This study did not find evidence for the hypothesis that maternal depression is associated with reduced height in children. Contrary to expectations, maternal postpartum depression was associated with greater child total height and leg length in this relatively privileged sample in a high income country. Postpartum depression was associated with 0.37 higher HAZ, which translates into an approximately 1.5 centimeter difference in 3-year-olds of average height (94.5 cm) in the US.
This finding was independent of potential confounders, including maternal sociodemographic factors and height as well as child size at birth. We found no evidence for mediation by duration of breastfeeding or age of introduction of solid foods, nor any evidence for reverse causation. Additional control for depression at 1 year postpartum did not diminish the estimated effect for postpartum depression at 6 months, nor was there a main effect of depressive symptoms at 1 year postpartum on height outcomes, suggesting that exposure to maternal depression earlier in life is more important.
Antenatal depression when defined by the more stringent criteria of EPDS>
15 was associated with greater leg length in children. Comparing results using alternate cut-off values for the EPDS suggests a dose-response relation between antenatal depressive symptoms and linear growth outcomes in children.
Our results contrast with several studies in developing countries that report either a cross-sectional or prospective association between maternal depressive symptoms or clinical depression and reduced child height or increased risk of stunting.
However, not all studies in developing countries support an association between maternal mental health and reduced height in children.
It should also be noted that maternal depression has been found to be associated with both reduced weight
(for a review, see Stewart, 2007 
) and increased
in different settings; thus, there is prior evidence that maternal depression may have different effects in different contexts.
It is unclear what mechanisms may explain divergent findings between developing countries and the US. One possible source of difference is risk of nutritional deficiency and serious childhood illness across these settings. In resource-poor settings, maternal depression may be associated with or lead to lack of sufficient food for the household or inadequate care of childhood illness, both of which may contribute to shorter stature in children. In Project Viva, a middle and upper class sample in the US, there are likely very few families who cannot obtain adequate food, though we do not have data to examine this issue directly. Similarly, severe childhood illness that may affect height is limited in the Project Viva sample. Other notable differences between the study population examined here and studies in low and middle income countries include high levels of maternal education, relatively low levels of maternal depression, and low rates of child stunting. We may speculate that in the rather privileged families enrolled in Project Viva, one threat (maternal depressive symptoms) is not enough to interrupt children's growth, while in developing countries in the context of several threats (including food insecurity, low education, and high rates of stunting) and fewer resources, maternal depression is an additional burden that influences children’s growth.
Another possible reason for the different findings is that many of the studies in developing countries used a dichotomous outcome of stunting, while we used height as a continuous outcome. We cannot examine whether this may help explain divergent results because only 7 subjects in our sample met criteria for stunting (HAZ<−2). Reports from Brazil, however, support the notion that maternal depression is associated with stunting,
but not height when examined as a linear outcome variable.
Future research may endeavor to examine these possible explanations further.
Interpretation of our results should be in light of the study's limitations. Mother-child pairs included in our analysis represent 37% of enrolled women. It is possible that this loss to follow-up introduced some bias, though it is unlikely that it induced a positive association between postpartum depression and child height. This loss to follow-up may limit the generalizability of our findings. The mothers included are generally well-educated, of middle to upper income, and all have health insurance. It is possible that the association between maternal depression and child height may be different in more at-risk populations. Similarly, though we statistically control for important variables related to maternal depression and height, residual confounding is always a concern. However, while residual confounding could have resulted in over- or under-estimates in our study, it is unlikely that the direction of effect would have changed with better control of confounding. Regarding our exposures, we rely on self-report of depressive symptoms, not clinically-defined depression, and depressive symptoms were assessed at only two time points in the perinatal period, which likely resulted in misclassification of exposure. This may be particularly important for postpartum depression: we assessed postpartum depression at 6 months, but the prevalence of postpartum depression is highest in the 2nd
Misclassification of our exposure is likely nondifferential with respect to the outcomes, which would attenuate results towards the null. Finally, due to the relative independence of antenatal and postpartum depression, our results generalize primarily to women who have either antenatal or postpartum depression, although inclusion of women with both did not materially alter the estimated effects in this cohort of women. Given these limitations as well as the unexpected findings, replication of these results in another US-based cohort is particularly important.
In considering the mechanisms underlying the current findings, although many factors influence height, very few are likely to mediate an effect of postpartum depression on linear growth. One possible pathway is suboptimal nutritional intake among children of depressed mothers. Depressed mothers may have difficulty recognizing signs of satiety in their children, use more mechanistic methods of feeding, or use restrictive feeding practices.
Secondarily, maternal depression negatively affects mother-child interactions,
which may have implications for the child's nutritional intake. Depressed mothers may have more unhealthful behaviors, such as dysregulated eating behaviors (including over-eating and eating high-calorie foods) and limited physical activity, and their children may have similar behavior patterns. It is possible that these behaviors lead to increased energy intake in infants; in a related analysis of Project Viva participants, maternal postpartum depression was associated with greater overall adiposity in children at age 3 years.
We may speculate that increased caloric intake could have contributed to the greater linear growth observed here through actions of growth hormone or insulin-like growth factors; however, this study did not measure caloric intake or growth hormone, thus we were not able to test these possible mechanisms. That children exposed to postpartum depression showed greater height as early as 6 months of age suggest that influences before this age are likely to be at play.
Another possible pathway is through cortisol. In two studies, postpartum depression was associated with increased cortisol and cortisol variability in newborns and adolescents.
Postpartum depression, through its adverse effects on parenting behavior and the social environment, can produce more stressful experiences for the child. Stressful experiences, in turn, lead to elevated cortisol levels and increased cortisol reactivity in children.
Cortisol has a complex relationship with growth hormone: while chronic hypercortisolism leads to reduced growth hormone and reduced growth, small increases in cortisol stimulate growth hormone secretion and production.
It is possible that increased cortisol in the children exposed to postpartum depression had a stimulating effect on growth hormone and thereby increased height. Unfortunately, we did not measure these hormones in the current study.
The current study has several strengths. Project Viva is a prospective study with repeated outcome measurements, which allowed us to establish temporal order between exposure and outcomes as well as examine change over time in outcomes. This study assessed depressive symptoms both during pregnancy and during the postpartum period, allowing us to assess the contribution of each exposure individually. In addition, the primary outcomes of this study were collected using research-standard protocols, improving the precision with which we estimate relations.
Our study did not support the hypothesis that maternal depression is associated with shorter stature in children. To our knowledge, this study is the first to report an association between maternal depression and increased height in children. As one of the first studies to examine these relationships in a US sample, these findings should be replicated in other, more diverse samples in the US and other developed nations. Our findings suggest that postpartum depression has important influences on behavior or physiology early in life that translate into different growth patterns in children. Public health implications of our findings await elucidation of the contexts in which and mechanisms through which maternal depression may affect growth in children. Future research should study possible mechanisms that may account for the different linear growth seen in children of depressed mothers, including mother-infant interactions, dysregulated feeding and/or eating behavior, as well as underlying hormonal differences.