through the comment form on our Contact page.
* header image from Francisco Osorlo at Creative Commons
- Mayo Clinic. Stress management. Viewed September 21, 2016.
- Thompson RA. Stress and child development. Future Child. 2014 Spring;24(1):41-59.
- Social Determinants of Health.World Health Organization. Viewed September 21, 2016.
- Morello-Frosch R, Shenassa ED. The environmental 'riskscape' and social inequality: implications for explaining maternal and child health disparities. Environmental Health Perspectives. 2006 Aug;114(8):1150-3.
- Braveman PA, Egerter SA, Mockenhaupt RE. Broadening the focus: the need to address the social determinants of health. American Journal of Preventive Medicine. 2011:40(1);S4–S18.
- Mair CA, Cutchin MP, Peek KM. Allostatic load in an environmental riskscape: The role of stressors and gender. Health & Place. 2001:17:978–987.
- Ward C. Marxism and Native Americans. Boston: South End Press, 1982.
- American Diabetes Association. Statistics About Diabetes. 2015. Viewed September 21, 2016; Centers for Disease Control. Chronic Disease Prevention and Health Promotion. 2015. Viewed September 21, 2016; Kessler RC, Berglund P, Demler O et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General Psychiatry. 2005:62(6);593–602; National Institute of Mental Health. Total Expenditures for the Five Most Costly Medical Conditions (1996 vs. 2006). Viewed September 21, 2016; Surveillance, Epidemiology, and End Results Program. SEER Stat Fact Sheets: All Cancer Sites. National Cancer Institute. National Institutes of Health. 2012. Viewed September 21, 2016.
- Paradies Y. A review of psychosocial stress and chronic disease for 4th world indigenous peoples and African Americans. Ethnicity & Disease. 2006;16(1);295–308.
- Glanz K, Rimer BK, Viswanath K (Editors). Health Behavior: Theory, Research, and Practice, 5th Edition. 2015. San Francisco, CA: Jossey-Bass.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Hunter RG, McEwen BS. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenomics. 2013:5(2);177–194; Harvard Medical School. Understanding the stress response. March 18, 2016. Harvard University. Viewed September 24, 2016.
- Harvard Medical School. Understanding the stress response. March 18, 2016. Harvard University. Viewed September 24, 2016.
- Gehlert S, Sohmer D, Sacks et. al. Targeting health disparities: a model linking upstream determinants to downstream interventions. Health Affairs (Project Hope). 2008:27(2);339–349; McLaren, L. Ecological perspectives in health research. Journal of Epidemiology & Community Health. 2005:59(1);6–14.
- Braveman PA, Egerter SA, Mockenhaupt RE. Broadening the focus: the need to address the social determinants of health. American Journal of Preventive Medicine. 2011:40(1);S4–S18; Ta-Nehisi Coates. The case for reparations. The Atlantic. 2014. Viewed 2015.
- Mair CA, Cutchin MP, Kristen Peek M. Allostatic load in an environmental riskscape: the role of stressors and gender. Health & Place. 2011:17(4);978–987.
- Hunn V, Harley D, Elliott W et al. Microaggression and the mitigation of psychological harm: four social workers’ exposition for care of clients, students, and faculty who suffer “a thousand little cuts.” The Journal of Pan African Studies. 2015:7(9);41.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Aneshensel CS. Toward explaining mental health disparities. Journal of Health and Social Behavior. 2009:50(4);377–394; Aneshensel CS. Social stress: theory and research. Annual Review of Sociology. 1992:18;15–38; McEwen BS, Gianaros PJ. Stress- and allostasis-induced brain plasticity. Annual Review of Medicine. 2011:62(1);431–445; McEwen BS, Wingfield JC. What is in a name? Integrating homeostasis, allostasis and stress. Hormones and Behavior. 2010:57(2);105–111; Rice VH. (Editor). Handbook of Stress, Doping, and Health: Implications for Nursing Research, Theory, and Practice 2nd Edition. 2011. Thousand Oaks: SAGE Publications; Seeman TE, Singer BH, Rowe JW et al. Price of adaptation--allostatic load and its health consequences. MacArthur studies of successful aging. Archives of Internal Medicine. 1997:157(19);2259–2268.
- Lyon B. Stress, Coping, and Health. In Handbook of Stress, Coping, and Health. 2012 SAGE Publications; McEwen BS, Wingfield JC. The concept of allostasis in biology and biomedicine. Hormones and Behavior. 2003: 43(1);2–15; Acuna-Alonzo V, Flores-Dorantes T, Kruit JK et. al. A functional ABCA1 gene variant is associated with low HDL-cholesterol levels and shows evidence of positive selection in Native Americans. Human Molecular Genetics. 2010:19(14);2877–2885; Karatsoreos IN, McEwen BS. Psychobiological allostasis: resistance, resilience and vulnerability. Trends in Cognitive Sciences. 2011:15(12);576–584; Mair CA, Cutchin MP, Kristen Peek M. Allostatic load in an environmental riskscape: The role of stressors and gender. Health & Place. 2011:17(4);978–987; McEwen BS, Gianaros PJ. Stress- and allostasis-induced brain plasticity. Annual Review of Medicine. 2011:62(1);431–445; McEwen BS, Wingfield JC. What is in a name? Integrating homeostasis, allostasis and stress. Hormones and Behavior. 2010:57(2);105–111; Seeman TE, Singer BH, Rowe JW et al. Price of adaptation--allostatic load and its health consequences. MacArthur studies of successful aging. Archives of Internal Medicine. 1997:157(19);2259–2268.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Lyon B. Stress, Coping, and Health. In Handbook of Stress, Coping, and Health. 2012 SAGE Publications.
- Hughes, V. Stress: The roots of resilience. Nature. 2012:490(7419);165–167.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185(1–2);61–71.
- Charmandari E, Kino T, Souvatzoglou E et al. Pediatric stress: hormonal mediators and human development. Hormone Research. 2003:59(4);161–179.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Francis RC. Epigenetics: How Environment Shapes Our Genes. 2012. New York: W. W. Norton; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185:61–71.
- Francis RC. Epigenetics: How Environment Shapes Our Genes. 2012. New York: W. W. Norton; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185:61–71.
- Hunter RG, McEwen BS. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenomics. 2013:5(2);177–194; Zhang TY, Labonté B, Wen XL, et al. Epigenetic mechanisms for the early environmental regulation of hippocampal glucocorticoid receptor gene expression in rodents and humans. Neuropsychopharmacology. 2013:38;111–123.
- Mitchell C, Hobcraft J, McLanahan SS et al. Social disadvantage, genetic sensitivity, and children’s telomere length. Proceedings of the National Academy of Sciences. 2014:111(16);5944–5949.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Mitchell C, Hobcraft J, McLanahan SS et al. Social disadvantage, genetic sensitivity, and children’s telomere length. Proceedings of the National Academy of Sciences. 2014:111(16);5944–5949.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Glei DA, Goldman N, Chuang Y-L et al. Do chronic stressors lead to physiological dysregulation? Testing the theory of allostatic load. Psychosomatic Medicine. 2007:69(8);769–776; Juster RP McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neuroscience & Biobehavioral Reviews. 2010:35(1);2–16; McEwen BS, Stellar E. Stress and the individual. Mechanisms leading to disease. Archives of Internal Medicine. 1993:153(18);2093–2101; McEwen BS, Wingfield JC. What is in a name? Integrating homeostasis, allostasis and stress. Hormones and Behavior. 2010:57(2);105–111.
- Karatsoreos IN, McEwen BS. Psychobiological allostasis: resistance, resilience and vulnerability. Trends in Cognitive Sciences. 2011:15(12);576–584; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185(1–2);61–71; Harvard Medical School. Understanding the stress response. March 18, 2016. Harvard University. Viewed September 24, 2016.
- Geronimus AT. Understanding and eliminating racial inequalities in women’s health in the United States: the role of the weathering conceptual framework. Journal of the American Medical Women’s Association. 2001:56(4);133–136,149–150.
- Geronimus AT, Hicken M, Keene D et. al. “Weathering” and age patterns of allostatic load scores among Blacks and Whites in the United States. American Journal of Public Health. 2006:96(5);826–833.
- Paradies Y. A review of psychosocial stress and chronic disease for 4th world indigenous peoples and African Americans. Ethnicity & Disease. 2006;16(1);295–308.
- McEwen BS, Wingfield JC. The concept of allostasis in biology and biomedicine. Hormones and Behavior. 2003: 43(1);2–15; Seeman TE, Singer BH, Rowe JW et al. Price of adaptation--allostatic load and its health consequences. MacArthur studies of successful aging. Archives of Internal Medicine. 1997:157(19);2259–2268.
- Juster RP, McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neuroscience & Biobehavioral Reviews. 2010:35(1);2–16; Karatsoreos IN, McEwen BS. Psychobiological allostasis: resistance, resilience and vulnerability. Trends in Cognitive Sciences. 2011:15(12);576–584; Rice VH (Editor). Handbook of stress, coping, and health: implications for nursing research, theory, and practice (2nd ed). 2012. Thousand Oaks: SAGE Publications.
- Rice VH (Editor). Handbook of stress, coping, and health: implications for nursing research, theory, and practice (2nd ed). 2012. Thousand Oaks: SAGE Publications.
- Karatsoreos IN, McEwen BS. Psychobiological allostasis: resistance, resilience and vulnerability. Trends in Cognitive Sciences. 2011:15(12);576–584; McEwen BS, Gianaros PJ. Stress- and allostasis-induced brain plasticity. Annual Review of Medicine. 2011:62(1);431–445; Rice VH (Editor). Handbook of stress, coping, and health: implications for nursing research, theory, and practice (2nd ed). 2012. Thousand Oaks: SAGE Publications.
- Charmandari E, Kino T, Souvatzoglou E et al. Pediatric stress: hormonal mediators and human development. Hormone Research. 2003:59(4);161–179.
- Martinez-Arguelles DB, Papadopoulos V. Epigenetic regulation of the expression of genes involved in steroid hormone biosynthesis and action. Steroids. 2010:75;467–476; Zhang TY, Labonté B, Wen XL, et al. Epigenetic mechanisms for the early environmental regulation of hippocampal glucocorticoid receptor gene expression in rodents and humans. Neuropsychopharmacology. 2013:38;111–123; Beato M, Herrlich P, Schütz G. Steroid hormone receptors: many actors in search of a plot. Cell. 1995:83; 851–857.
- Martinez-Arguelles DB, Papadopoulos V. Epigenetic regulation of the expression of genes involved in steroid hormone biosynthesis and action. Steroids. 2010:75;467–476; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185:61–71.
- Beato M, Herrlich P, Schütz G. Steroid hormone receptors: many actors in search of a plot. Cell. 1995:83; 851–857; Tronche F et al. Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety. Nature Genetics. 1999 Sep;23(1):99-103.
- Martinez-Arguelles DB, Papadopoulos V. Epigenetic regulation of the expression of genes involved in steroid hormone biosynthesis and action. Steroids. 2010:75;467–476; Alheim K, Corness J, Samuelsson MK. Identification of a functional glucocorticoid response element in the promoter of the cyclin-dependent kinase inhibitor p57Kip2. Journal of Molecular Endocrinology. 2003:30;359–368.
- Juster RP McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neuroscience & Biobehavioral Reviews. 2010:35(1);2–16; Seeman TE, Singer BH, Rowe JW et al. Price of adaptation--allostatic load and its health consequences. MacArthur studies of successful aging. Archives of Internal Medicine.1997:157(19);2259–2268.
- Kopp MS, Réthelyi J. Where psychology meets physiology: chronic stress and premature mortality—the Central-Eastern European health paradox. Brain Research Bulletin. 2004:62(5);351–367; Paradies Y. Ethnicity & Disease. 2006;16(1);295–308.
- Felitti VJ, Anda RF, Nordenberg D et al. Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. American Journal of Preventive Medicine.1998:14(4);245–258.
- Aneshensel CS. Social stress: theory and research. Annual Review of Sociology. 1992:18;15–38; Geronimus AT. Understanding and eliminating racial inequalities in women’s health in the United States: the role of the weathering conceptual framework. Journal of the American Medical Women’s Association. 2001:56(4);133–136,149–150; Gielen AC, O’Campo PJ, Faden RR et al. Interpersonal conflict and physical violence during the childbearing year. Social Science & Medicine. 1994:39(6);781–787; Park H, Kim MT. Impact of social role strain, depression, social support and age on diabetes self-efficacy in Korean Women with type 2 diabetes. The Journal of Cardiovascular Nursing. 2012:27(1);76–83.
- Aneshensel CS. toward explaining mental health disparities. Journal of Health and Social Behavior. 2009:50(4);377–394; Braveman PA, Cubbin C, Egerter S et al. Socioeconomic disparities in health in the United States: what the patterns tell us. American Journal of Public Health. 2010:100(S1);S186–S196; Braveman PA, Egerter SA, Mockenhaupt RE. Broadening the focus: the need to address the social determinants of health. American Journal of Preventive Medicine. 2011:40(1);S4–S18.
- Link BG, Phelan JC. McKeown and the idea that social conditions are fundamental causes of disease. American Journal of Public Health. 2002:92(5);730–732; Marmot M. Social determinants of health inequalities. The Lancet. 2005:365(9464);1099–1104; Marmot, M. Achieving health equity: from root causes to fair outcomes. The Lancet. 2007:370(9593);1153–1163; Phelan JC, Link BG, Tehranifar P. Social conditions as fundamental causes of health inequalities: theory, evidence, and policy implications. Journal of Health and Social Behavior. 2010:51(1 Suppl);S28–S40.
- Kim P, Evans G, Angstadt M. Effects of childhood poverty and chronic stress on emotion regulatory brain function in adulthood. Proceedings of the National Academy of Sciences of the United States of America. 2013:110(46);18442-18447.
- Perera F, Herbstman J. Prenatal environmental exposures, epigenetics, and disease. Reproductive Toxicology. 2001:31(3);363–373.
- Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185(1–2);61–71.
- Meaney MJ. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Annual Review of Neuroscience. 2001:24;1161–1192.
- Ellis BJ, Boyce WT. Biological sensitivity to context. Current Directions in Psychological Science. 2008:17(3);183–187.
- Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592.
- Barnes SK, Ozanne SE. Pathways linking the early environment to long-term health and lifespan. Progress in Biophysics and Molecular Biology. 2011:106(1);323–336; Del Giudice M, Ellis BJ, Shirtcliff EA. The Adaptive Calibration Model of stress responsivity. Neuroscience & Biobehavioral Reviews. 2011:35(7);1562–1592; Hunter RG, McEwen BS. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenomics. 2013:5(2);177–194; Kim P, Evans G, Angstadt M. Effects of childhood poverty and chronic stress on emotion regulatory brain function in adulthood. Proceedings of the National Academy of Sciences of the United States of America. 2013:110(46);18442-18447.
- McLaughlin KA, Conron KJ, Koenen KC et al. Childhood adversity, adult stressful life events, and risk of past-year psychiatric disorder: a test of the stress sensitization hypothesis in a population-based sample of adults. Psychological Medicine. 2010:40(10);1647–1658.
- Barnes SK, Ozanne SE. Pathways linking the early environment to long-term health and lifespan. Progress in Biophysics and Molecular Biology. 2011:106(1);323–336; Brown R. The Intergenerational Impact of Terror: Does the 9/11 Tragedy Reverberate into the Outcomes of the Next Generation? April 2012. Duke University. Viewed September 28 2016; Seckl JR. Glucocorticoid programming of the fetus; adult phenotypes and molecular mechanisms. Molecular and Cellular Endocrinology. 2001:185(1–2);61–71.
- Meaney MJ. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Annual Review of Neuroscience. 2001:24;1161–1192; Zhang TY, Labonté B, Wen XL, et al. Epigenetic mechanisms for the early environmental regulation of hippocampal glucocorticoid receptor gene expression in rodents and humans. Neuropsychopharmacology. 2013:38;111–123.
- Papaioannou A, Dafni U, Alikaridis F et al. Effects of neonatal handling on basal and stress-induced monoamine levels in the male and female rat brain. Neuroscience. 2002:114(1);195–206.
- Pérez-Ortiz JM, García-Gutiérrez MS, Navarrete et al. Gene and protein alterations of FKBP5 and glucocorticoid receptor in the amygdala of suicide victims. Psychoneuroendocrinology. 2013:38(8);1251–1258.
- Labonté B, Suderman M, Maussion G et al. Genome-wide methylation changes in the brains of suicide completers. American Journal of Psychiatry. 2013:170(5);511–520; Schneider E, El Hajj N, Müller F et al. Epigenetic dysregulation in the prefrontal cortex of suicide completers. Cytogenetic and Genome Research. 2015.
- Perera F, Herbstman J. Prenatal environmental exposures, epigenetics, and disease. Reproductive Toxicology. 2001:31(3);363–373.
- Hunter RG, McEwen BS. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenomics. 2013:5(2);177–194.
- Francis RC. Epigenetics: How Environment Shapes Our Genes. 2012. New York: W. W. Norton; Meaney MJ. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Annual Review of Neuroscience. 2001:24;1161–1192.
- Hunter RG, McEwen BS. Stress and anxiety across the lifespan: structural plasticity and epigenetic regulation. Epigenomics. 2013:5(2);177–194;
- Zhang TY, Labonté B, Wen XL, et al. Epigenetic mechanisms for the early environmental regulation of hippocampal glucocorticoid receptor gene expression in rodents and humans. Neuropsychopharmacology. 2013:38;111–123;
- Meštrović T. Telomere function. News Medical Life Sciences. November 19, 2015. Viewed September 28 2016.
- Epel ES, Blackburn EH, Lin J et al. Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences. 2004:101(49);17312–17315.
- Mitchell C, Hobcraft J, McLanahan SS et al. Social disadvantage, genetic sensitivity, and children’s telomere length. Proceedings of the National Academy of Sciences. 2014:111(16);5944–5949.
- Luby J, Belden A, Botteron K et al. The effects of poverty on childhood brain development: the mediating effect of caregiving and stressful life events. JAMA Pediatrics. 2013:167(12);1135–1142.
- Public Health Emergency: Community Resilience. US Department of Health & Human Services. June 9, 2015. Viewed September 21, 2016.
- Public Health Emergency: Community Resilience. US Department of Health & Human Services. June 9, 2015. Viewed September 21, 2016.
- Proceedings of the EPA workshop on interactions between social stress and environmental hazards. Environmental Protection Agency. May 14-15, 2012. Prepared by Industrial Economics, Incorporated.
- Islam T, Urman R, Gauderman WJ et al. Parental stress increases the detrimental effects of traffic exposure on children’s lung function. American Journal of Respiratory and Critical Care Medicine. 2011:184;822-827.
- Vishnevetssky J, Tang, D., Chang, H et al. Combined effects of prenatal polycyclic aromatic hydrocarbons and material hardship on child IQ. Neurotoxicology and Teratology. 2015:49;74-80.
- World Health Organization. Risks to mental health: an overview of vulnerabilities and risk factors. 2012. Viewed August 25 2016.
- Violence against women. World Health Organization. 2016. Viewed September 21, 2016.
- Truman JL, Morgan RE. Nonfatal domestic violence, 2003-2012. US Department of Justice. April 2014. NCJ 244697.
- Domestic Violence National Statistics. National Coalition Against Domestic Violence. 2015. Viewed September 21, 2016.
- Truman JL, Morgan RE. Nonfatal domestic violence, 2003-2012. US Department of Justice. April 2014. NCJ 244697.
- Truman JL, Morgan RE. Nonfatal domestic violence, 2003-2012. US Department of Justice. April 2014. NCJ 244697.
- Domestic Violence National Statistics. National Coalition Against Domestic Violence. 2015. Viewed September 21, 2016.
- Truman JL, Morgan RE. Nonfatal domestic violence, 2003-2012. US Department of Justice. April 2014. NCJ 244697.
- Truman JL, Morgan RE. Nonfatal domestic violence, 2003-2012. US Department of Justice. April 2014. NCJ 244697.
- Violence against women. World Health Organization. 2016. Viewed September 2016.
- National Center for Injury Prevention and Control. Costs of Intimate Partner Violence against Women in the United States. Atlanta (GA): Centers for Disease Control and Prevention; 2003. Viewed September 21, 2016.
- Centers for Disease Control and Prevention. Intimate Partner Violence: Consequences. March 3, 2015. Viewed September 21, 2016.
- Injury Prevention & Control: Division of Violence Prevention. Child Abuse and Neglect Prevention. May 25, 2016. Viewed September 26, 2016.
- Injury Prevention & Control: Division of Violence Prevention. Child Abuse and Neglect Prevention. May 25, 2016. Viewed September 26, 2016.
- Injury Prevention & Control: Division of Violence Prevention. Youth Violence. Centers for Disease Control and Prevention. May 24, 2016. Viewed September 26, 2016.
- Injury Prevention & Control: Division of Violence Prevention. Youth Violence. Centers for Disease Control and Prevention. May 24, 2016. Viewed September 26, 2016.
- Injury Prevention & Control: Division of Violence Prevention. About the CDC-Kaiser ACE Study. Centers for Disease Control and Prevention. June 14, 2016. Viewed September 27, 2016.
- Injury Prevention & Control: Division of Violence Prevention. About the CDC-Kaiser ACE Study. Centers for Disease Control and Prevention. June 14, 2016. Viewed September 27, 2016.
- Ross T et al. Creating Safe and Healthy Living Environments for Low-Income Families. Center for American Progress. July 2016. Viewed August 25, 2016.
- Ross T et al. Creating Safe and Healthy Living Environments for Low-Income Families. Center for American Progress. July 2016. Viewed August 25, 2016.
- Beyer K, Wallis AB, Hamberger LK. Neighborhood environment and intimate partner violence: a systematic review. Trauma, Violence, & Abuse. 2015:16(1); 16-47.
- Beyer K, Wallis AB, Hamberger LK. Neighborhood environment and intimate partner violence: a systematic review. Trauma, Violence, & Abuse. 2015:16(1); 16-47.
- Mays VM et al. Race, race-based discrimination, and health outcomes among African Americans. Annual Review of Psychology. 2007;58:201-225; World Health Organization. Risks to mental health: an overview of vulnerabilities and risk factors. 2012. Viewed August 25 2016.
- The Workplace and Health. NPR, Robert Wood Johnson Foundation, Harvard T.H. Chan School of Public Health. July 2016. Viewed July 28, 2016.
- National Institute on Drug Abuse. Stress and Substance Abuse: A Special Report After the 9/11 Terrorist Attacks. National Institutes of Health. Viewed September 28, 2016.
- Sinha R, Jastreboff A. Stress as a common risk factor for obesity and addiction. Biology of Psychiatry. 2013:79(9);827-835.
- Tips from former smokers. Stress and Smoking. Centers for Disease Control and Prevention. 2015. Viewed September 28, 2016.
- National Institute on Drug Abuse. Stress and Substance Abuse: A Special Report After the 9/11 Terrorist Attacks. National Institutes of Health. Viewed September 28, 2016.
- National Institute on Drug Abuse. Stress and Substance Abuse: A Special Report After the 9/11 Terrorist Attacks. National Institutes of Health. Viewed September 28, 2016.
- Conway CC, Keenan-Miller D, Hammen C, et al. Coaction of stress and serotonin transporter genotype in predicting aggression in the transition to adulthood. Journal of Clinical and Child Adolescent Psychology. 2012:41(1);53-63.
- Caspi A, McClay J, Moffitt TE, et al. Role of genotype in the cycle of violence in maltreated children. Science. 2002:297;851-854.
- Violence and Injury Prevention Programme. The Cycles of Violence. World Health Organization. 2007. Viewed September 28, 2016
- Violence and Injury Prevention Programme. The Cycles of Violence. World Health Organization. 2007. Viewed September 28, 2016.
- Violence and Injury Prevention Programme. The Cycles of Violence. World Health Organization. 2007. Viewed September 28, 2016.
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