2b. Pathways to Population Health Inequities: Adverse Childhood Experiences and Psychosocial Stress  

Adverse Childhood Experiences: How an unhealthy beginning can determine future health outcomes

As your readings note, the lifecourse perspective, an increasingly studied approach to understanding population health inequities, is premised on research linking the health status of adults to adverse early life experiences. Specifically, exposure to unfavourable health and social conditions, including low socioeconomic status (SES), during fetal and early child development may trigger a process of “biological embedding” that “gets under the skin” of vulnerable populations, thereby contributing to a social gradient in health outcomes, both developmentally and throughout the lifespan.1-3

A growing body of evidence indicates that children raised in unfavourable circumstances have increased susceptibility to chronic diseases of aging, such as cardiovascular disease (CVD) and diabetes, upon reaching their fifth and sixth decades of life.4 The importance of early childhood development is reinforced by research findings that these inequities are generally independent of SES in adulthood. For example, the Precursors study tracking over 1131 Johns Hopkins medical graduates for over four decades found that, even among a highly educated, high SES cohort of physicians, low early life SES was linked to a 2.4-fold increased risk of coronary heart disease by age 50.5

Several decades of neurobiological research have pointed to how, when, and by what means adverse prenatal and early childhood experience influence key systems to produce inequities in health outcomes. Higher levels of cortisol, a steroid hormone released in response to stress, have been found among individuals with low early-life SES6–8, childhood adversity9, and mothers who suffered from depression10.  

 
Infant cortisol levels by SES and time of day showing a decline from 0.6 mg/dL in am to 0.3 mg/dL in pm
Figure 1. Infant Cortisol Levels: High vs Low SES (Clearfield et al, 2014)8
 

Heightened cortisol levels are one marker of increased allostatic load, the cumulative physiological “wear and tear” across multiple biological systems over time.11 A review of the evidence by Seeman et al (2010) found associations between low SES and a greater cumulative allostatic load throughout the lifecourse.12

Stress and Illness

Individuals suffering from inequitable access to the social determinants of health are also more vulnerable to high levels of physiological and psychological stress. Stressful experiences can result from coping with conditions of low income, poor quality housing, food insecurity, inadequate working conditions, insecure employment, and various forms of discrimination. A lack of supportive relationships, social isolation, and mistrust of others further increases stress.1

As is the case with adverse early life experiences, research implicates chronic adult stress in the causal pathways linking poor health outcomes to key biological triggers.13 For example, low SES has been associated with the release of cortisol, cytokines, and other substances that can compromise immune defenses, vital organs, and physiologic systems.12,13

At a psychological level, stressful and poor living conditions can cause feelings of shame, insecurity, and worthlessness. Uncertainty about the future raises anxiety, which, in turn, increases exhaustion and makes everyday coping more challenging. People who experience high levels of stress often attempt to relieve these pressures by adopting unhealthy coping behaviours, such as the excessive use of alcohol and recreational drugs, smoking, and overeating sugar, fat, and carbohydrates. While these behaviours are generally known to be health damaging, they are effective in bringing momentary relief from psychosocial stress. Damaging behaviours can be seen as coping mechanisms to adverse life circumstances even though they ultimately make the situation worse.1, 14

The following diagram illustrates how the living and working conditions we experience can shape our health. These processes operate through material, psychosocial, and behavioural pathways. During all stages of life, genetics, early life experiences, and cultural factors are also strong influences upon health.14 

 
Shows how the organization of society influences the living and working conditions we experience that then go on to shape health.
Figure 2. Social Determinants of Health and the Pathways to Health and Illness
 

References

  1. Mikkonen, J., & Raphael, D. (2010). Social determinants of health: The Canadian facts. Toronto: York University School of Health Policy and Management. Retrieved from: http://thecanadianfacts.org/the_canadian_facts.pdf 
  2. Hertzman, C., & Boyce, T. (2010). How experience gets under the skin to create gradients in developmental health. Annual Review of Public Health, 31, 329–347.
  3. Kim, P., Evans, G.W., Angstadt, M., Ho, S.S., Sripada, C.S., Swain, J.E., … & Phan, K.L.. (2013). Effects of childhood poverty and chronic stress on emotion regulatory brain function in adulthood. Proceedings of the National Academy of Sciences, 110(46), 18442–18447.
  4. Galobardes, B., Smith, G.D., & Lynch, J.W. (2006). Systematic review of the influence of childhood socioeconomic circumstances on risk for cardiovascular disease in adulthood. Annals of Epidemiology 16(2), 91–104.
  5. Kittleson, M.M., Meoni, L.A., Wang, N.Y., Chu, A.Y., Ford, D.E., & Klag, M.J. (2006). Association of childhood socioeconomic status with subsequent coronary heart disease in physicians. Archives of Internal Medicine, 166(21), 2356–2361.
  6. Lupien, S.J., King, S., Meaney, M.J., & McEwen, B.S. (2001). Can poverty get under your skin? Basal cortisol levels and cognitive function in children from low and high socioeconomic status. Development and psychopathology, 13(3), 653–676.
  7. Miller, G.E., Chen, E., Fok, A.K., Walker, H., Lim, A., Nicholls, E.F., ... & Kobor, M.S. (2009). Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling. Proceedings of the National Academy of Sciences, 106(34), 14716–14721.
  8. Clearfield, M.W., Carter-Rodriguez, A., Merali, A.R., & Shober, R. (2014). The effects of SES on infant and maternal diurnal salivary cortisol output. Infant Behavior and Development, 37(3), 298–304.
  9. Evans, G.W., & Kim, P. (2007). Childhood poverty and health: Cumulative risk exposure and stress dysregulation. Psychological Science, 18(11), 953–957.
  10. Essex, M.J., Klein, M.H., Cho, E., & Kalin, N. H. (2002). Maternal stress beginning in infancy may sensitize children to later stress exposure: Effects on cortisol and behavior. Biological psychiatry, 52(8), 776-784.
  11. McEwen, B.S., & Stellar, E. (1993). Stress and the individual: Mechanisms leading to disease. Archives of internal medicine, 153(18), 2093–2101.
  12. Seeman, T., Epel, E., Gruenewald, T., Karlamangla, A., & McEwen, B.S. (2010). Socio‐economic differentials in peripheral biology: Cumulative allostatic load. Annals of the New York Academy of Sciences, 1186, 223–239.
  13. McEwen, B.S., & Gianaros, P.J. (2010). Central role of the brain in stress and adaptation: links to socioeconomic status, health, and disease. Annals of the New York Academy of Sciences, 1186, 190–222.
  14. Brunner, E., & Marmot, M. (2006). Social organization, stress and health. In M. Marmot and R. Wilkinson (Eds.), Social Determinants of Health (2nd ed., pp. 6–130). New York: Oxford University Press.