Explaining the link between poor growth, social deprivation and cardiovascular disease.
Lead Research Organisation:
Medical Research Council
Department Name: UNLISTED
Abstract
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Technical Summary
Background Controversy exists over the initiation and progression of cardiovascular disease (CVD) risk. This has been stimulated by three parallel lines of epidemiological investigation: tracking, programming, and environmental disadvantage at different ages. In this proposal, these three approaches are brought together in a lifecourse perspective to identify underlying mechanisms. Whilst it is well recognised that short height is associated with an increased risk of CVD, the relative contribution of these three pathways and the mechanisms involved remain unclear.
Hypothesis Poor growth in childhood alters arterial structure and function and specific growth limiting factors in childhood lead to a tracking of CVD risk throughout the life course. We also hypothesise that this excess risk acquired in early life is modified by adult socio-economic status and related health behaviour. We will use existing data from 3 prospective cohort studies to address complementary aspects of our underlying hypothesis.
Objectives We will bring together three key epidemiological approaches in order:
1. To identify growth-limiting factors in early life, that are associated with cardiovascular risk factors in middle age (blood pressure, HDL- and LDL-cholesterol, central and total obesity, glycosylated hemoglobin HbA1c).
2. To identify determinants of tracking of risk (hypertension and pulse pressure) over the life course.
3. To compare the influence of poor growth on measures of arterial structure (intima media thickness) and function (arterial distensibility and flow mediated dilatation).
4. To investigate whether the association between an early biological risk associated with poor growth and cardiovascular mortality is modified by adult socio-economic position.
Methods
1, 2 1946 Birth Cohort Study (MRC NSHD), which followed up 2547 women and 2815 men from birth until 53 years.
3 Subsample of the Whitehall II Study (168 men, 115 women, age 45-67 years), with measures of carotid artery intima media thickness and distensibility and brachial artery flow mediated dilatation.
4 Whitehall II Study 10,308 non-industrial civil servants recruited between 1985-1988 and Original Whitehall Study, which followed up 18001 men aged 45-69 years over 25 years for cardiovascular mortality.
Scientific opportunity The MRC and other funders have given program support to these UK cohorts; the collaborative analyses, proposed here for the first time, will enhance the scientific return for this investment. The 1946 birth cohort is the oldest ongoing birth cohort study internationally.
Public health importance This proposal will inform interventions for public health policy by identifying modifiable childhood factors, associated with poor growth, that lead to a tracking of cardiovascular risk over the lifecourse and premature mortality.
Hypothesis Poor growth in childhood alters arterial structure and function and specific growth limiting factors in childhood lead to a tracking of CVD risk throughout the life course. We also hypothesise that this excess risk acquired in early life is modified by adult socio-economic status and related health behaviour. We will use existing data from 3 prospective cohort studies to address complementary aspects of our underlying hypothesis.
Objectives We will bring together three key epidemiological approaches in order:
1. To identify growth-limiting factors in early life, that are associated with cardiovascular risk factors in middle age (blood pressure, HDL- and LDL-cholesterol, central and total obesity, glycosylated hemoglobin HbA1c).
2. To identify determinants of tracking of risk (hypertension and pulse pressure) over the life course.
3. To compare the influence of poor growth on measures of arterial structure (intima media thickness) and function (arterial distensibility and flow mediated dilatation).
4. To investigate whether the association between an early biological risk associated with poor growth and cardiovascular mortality is modified by adult socio-economic position.
Methods
1, 2 1946 Birth Cohort Study (MRC NSHD), which followed up 2547 women and 2815 men from birth until 53 years.
3 Subsample of the Whitehall II Study (168 men, 115 women, age 45-67 years), with measures of carotid artery intima media thickness and distensibility and brachial artery flow mediated dilatation.
4 Whitehall II Study 10,308 non-industrial civil servants recruited between 1985-1988 and Original Whitehall Study, which followed up 18001 men aged 45-69 years over 25 years for cardiovascular mortality.
Scientific opportunity The MRC and other funders have given program support to these UK cohorts; the collaborative analyses, proposed here for the first time, will enhance the scientific return for this investment. The 1946 birth cohort is the oldest ongoing birth cohort study internationally.
Public health importance This proposal will inform interventions for public health policy by identifying modifiable childhood factors, associated with poor growth, that lead to a tracking of cardiovascular risk over the lifecourse and premature mortality.
