Transcript Early origins of health disparities: infectious burden and

Origins of the “flame within”:
Social and Physical Correlates of
Inflammation in U.S. Children.
Jennifer Beam Dowd, Hunter College,
CUNY Institute for Demographic Research (CIDR)
Anna Zajacova, Allison Aiello, Center for Social Epidemiology and
Population Health, University of Michigan
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Background and Motivation
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Disparities in health by SES in the U.S. begin in childhood (Case,
Lubotsky, Paxson 2002)
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Biological pathways linking SES to health, especially in children, are not
clear.
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Early environments can shape developing physiological systems (critical
and sensitive periods)
Background
Data/Methods Results
Conclusions
Inflammation:
S Integral part of the human stress and immune response
S Pro-inflammatory cytokines regulate the production of acute-phase
proteins such as C-reactive protein (CRP) which fight infection and
promote repair of damaged issues.
S Little is known about the predictors of low-grade inflammation in
children
Background
Data/Methods
Results
Conclusion
Contributors to inflammation
S Independent predictors of increased inflammation in adults:
S Higher BMI (inflammatory cytokines expressed in adipose
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tissue)
Smoking
Poor sleep quality/short sleep
Diet high in saturated and trans fat
Chronic Infections
Background
Data/Methods
Results
Conclusion
Health Consequences of Inflammation
S Elevated CRP is associated with risk of:
S myocardial infarction, stroke, atherosclerosis
S insulin resistance, Type II diabetes
S vascular dementia, Alzheimer’s disease.
S Life-long inflammatory burden may shape later life
patterns of aging and mortality. (Crimmins and Finch 2006).
Background
Data/Methods
Results
Conclusion
“Inflamm-aging”
S Chronic immune activation, including a persistent
inflammatory status, may drive what we considered
“age” related declines in functioning and immune
response–
S Thus large differences across groups
(race/ethnicity/SES) in burden of inflammation could
play a role in observed differences in aging rates and
longevity.
Background
Data/Methods
Results
Conclusion
SES differences in Infection Burden
in U.S. children:
Previous Work
S Lower SES associated with higher CRP in U.S. adults
S Mixed results for race/ethnicity-some studies show highest
levels for blacks, some for Hispanics
S European studies have not found social inequalities in CRP
in childhood, differences emerge later.
S To our knowledge, no existing studies looking at CRP
disparities in U.S. children
Background
Data/Methods
Results
Conclusion
Primary Research Questions
S Are physical (infections, BMI, etc) and social (family
income, race/ethnicity) risk factors associated with
inflammation in U.S. children?
S Do physical risk factors mediate the relationship between
social factors and levels of inflammation in U.S. children?
Background
Data/Methods
Results
Conclusion
Secondary Question
S Hygiene hypothesis: Mixed evidence on whether higher
infectious burden in childhood promotes better or worse
regulation of inflammation later in life—
S Are chronic infections related to inflammation in U.S.
children? Are proxy measures of pathogen exposure related
to inflammation in U.S. children?
Background
Data/Methods
Results
Conclusion
Data
S National Health and Nutrition Examination Survey
(NHANES), 1999-2004
S Cross-sectional, representative sample of non-
institutionalized U.S. population
S Face-to-face interview, medical exam, collection of blood
and urine
S Our sample consists of children aged 3-17, N= 6338
Background
Data/Methods
Results
Conclusion
Measures: Outcome
High Sensitivity C-reactive Protein (CRP) mg/L:
Distribution is right-skewed, transformed to Ln(CRP)
Background
Data/Methods
Results
Conclusion
Measures: Physical Predictors
S Infections: Positive Serostatus for
Cytomegalovirus (CMV)
Herpes Simplex Virus Type 1 (HSV-1)
Helicobacter Pylori (H Pylori)
Cryptosporidium
Toxoplasmosis
Hepatitis A Virus (HAV)
S Infectious Burden (Factor Score)
Background
Data/Methods
Results
Conclusion
Measures: Physical Predictors
S Body Mass Index (BMI) (kg/m2)
S Illness in the last 30 days (0/1)
S Low birth weight (0/1)
S Mother Smoked during pregnancy (0/1)
S Currently a smoker in the Household (0/1)
S Cotinine (log transformed)
S Triclosan (log transformed, N=557)
S White Blood Cell Count
S Vitamin D (log transformed)
Background
Data/Methods
Results
Conclusion
Measures: Social Predictors
Age (continuous)
Sex
Foreign Born (0/1)
Household size (continuous)
Race/ethnicity (White/Black/Mexican-American)
SES:
S Poverty-Income Ratio (Ratio of Family Income to Poverty
Line)
S Years of Education of the Household Reference Person
Background
Data/Methods
Results
Conclusion
Methods
S OLS Regressions:
Ln(CRP)= α + β1(Social) +β2(Physical) + ε
S Infection burden score created with M-Plus, confirmatory factor
analysis with full-information maximum likelihood estimation
S All analyses conducted with STATA 10.0 SVY commands to account
for complex survey design
Background
Data/Methods
Results
Conclusion
Descriptive
Statistics
Results
Results
Conclusions
S BMI and current/recent illness are strong predictors of CRP
in U.S. children
S Differences in CRP levels by income largely accounted for by
BMI and recent illness.
S Higher levels for Mexican-American race/ethnicity not
explained by physical vars.
Conclusions
S Hygiene Hypothesis: Still a mystery
S --Pro: increased HH size associated with lower CRP, Being
foreign-born associated with lower CRP
S --Cons: infection coefficients all reflect positive effects on
CRP, foreign-born effect explained by BMI, Triclosan
coefficient negative
Conclusions/Next Steps
S Higher BMI and potentially more frequent acute infections
contribute to greater levels of low-grade inflammation among
U.S. children with lower family income.
S What explains higher levels for Mexican-American children?
S Potential life-course health implications: aging, CVD,
cognition and learning?
Acknowledgements
S Thanks to collaborators Anna Zajacova and Allison Aiello,
Research assistance from Megan Todd
S Support from the NIH: 1R21NR011181-01