Lactation and maternal measures of subclinical cardiovascular disease

Abstract

Objective: To examine the relationship between lactation and subclinical cardiovascular disease in a population free of clinical cardiovascular disease.

Methods: We conducted a cross-sectional analysis of 297 women who reported at least one live birth on enrollment in the Study of Women Across the Nation-Heart Study. Participants were mothers aged 45-58 years who were free of clinical cardiovascular disease. History of lactation was self-reported. Electron beam tomography was used to assess coronary and aortic calcification. B-mode ultrasonography was used to assess carotid adventitial diameter, intima-media thickness, and carotid plaque. Multivariable linear and logistic regression models were used to estimate whether lactation was independently associated with markers of subclinical cardiovascular disease.

Results: In unadjusted models, compared with mothers who had breastfed all of their children for at least 3 months, mothers who had not breastfed were more likely to have coronary artery calcification (17% compared with 32%), aortic calcification (17% compared with 39%), carotid plaque (10% compared with 18%), and larger carotid adventitial diameters (mean+/-standard deviation 6.63+/-0.59 compared with 6.87+/-0.60 mm). After adjusting for measures of socioeconomic status and lifestyle and family history variables, mothers who had not breastfed remained more likely to have aortic calcification (odds ratio [OR] 3.85, 95% confidence interval [CI] 1.47-10.00) and coronary artery calcification (OR 2.78, 95% CI 1.05-7.14) than mothers who had consistently breastfed. After further adjustment for body mass index and traditional risk factors for cardiovascular disease, mothers who had not breastfed remained more likely to have aortic calcification than mothers who had consistently breastfed (OR 5.26, 95% CI 1.47-20.00).

Conclusion: Mothers who do not breastfeed their infants seem to be at increased risk of vascular changes associated with future cardiovascular disease.

Level of evidence: II.