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Dutch women with a low birth weight have an increased risk of myocardial infarction later in life
– Reported, February 04, 2012
Nationwide population-based case-control study. Patients and controls: 152 patients with a first myocardial infarction before the age of 50 years in the Netherlands. 568 control women who had not had a myocardial infarction stratified for age, calendar year of the index event, and area of residence.
Birth weight in the patient group was significantly lower than in control women (3214 vs. 3370 gram, mean difference -156.3 gram (95%CI -9.5 to -303.1). The odds ratio for myocardial infarction, associated with a birth weight lower than 3000 gram (20th percentile in controls) compared to higher than 3000 gram was 1.7 (95%CI 1.1ñ2.7), while the odds ratio for myocardial infarction for children with a low birth weight (< 2000 g) compared to a birth weight = 2000 g was 2.4 (95%CI 1.0 ñ 5.8). Both figures did not change after adjustment for putative confounders (age, education level, body mass index, waist-hip ratio, hypertension, diabetes, hypercholesterolemia, smoking, and family history of cardiovascular disease).
Low birth weight is associated with an increased risk of myocardial infarction before age of 50 in Dutch women.
Intrauterine malnutrition, as reflected by birth weight and abnormal thinness at birth, has been associated with an increased incidence of risk factors for arterial disease, i.e. hypertension, impaired glucose tolerance, diabetes and to a lesser extent hyperlipidemia and body fat distribution in adulthood. This observation has become known as the ‘fetal origins of adult disease’ or ‘Barker hypothesis’, which suggests that several of the major diseases of later life, including coronary heart disease, stroke and cardiovascular death, originate in impaired intrauterine growth and development . In cohort studies, Barker in England and Finland, Rich-Edwards et al. as part of the Nurses’ Health Study in the USA and Leon et al. from Uppsala in Sweden showed an inverse relationship between birth weight and the clinical endpoint ischemic heart disease. Leon et al. found a significant relationship only among male singletons and adjusted their results for gestational age and socioeconomic confounding. The association was not found in a cohort study from Gothenburg.
The characteristics of 152 women with myocardial infarction and 568 control women at the index date.At the moment of completing the questionnaire, patients were aged 32ñ59 years (mean 50), and control women 25ñ60 years (mean 47). The mean body mass index was 25.1 kg/m2 for the patients and 23.4 kg/m2 for control women, mean difference 1.76 kg/m2 (95%CI 1.05ñ2.47), p < 0.001. Ninety-seven patients (64%) and 415 (73%) controls could give their birth weight. Compared with control women, patients had a significantly lower mean birth weight (3214 vs. 3370 g, mean difference -156.3 g (95%CI -9.5 to -303.1). The odds ratio for myocardial infarction for children with a low birth weight (< 2000 g) compared to a birth weight = 2000 g was 2.4 (95%CI 1.0 to 5.8). After adjustment for putative confounders (age, education level, body mass index, waist-hip ratio, hypertension, diabetes, hypercholesterolemia, smoking, and family history of cardiovascular disease) the odds ratio did not change. Odds ratios for myocardial infarction in different categories of birth weight as compared to the reference category (birth weight higher than 3884 g) were 1.3 (95%CI 0.5ñ3.3) for a birth weight 3500 to 3883 g, 1.4 (95%CI 0.6ñ3.4) for a birth weight 3200 to 3499 g, 1.7 (95%CI 0.6ñ5.1) for a birth weight 3000 to 3199 g, and 2.3 (95%CI 1.0ñ5.4) for a birth weight lower than 3000 g (Table 2). The risk of myocardial infarction was 6.2 fold increased (95%CI 2.7ñ13.9) among women with low birth weight and a low educational level compared to women with a high birth weight and a high educational level (reference category).
In this case control study we have found that women with a low birth weight had a higher risk of myocardial infarction than women with a higher birth weight. The data confirm the association found in cohort studies and as such support the ‘fetal origins of adult disease’ or ‘Barker hypothesis’.
A limitation of the study is that we have no information on gestational age. However, recently it has been demonstrated that both children who had been born prematurely and children who are small for gestational age had a reduction in insulin resistance. The self-report of birth weights as well as the rather high percentage of missing values for birth weight may also limit the study, but the random events among cases and controls cannot explain our results. Socio-economic factors associated with low birth weight are also associated to risk factors for arterial disease later in life. As pointed out by several others, it will be nearly impossible to disentangle these effects .
In the present study we confirmed an interactive effect between low birth weight and a low educational level on the risk of myocardial infarction in women. However, when we adjusted for age, education level, body mass index, waist-hip ratio, hypertension, diabetes, hypercholesterolemia, smoking, and family history of cardiovascular disease, factors of which some may partly been seen as (the result of) socio-economic/environmental and genetic factors, we still observed an association between low birth weight and a higher risk of myocardial infarction. This is in agreement with others who also found that genetic and socio-economic circumstances at birth and in adult life can not completely explain the association between low birth weight and disease late in life.
Study shows that a low birth weight (<2000 g) is associated with a 2.4 fold higher risk of myocardial infarction before the age of 50 as compared with a birth weight = 2000 g. Because the risk of cardiovascular disease is known to increase with an increasing number of risk factors, women with a low birth weight should try to avoid acquired risk factors, like smoking and obesity. In addition, extra attention should be given in detecting diabetes or hypertension at a later stage in life and in detecting exaggerated growth during childhood, as these individuals seem most prone to develop disease later on in life.
Credits: Bea C Tanis, Kitty Kapiteijn, Ronella M Hage, Frits R Rosendaal,and Frans M Helmerhorst
More information at: http://www.reproductive-health-journal.com/content/2/1/1
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