The goal of this study was to examine whether depressive symptoms during pregnancy are inversely associated with breast milk LCPUFA concentrations. We found this to be true for DHA when depressive symptoms were measured at < 20 weeks of pregnancy but not for symptoms measured at 24 to 29 weeks. The association with symptoms at < 20 weeks applied across the range of CES-D scores; it appeared to be linear—that is, not confined to women scoring 16+. We observed no associations between depressive symptoms at either time point and concentrations of other fatty acids in adjusted models.
Some proportion of women who experience elevated depressive symptoms late in pregnancy are women who have been chronically depressed and whose symptoms may be rooted in factors unrelated to and preceding the pregnancy, while other women have no history of depression but start to experience symptoms as hormonal triggers or psychosocial influences (eg, absence of a partner, financial worries) build as delivery nears.29
Our null results for symptoms measured around the beginning of the third trimester might be explained by the fact that women with elevated depressive symptoms detected early in pregnancy may be more reflective of the chronically depressed group, while the women with elevated symptoms later in pregnancy come from both these groups. Because breast milk DHA levels largely reflect fatty acid stores laid down over many years, low breast milk DHA may reflect chronic depression more closely than transient depressive symptoms during pregnancy. Again, it could be that (1) chronically low dietary intake or abnormal fatty acid metabolism could affect cell membrane phospholipid composition and function in the brain and cause depression or (2) chronic depression reinforces a diet low in ω-3 fatty acids or adversely affects fatty acid metabolism as reflected in low ω-3 levels. Alternatively, our positive result for depressive symptoms early in pregnancy could be spurious.
We evaluated the possibility that women who never initiated breastfeeding, who quit before 4 months, or who declined or were unable to provide a breast milk sample might have been more likely to have elevated depressive symptoms during pregnancy. These women scored slightly higher on the CES-D at both pregnancy time points. Because these women were not part of the analytic sample, our results may be biased toward the null and underestimate the true association.
No previous studies have examined depressive symptoms during pregnancy and breast milk fatty acid concentrations. One previous cross-sectional study of clinically depressed women found an inverse association between plasma DHA, total ω-3, or ω-6:ω-3 and depressive symptoms in the third trimester, but it did not examine symptoms earlier in pregnancy, nor did it examine breast milk concentrations.16
Of several previous observational postpartum studies, 1 observed no association between postpartum depression and concurrent DHA status, while 2 observed that decreasing plasma DHA levels were accompanied by increasing depressive symptoms.13–15
Another study found an association on an ecologic level between national postpartum depression point prevalence estimates and breast milk composition reported by one or more studies aggregated in each of 16 countries.30
Our study is unique in that it examined the association between depressive symptoms and milk concentrations at the individual level.
By using a screening instrument to identify depressive symptoms, we included women with a range of depressive symptoms, rather than only women who met a clinical definition for major depression. Observing the association between DHA and depressive symptoms at subclinical levels suggests that a larger proportion of individuals might be affected, not only those who are clinically depressed. However, the use of this screener may underestimate the association among the most severely depressed women and is a limitation of our study. The proportion of women who experienced significant depressive symptoms in this study is similar to population-based studies of pregnancy,31,32
and the DHA concentration in the breast milk samples in this study was in the range of other US studies.33
Other limitations include the lack of information about depressive symptoms before pregnancy began. This information would have allowed us to examine depressive symptoms of a more chronic nature compared to newly emerging symptoms during pregnancy. Also, our limited sample size and relatively small number of women who experienced elevated symptoms at both pregnancy time points prevented in-depth analysis of the more severe symptoms levels.
While there is growing interest in the relation between depression and DHA, research has not revealed the temporal direction of the association. Most previous studies that examined the association between perinatal depressive symptoms and DHA status measured DHA at the same time or long before symptoms were measured. We examined the association longitudinally by assessing depressive symptoms during pregnancy and measuring fatty acid status postpartum. In this way, depressive symptoms present months before the measurement of DHA status may be meaningful, even if symptoms measured closer in time are not associated with DHA status. Because depressive symptoms often reflect a chronic condition and fatty acid levels are, at least in part, a product of lifetime diet, it is difficult for even a lengthy longitudinal study to resolve the temporal sequence of these factors. However, this study found that depressive symptoms were present at a time point at least as early as the fatty acid profile (lower DHA). Additional research into the biological mechanisms underlying this association, as well as long prospective studies, will help clarify these uncertainties over temporality and causality.