SES and health across the life course

Summary prepared by Karen Matthews. Last revised April, 2005.

a) What is the evidence?
b) Where are the holes?
c) Why are these questions important?
d) Citations

The association of SES and health begins at birth and extends through the life span but the strength and nature of the relationship varies at different stages of the life course.   The Network hypothesizes that the effects of child and adult SES are not redundant but rather may have cumulative effects, underscoring the value of examining trajectories of SES along with trajectories of risk. 

What is the evidence?

An enormous literature dating from the middle ages documents that SES has a profound influence on the health of adults.  Individuals lower in SES experience higher levels of morbidity and mortality in almost every disease category than individuals higher in SES.  Although the focus of fewer investigations, children and adolescents lower in SES also experience higher rates of all-cause mortality and poor subjective health.   These patterns occur whether SES is measured by education, occupation, or income.  Lower SES children and adolescents are more functionally impaired and have more school absences, more chronic conditions, such as severe asthma, vision and hearing disorders, higher blood levels, higher rates of injury, and lower birth weight (except Hispanics) than their high SES counterparts.   SES also affects children’s and adolescent’s health behaviors, such as cigarette smoking and inactivity, and access to and use of formal health care, such as prenatal care in the first trimester.  There are exceptions to the pattern, however.  Allergies, prevalence of asthma, myopia, Hodgkin’s disease and acute lymphoblastic leukemia are higher among higher SES children in some studies.

The strength and nature of the relationship may vary at different stages of the life course.  With regard to childhood, it is plausible that the associations between SES and health vary in early childhood vs adolescence because of the dramatic developmental changes that occur.   Indeed, it appears that rates of injury and high blood pressure are more strongly associated with SES in childhood than in adolescence, severe asthma is related to SES in both periods, and smoking and physical inactivity are more strongly related with SES in adolescence.  Different mechanisms correlated with SES may aid understanding why these associations are apparent.  Mechanisms related to family relationships, housing characteristics, and childcare practices that are associated with SES may be important to understanding stronger associations with SES in childhood, whereas mechanisms related to peer relationships, neighborhood characteristics, and health habits may be important to understanding stronger associations with SES in adolescence.

With regard to the influence of SES according to stages of the life course extending into adulthood, a number of different perspectives have been offered.    One is that child and adult SES are somewhat redundant and do not have unique predictive value.  Underlying this perspective is that high SES in childhood predicts the ability to attain economic and educational advantages in adulthood, which, in turn, confer better health and longevity.  While clearly there are strong associations between child and adult SES, they are not completely overlapping.   A second perspective in the extreme is that childhood SES is the critical period for many outcomes and that adult SES is redundant.   This perspective is supported by analyses showing that early childhood SES continues to exert an impact on health in adulthood, even when adult SES is taken into account.  It should be noted that there are few formal tests of adulthood SES and adult health, adjusting for childhood SES.  A recent review of the effects of childhood SES on adult mortality shows that the effects of childhood SES are stronger for some causes of mortality, i.e. stomach cancer and hemorrhagic stroke.   Another perspective is an accumulation model, which argues that the longer the exposure to lower SES the greater the resultant health disadvantage.  Note that this is not a critical period hypothesis—just an additive hypothesis.  Most tests of this model are based on repeated measures of adulthood SES and show that the more often individuals are in lower SES categories the worse the physical and psychological functioning.   The adult mortality literature suggests the risk for coronary heart disease and obstructive pulmonary disease is associated with both low SES during early and adult life.   Finally, a bidirectional model emphasizes the reciprocal relationship between economic and health advantages across the life span.   For example, data from large survey studies of children show that household income is related to children’s subjective health and becomes more pronounced with age.  A substantial component of the increasing age-related relationship between income and subjective health can be explained by the arrival and impact of chronic health problems in childhood, especially on the ability to obtain adequate education.  

Where are the holes? 

We have just begun to understand the impact of the life course on associations between SES and health.   Most of the work on the life course perspective has been conducted in samples of European origin and outside the United States.  The associations between SES and health across the life span in diverse ethnic groups are unknown, although some data suggest that African Americans have flatter gradients than do whites for some outcomes, e.g. obesity.  Longitudinal studies examining the impact of the life course on multiple health outcomes and testing possible mechanisms have been few in number.  Analyses typically have not pitted various models against one another.  While it is clear that childhood SES has effects on some outcomes independent of adult SES, the reverse is not well studied.  The effects of childhood and adult SES on plausible mechanisms are not studied with few exceptions.  Finally, the challenge of the work is increased by the fact that the adverse circumstances experienced by low SES in childhood may be very different in one generation vs. another and therefore will not have similar health effects.  For example, childhood adversity during World War II may be associated with different adult health consequences than adversity experienced by the current generation of children exposed to low SES environments.

Why are these questions important?

Addressing these issues is not simply academic.  It is important to understand the life course in order to identify the optimal times for intervention, and the most likely processes for social/behavioral change.  If the association between SES and health becomes stronger with age, the question arises if it is ever too late for interventions.  Furthermore, if some groups seem to be immune to the effects of low SES, there may be protective factors that can also be encouraged in more vulnerable groups.  Addressing these questions has important policy implications.  Child poverty has increased markedly since the 1960s in the United States and United Kingdom such that 15-20% of children now live in poverty.  Tax and transfer policies have had little effect on these rates, whereas in Sweden the market-generated child poverty of 24% is reduced to below 3% by tax and transfer policies.  If early life SES environments have a lasting impact on adult health, the ever escalating costs of health care could be impacted by health policy change that reduces the proportions of children raised in poverty. 

Citations:

Case A, Lubotsky D, Paxson C.  Economic status and health in childhood: The origins of the gradient.  Is Economic Rev 2002, 92: 1308-1334.

Chen E, Matthews KA, Boyce WT.  Socioeconomic differences in children’s health: How and why do these relationships change with age?  Psych Bull 2002,128: 295-329.

Gallopades B, Lynch JW, Dave Smith G.  Childhood socioeconomic circumstances and cause-specific mortality in adulthood: Systematic review and interpretation.  Epid Reviews 2004, 26: 7-21.

Kuh D, Ben-Shlomo Y.  A life course approach to chronic disease epidemiology.  Oxford University Press:New York, 1997.

Power C, Hertzman C  Social and biological pathways linking early life and adult disease.  Br Med Mull 1997, 53:210-221.

West P.  Health inequalities in the early years: Is there equalization in youth?  Soc Sci Med 1997, 44: 833-858.