What is postpartum depression? It depends who you ask. If you ask me, I’m likely to describe a number of potential contributors that can ultimately be tagged with the impressionist psychiatric descriptor of postpartum depression, anxiety, and psychosis. These terms tell us little to nothing about what's actually going on in a woman’s body, yet the gold standard of treatment is medications that may only be riding a placebo effect, and may put that woman — and even her family — at risk, all while neglecting to investigate underlying drivers. It’s time to demand a more personalized and biochemically updated perspective on this syndrome that afflicts 10-15% of women.
In my communication with perinatal psychiatrists, and in reading the updated literature that attempts to identify predictive factors and best treatments, I'm struck by how one-dimensional this research is. Here are my complaints:
Research on pregnancy-related mood disorders rarely controls for metabolic and inflammatory markers that we know to be derailed in the setting of most of what we call depression.
It rarely, if ever, controls for dietary and environmental exposures (filtered water, plastics, and pesticides).
When studying natural agents, studies fail to apply a multi-interventional approach that includes lifestyle changes and a number of synergistic nutrients. The more we think about natural supplements the way we do medication — one pill for one disease — the further we get from understanding and appreciating their true potential.
You can imagine my excitement when I read Homocysteine and serotonin: Association with Postpartum Depression one weekend. Here, researchers state what I've come to believe is the most promising gauge of risk to baby and mother: elevated inflammatory markers. They state, “One of the biological factors for PPD may be higher levels of homocysteine,” and go on to discuss the results of their study, which assessed Edinburgh-confirmed postpartum depression and found elevated homocysteine at both 1-2 days postpartum and 6 weeks after delivery.
The babies of these mothers also had lower APGAR scores. Unsurprisingly to me, serotonin played a less predictable role (because depression is not a serotonin deficiency!). Let’s understand why homocysteine is a good candidate marker for a complex inflammatory syndrome that likely involves diet- and environment-driven immune reactivity inside and outside the brain:
An amino acid pathway, the methionine-homocysteine pathway plays a critical role in widespread bodily functions including production of the body’s principal methyl-donor, SAMe, and the body’s primary antioxidant glutathione. Through these two responsibilities, recycling of homocysteine accomplishes the following (and more) brain-relevant tasks: