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Fetal exposure, heredity and risk indicators for cardiovascular disease in a Swedish welfare cohort
I Mogren1, U Högberg, B Stegmayr
1Department of Clinical Science, Obstetrics and Gynecology, Umeå University, S-90185 Umeå, Sweden.
Insights
Low birthweight (LBW) is linked to higher blood pressure and cholesterol levels in middle age. However, heredity plays a more significant role in elevated systolic blood pressure (SBP) than LBW.
Area of Science:
- Cardiovascular Epidemiology
- Developmental Origins of Health and Disease (DOHaD)
Background:
- Investigating the association between low birthweight (LBW) and cardiovascular disease (CVD) risk factors in middle age within a welfare society.
- Examining potential interactions between LBW and genetic predisposition for myocardial infarction or stroke.
Purpose of the Study:
- To determine if LBW in newborns is associated with CVD risk indicators in early middle age.
- To explore the interplay between LBW and heredity on cardiovascular risk markers.
Main Methods:
- Longitudinal study identifying subjects from a birth register and the Västerbotten Intervention Program (n=7876).
- Assessed outcomes including systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), cholesterol, and triglycerides at ages 29-41.
- Analyzed outcomes in relation to birthweight status.
Main Results:
- LBW was associated with increased SBP and DBP.
- Elevated triglycerides were observed in women with LBW, and elevated total cholesterol in men with LBW.
- A synergistic effect between LBW and heredity was noted for SBP levels; BMI did not differ significantly.
Conclusions:
- The 'fetal origins' hypothesis is supported for middle-aged individuals in a welfare society.
- While LBW has associations, heredity is a more significant public health factor for elevated SBP.
- Population attributable risks from LBW exposure were relatively small.
Background:
The overall aim was to test whether low birthweight (LBW) in newborns is associated with the risk indicators for cardiovascular disease in early middle age, even in a welfare society. Further, a possible interaction of LBW and heredity for myocardial infarction or stroke was investigated.
Methods:
Overall, subjects were identified as newborns in a local birth register, and as adult participants, in the Västerbotten Intervention Program (n = 7876). Outcome measures such as systolic (SBP) and diastolic blood pressures (DBP), body mass index (BMI), cholesterol, triglycerides and anthropometrics were investigated (at age 29-41 years) in relation to LBW.
Results:
Low birthweight was associated with increased SBP and DBP. Triglycerides were elevated among women with LBW and total cholesterol was elevated in men with LBW. Heredity for myocardial infarction or stroke interacted with LBW, and indicated a synergistic effect on the level of SBP. The BMI did not differ between LBW and normal birthweight subjects.
Conclusions:
Our interpretation is that the 'fetal origins' hypothesis' is valid for middle-age subjects who grow up in a welfare society. The population attributable proportions that result from different exposures to LBW were relatively small overall; from a public health perspective, heredity was more important than LBW for elevated SBP.
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