Pregnancy induces significant metabolic changes. The concentrations of lipids, lipoproteins and apolipoproteins in the plasma increase appreciably during pregnancy. The lipid levels are affected by maternal hormonal changes (rise in insulin, progesterone, 17-β estradiol and Human Placental Lactogen). Other maternal factors such as BMI (body mass index), maternal weight gain, maternal nutrition, pre-pregnancy lipid levels and various medical complications of pregnancy may also have significant effects on lipid metabolism and plasma levels [10].
Until the CARDIA study by Gunderson et al [11, 12] evidence regarding the association between parity and the risk of cardiovascular disease in women has been conflicting. That prospective study, among 1952 American women, examined lipid changes over a 10 year period, and adjusted the results to allow for various confounding factors. For both white and non-white populations a decline of 3 to 4 mg/dL in HDL-C was seen during the first pregnancy compared with nulliparous women. Higher order births were not associated with a greater decline in HDL cholesterol.
We assessed the influence of consecutive pregnancies on lipid changes. In our study population the total cholesterol generally increased during pregnancy by approximately 40% and returned to pre-pregnancy levels within one year postpartum. We noted a slight decrease during the first trimester, an observation described in other studies [13, 14].A possible explanation for the decrement during the first trimester may be a decreased intake of food due to nausea and vomiting, which characterize the early stages of pregnancy (10).
LDL-C demonstrates a similar pattern to total cholesterol, with an average increase of approximately 23% in the third trimester. However, after the first year postpartum, the levels of LDL-C continue to decline even below pre-pregnancy levels.
Triglyceride levels, as also shown in other studies [1, 14], doubled in the third trimester. However, we also demonstrated an initial decrease in TG levels in the first trimester, a pattern not shown in previous studies [1, 14]. Apparently, consecutive pregnancies do not influence baseline (non-pregnant) TG levels. These findings are consistent with the findings of Gunderson et al [11, 12].
HDL-C levels mainly rise in the second trimester, but begin to decline from the third trimester, reaching their nadir one year postpartum. Interestingly, our results show that with each consecutive pregnancy HDL-C rises to lesser extent, and the nadir is lower. These changes may be a risk factor for future atherosclerosis.
This study has several limitations. The first is that it lacks a non-pregnant control group in the same period. It is known that aging is a significant factor affecting changes in the lipid profile - a factor we did not analyze. We also lack data about weight changes during this six-year period, as well as information on the diet of the subjects - factors that may affect the lipid profile [15]). Another possible explanation for the changes we found may be the decline in physical activity due to increased demands of the growing family over time.
Our study has some other limitations. This is a retrospective study and the effect of factors such as breast feeding and birth control pills were not available for adjustment [10–12].We controlled the women to their own pre-pregnancy lipid levels rather than comparing to a nulliparous group, which would provide another perspective of the change in the lipid profile with age.
Our study reinforces the results of previous studies [14, 15] supporting the hypothesis that pregnancy exerts persistent adverse effects on HDL cholesterol. We demonstrate a cumulative effect of consecutive pregnancies on lowering HDL cholesterol levels. This effect may have negative implications on future cardiovascular health.