Transcript Slide 1

Audra D. Robertson, MD, MPH
Brigham and Women’s Hospital
Harvard Medical School
April 8, 2010
Babies born to Black women
in the US, Texas, and Tarrant County are
more than twice as likely to die in the
first year of life compared to babies born
to White women.
In Boston, three times as likely.
Infant mortality is a significant indicator
of a community’s health and
social welfare
1. Defining the disparity

Review national, state, local data to identify the disparity
2. Understanding the cause of the disparity


Preterm Birth
Risk versus Care
3. Addressing the disparity


Understanding the life course approach
Stress and preterm birth
▪

Barker Hypothesis, Allostatic Load, Weathering
Implementing a Life Course Approach
4. Discussion

Infant death:
Death of an infant in the 1st year of life

Infant mortality rate:
Number of infant deaths per 1,000 live
births.

Term birth:
Birth from 37 to 41 completed weeks of
gestation.

Preterm birth:
Birth before 37 weeks

Very preterm birth:
Birth before 32 weeks

Late preterm birth:
Birth from 34 to 36 weeks
DHHS NCHS National Vital Statistics Reports, 2002
Singapore
Sweden
Hong Kong
Japan
Finland
Norway
Czech Republic
Portugal
France
Belgium
Greece
Germany
Ireland
Spain
Switzerland
Austria
Denmark
Israel
Italy
Netherlands
England
Australia
New Zealand
Scotland
Canada
Hungary
Cuba
N. Ireland
Poland
United States
Slovakia
IMR: Deaths per 1,000 live births
2.1
2.4
2.4
2.8
3
3.1
3.4
3.5
3.6
3.7
3.8
3.9
4
4.1
4.2
4.2
4.4
4.6
4.7
4.9
5
5
5.1
5.2
5.4
6.2
6.2
6.3
6.4
6.9
7.2
0
United States, Table 1: Health 2008
1
2
3
4
5
6
7
8
16
Black
White
14
12
10
2.4x
3.7x
2.3x
2.3x
8
HP 2010
6
4.5
4
2
0
US (1)
1National Center for
Boston (2)
TX (3)
Health Statistics, 2007
Public Health, 2008
3Texas Dept of State Health Services and Tarrant County Public Health, 2009
2Massachusetts Dept of
Tarrant
County (3)
A Case of Infant Mortality

A healthy 34 year-old African American woman presented
to a teaching hospital with bleeding and abdominal pain
at 27 weeks gestation

Despite current medical intervention, she delivered a
ounce boy prematurely

He lived 24 days

The mother has yet to recover emotionally from this loss
All Races………………………………….…….
White ..……………………………………..…..
Black …………………………………………….
Native American ……………………………
Asian …………………………………………….
Hispanic …………………………………………
Mexican …..…………………………………
Puerto Rican …………………………….…
Cuban ………………………………………..
Central and South American ………….
2
National Center for Health Statistics, 2010
1995
2005
7.6
6.3
14.6
9.0
5.3
6.3
6.0
8.9
5.3
5.5
6.9
5.7
13.6
8.1
4.9
5.6
5.5
8.3
4.4
4.7
Hispanic groups have lower socioeconomic status,
but better than expected health and mortality
outcomes
 Explanation (unknown)

 Healthy migrant effect
 Return migration effect
 Social capital, resiliency
Reasons for this paradox are likely to be
multifactorial and social in origin
 Outcomes worsen after acculturation

1. Defining the disparity

Review national, state, local data to identify the disparity
2. Understanding the cause of the disparity


Preterm Birth
Risk versus Care
3. Addressing the disparity


Understanding the life course approach
Stress and preterm birth
▪

Barker Hypothesis, Allostatic Load, Weathering
Implementing a Life Course Approach
4. Discussion
Infant Death
(Death in 1st year of life)
Neonatal
Postnatal
(<28 days of life)
(28 days – 11 months)
Birth defect
Birth defect
Premature birth
Sudden Infant
Death (SIDS)
46%
CDC/NCHS National Vital Statistics System, 2008
The Cost of Preterm Births

Estimated total annual health care charges for
babies born in the US:
Estimated $52 Billion (for 4.3 million live births)

Total cost for babies born premature
$26 Billion (for 546,000 preterm births)

Average health care cost for a baby born healthy
$4,551

Average health care cost for a baby born premature
$49,000
Source: March of Dimes 2009, AHRQ Healthcare Costs and Utilization 2007, and Institute of Medicine 2006
Gene
Poverty
Risk
Environment
Education
Stress
Premature Birth
& Low Birth
NeuroEndocrine
Immune/
Inflammatory
Generational
Effect
Weight
Differences in access
to care
Care
Differences in care
received
Bias

Collins and David NEJM 1997
 Examined LBW of African-born blacks living in U.S.,
U.S. born African Americans, and U.S. born whites.
 LBW among African-born blacks closer to U.S. born
whites, but by 2nd generation black to white gap
started to emerge.
Collins and David NEJM 1997
Gene
Poverty
Risk
Environment
Education
Stress
Premature Birth
& Low Birth
NeuroEndocrine
Immune/
Inflammatory
Generational
Effect
Weight
Differences in access
to care
Care
Differences in care
received
Bias
Gene
Poverty
Risk
Environment
Education
Stress
Premature Birth
& Low Birth
NeuroEndocrine
Immune/
Inflammatory
Generational
Effect
Weight
Differences in access
to care
Care
Differences in care
received
Bias

Collins et al. 1997
 Women with 16 years or more Education
 Small-for-Dates Rate
▪ African-Americans
▪ Whites
▪ Odds Ratio
2.8%
1.2%
2.9 (CI 1.4-4.5)
3
2.5
2
1.5
1
0.5
0
<High High School Some
School
College
Education
Adapted from D. Williams
College
grad. +
B/W Ratio
Deaths per 1,000 population
20
18
16
14
12
10
8
6
4
2
0
White
Black
B/W Ratio
Gene
Poverty
Risk
Environment
Education
Stress
Premature Birth
& Low Birth
NeuroEndocrine
Immune/
Inflammatory
Generational
Effect
Weight
Differences in access
to care
Care
Differences in care
received
Bias
Gene
Poverty
Risk
Environment
Education
Stress
Premature Birth
& Low Birth
NeuroEndocrine
Immune/
Inflammatory
Generational
Effect
Weight
Differences in access
to care
Care
Differences in care
received
Bias
1. Defining the disparity

Review national, state, local data to identify the disparity
2. Understanding the cause of the disparity

Preterm Birth
Risk versus Care

3. Addressing the disparity

Understanding the life course approach
Stress and preterm birth

▪

Barker Hypothesis, Allostatic Load, Weathering
Implementing a Life Course Approach
4. Discussion

Health is shaped by the biological, behavioral/social
and psychosocial pathways operating throughout
life, as well as across generations

Study of independent, cumulative and interactive
effects of biological, social and psychological risk
factors/exposures during gestation, childhood,
adolescence, young adulthood and later adult life on
women's health and birth outcomes
Kuh D and Hardy R. A Life Course Approach to Women’s Health. 2002
Understanding the exposure–outcome
associations across an individual lifespan
accounting for:



critical or sensitive period of exposure
exposure trajectory
intensity of exposure over time (accumulation)
Kuh D and Hardy R. A Life Course Approach to Women’s Health. 2002
•View life, not in stages, but as integrated continuum
•Begin to understand critical/sensitive periods of risk as well as cumulative effects
Embryo
Child
Adolescence
e.g. Mental Health
e.g. Environmental Pollution
i.e. Barker Hypothesis
Young Adult /
Adult
Pre-conception
Prenatal
Inter-conception


Reproductive capacity begins with menarche
and ends with menopause
Yet, reproductive health begins in utero and is
influenced by:
 Life circumstances such as neighborhood
environment, relationship interactions and social
support structures
 An individual's stress coping skills and disposition
Mishra G, Cooper R, and Kuh D. Maturitas 65;2:2010 (92-97)

A large body of evidence supports maternal
psychosocial stress as an independent and
significant risk factor for preterm birth1

Evidence supports a correlation between maternal
psychological stress and the placental–adrenal
endocrine axis 2

Research implicates CRH as a contributor to the
initiation of labor in term and preterm birth3
1 Hedegaard, 1993; Hobel, 2003; Ruiz, 2003; Zambrana, 1999
2 Lockwood, 1999; Wadhwa et al, 2001
3 Holzman, 2001; McGrath, 2002; Moawad, 2002

The fetal origins of adult disease

Biologic Programming
Exposures during critical periods of growth and
development in utero may “program” the structure or
function of organs, tissues, or body systems

Previous Theory
 adult lifestyle model
 social causation
Barker DJP. Fetal and infant origins of adult disease. London: British Medical Publishing Group, 1992.
Physiologic Response
Physiologic Response
Stress
Recovery
No Recovery
Time
“Stressed”
 Increased cardiac output
“Stressed Out”
 Hypertension, CV disease, MI
 Increased available glucose
 Obesity, glucose intolerance & insulin
 Enhanced immune function
 Growth of neurons
Adapted from M. Lu and B McEwen
resistance
 Infection & inflammation
 Atrophy & death of neurons

Homeostasis: remaining stable by constancy

Allostasis: fluctuation of the physiologic systems
within the body to meet demands from external
forces, causes activation of neural, neuroendocrine
and neuroendocrine-immune mechanisms

Allostatic Load: the physiologic “cost” of an
individuals reaction to repeated challenge (thus
chronic exposure to fluctuating or heightened
neural or neuroendocrine responses)
McEwen BS. Ann N Y Acad Sci. 1998

An individual may age prematurely because of
exposure to chronic stress early in life

Stress Age versus Chronologic Age

Geronimus and Weathering
 associated with adverse pregnancy outcomes and
hypertension among black and poor women

McEwen and Allostatic load
 the cumulative wear and tear that the body experiences as
a result of daily life
Geronimus AT.Ethn Dis 1992 and McEwen Metabolism 2003





The Barker Hypothesis of the fetal origins of adult disease
The HPA axis remains plastic throughout life and is molded
and remodeled by environmental exposures
Animal studies support that chronic stress can program the
fetal brain’s reaction to novel stressors
Stress exposure up-regulates gene expression of CRH which
may create exaggerated physiologic responses to stressors
Thus, programming future stress responses
Rosen JB et al. Behav Neurosci 1996.
White
Age 0
Reproductive Potential
African
American
Risk Factors
Protective Factors
African
American
Perinatal
Childhood
Adolescence
Life Course
Adapted from Lu and Halfon. Matern Child Health J. 2003;7:13-30.
Young Adult/ Adult
Adapted from McGinnis et al., Health Affairs 2002
• Address the root cases
• Chronic Maternal Stress
• Preterm birth and low birth weight birth
• Address social determinant of health
• Incorporate a life course approach to scientific
investigation, program integration, and policy development
Embryo
Child
Adolescence
Young Adult /
Adult
Atwood K et el. Am J of Pub Health 1997. 87(10):1603-6 .
Richmond and Kotelchuck. from Oxford Textbook of Public Health. 1991
Knowledge Base
Prevention
Priorities

Reduce the number of high-risk pregnancies
 Preconception Health
 Optimal Social Determinants of Health
 Optimal Reproductive Life Plan

Reduce LBW and preterm birth
 Health promotion
 Optimal PNC (e.g. progesterone for previous PTB, group prenatal care)

Improve birthweight specific survival
 Access to quality OB care and high volume NICU -> Regionalized care

Reduce death from sudden infant death syndrome
 Support services, parent education, and health promotion
1. Provide inter-conception care to women with prior adverse pregnancy
outcomes
2. Increase access to preconception care for African American women
3. Improve the quality of prenatal care
4. Expand healthcare access over the life course
5. Strengthen father involvement in African American families
6. Enhance service coordination and systems integration
7. Create reproductive social capital in African American communities
8. Invest in community building and urban renewal
9. Close the education gap
10. Reduce poverty among Black families
11. Support working mothers and families
12. Undo racism
Lu MC, Kotelchuck M, Hogan V, Jones L, Jones C, Halfon N. Closing the Black-White gap in birth outcomes:
A life-course approach. Ethnicity and Disease. 2008
Audra D. Robertson, MD, MPH
Brigham and Women’s Hospital
Harvard Medical School
April 8, 2010