mommy brain

Perinatal Mood, Cognition and Hormones

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While searching through old research files for an article I am writing on mitochondria and hormones, I stumbled upon the presentation notes for my thesis defense. I thought some of our readers might find them interesting. Although, I was not able to find the original PowerPoint presentation, I did find a later presentation that included my thesis and dissertation research, along with the some background information on neuroendocrinology. You can read my thesis here and/or the articles published from that research here and here. I added a few subheadings for readability, but otherwise, the presentation remains unchanged.

Perinatal Mood, Cognition, and Hormones

The purpose of this study was to identify the cognitive and emotional changes associated with pregnancy hormones both during pregnancy and postpartum and to identify early markers for perinatal mood dysfunction.

This research was based upon several physiological presumptions regarding pregnancy and postpartum. Conventional wisdom holds that during pregnancy reproductive hormones increase exponentially to support the pregnancy. It also posits that after delivery those levels decrease rapidly to below normally circulating levels and remain low until breastfeeding ceases and menstruation begins.

Animal research shows that many reproductive hormones are neuroactive and potently modulate numerous neurotransmitters systems. Given the large and sustained increased in such hormones followed by the precipitous decline, one would expect clear behavioral changes associated both with the elevated and diminished states of circulating hormones. We would also expect that the change from high hormone to low hormone state would mimic an addiction/withdrawal syndrome.

Numerous animal studies indicated that this was the case, but the connection between hormones and behavior in human studies was inconsistent and inconclusive for many reasons outlined in my research. The most important failing of previous research has been the lack of theory or evidence-based design. That is, not only has previous research failed to recognize, and hence, postulate neurosteroid/neurotransmitter mediated behaviors, but often failed to recognize the clearly articulated affective dysregulation presented regularly in clinical case research.

The question of which hormones modulate which neurotransmitters and to what behavioral consequences has not been asked, nor has the possibility that perinatal mood might be altered across several domains ever been addressed. Instead, most if not all, research focuses exclusively on progesterone and estradiol without so much as even speculating which neural circuits might be involved. Moreover, despite ample clinical evidence to the contrary, most research thus far measured and continues to measure only anhedonic depressive symptoms.

This study was different. Because extensive clinical case research revealed that perinatal mood was more often than not comprised of multiple syndromes of which depression was merely a part, I expanded the psychiatric domains measured to include assessment of 9 common psychiatric modalities and utilized a standardized and validated measure.

Additionally, previous studies measured only progesterone and/or estradiol. This study measured five hormones, progesterone, DHEAS, estrone, estradiol, estriol and testosterone.  The timing of assessment in other studies has been inconsistent and again not obviously evidence based. With approximately, 70% of all cases of postpartum psychosis occurring in first two weeks post-delivery, I thought it was important to measure within that time frame to capture those changes. Since case reports reveal premorbid symptoms during late pregnancy, I also measured at 37 weeks of pregnancy.

This study utilized salivary assays to measure hormone levels and controlled time of day and food intake. All previous studies measured hormones at non-standardized times and did not control food intake. Hormones have diurnal rhythms, and food intake, particularly with salivary assays will comprise results.

But perhaps the most important difference between this and previous studies is that this study was designed, all instruments were selected and the timing of testing was determined, based upon the presumed neuromodulatory activity of these hormones and the predicted concomitant behaviors associated therein, using an addiction/withdrawal framework. Thus it was imperative to test in the immediate postpartum so as to capture changes before neurological and behavioral adaptation occur.

It’s All About GABA

Given these considerations, much of the study design was based upon progesterone’s capacity to modulate the GABA system.

Progesterone is a potent allosteric GABAa agonist and anxiolytic. However, chronically elevated progesterone becomes anxiogenic via its actions on receptor conformation. It was postulated that during the course of pregnancy, the women would be the beneficiaries of the progesterone’s anxiolytic actions, but that towards the end of the pregnancy, as receptor conformation changed, the GABAa receptor would become immune not only to progesterone’s actions but GABA’s actions as well with the net behavioral effect of increased anxiety.

Postpartum, when progesterone was withdrawn the lack of CNS GABA transmission would induce hyper-excitability across several CNS systems that would be expressed in elevated anxiety symptoms and mood lability.

Major Findings: It’s Not Progesterone or Estradiol and It’s Not Depression

What I didn’t know going into this study was that DHEAS also modulated GABAa but did so antagonistically. What I also didn’t know, and what is in fact the first major finding of this study, was that circulating DHEAS levels increased throughout pregnancy and postpartum. All previous research indicated that DHEAS increased over the first two trimesters, decreased during the third and returned to normal immediately proceeding delivery. This was not the case. Although I have only two test times, DHEAS levels were clearly very high at 37 weeks, and increased postpartum by an average of 34%. Indeed only 6 participants showed waning postpartum DHEAS levels.

Returning to the GABA hypothesis, as is now becoming clear, during most of the pregnancy progesterone positively modulates GABA transmission. Toward the end of pregnancy when progesterone levels presumably level off but are nonetheless at supra-physiological levels, the chronicity of exposure elicits conformational changes in the receptor making it unresponsive to progesterone and according to animal research unresponsive to benzodiazepines as well. Concurrently, DHEAS levels are increasing and are now blocking whatever limited GABA transmission exists. Parturition occurs, progesterone levels diminish by some 93% while DHEAS levels continue to increase. So now whatever remaining GABA binding sites are still available become blocked and CNS hyper-excitability ensues leading to the behavioral lability seen in almost all women during the first two weeks postpartum.

The behavioral sequelae of these rather dramatic physiological changes include increased anxiety, phobia, OCD, paranoia psychoticism, and importantly many physiological symptoms tapped by the somatization scale of the SCL-90R, particularly cardiovascular dysregulation, increased heart rate, respiration, sweating, etc.

Postpartum, even in asymptomatic women, that is the 80% of women who experience what is imprecisely called “baby-blues” is often marked by hyper-excitability and mood lability as much or more so that anhedonia and depression. This is with good reason given the neurochemical and physiological changes occurring as these hormones adapt to the non-pregnant state.

Thus, the second major finding in this study was that although depression was certainly present, it was by no means the sole determinant and I would argue not even the primary or causative factor in the observed mood dysregulation postpartum. This is really important because insofar as previous and indeed current research continues to focus on postpartum depression rather than perinatal mood more broadly, hundreds of thousands of women get misdiagnosed, under-diagnosed and inappropriately treated. The findings from this study indicate that not only do negative mood symptoms begin in late pregnancy but that the disorder itself is characterized as much by anxiety or positive type symptoms as it is by depressive and anhedonic type symptoms.

The third major finding of this study was the connection between late pregnancy and post-delivery hormones to negative mood. As was outlined in my research, the design of this study was very strongly based upon the neuromodulatory capacity of progesterone on the GABAa system. Results from this research indicate that progesterone was not correlated with negative mood and thus I was wrong about progesterone. Nevertheless, I was correct about GABA being a major player in perinatal mood dysregulation.

Recent research suggests that DHEAS is a potent GABAa antagonist similar to the drug picrotoxin. That is, it is capable of binding to a site deep within the receptor, thereby limiting GABA influx.

Given DHEAS’ influence on GABA, its increase late pregnancy and post-delivery, one would expect clear and consistent correlations between DHEAS levels and mood. That is exactly what I found. Pre-delivery DHEAS was correlated with paranoia and psychoticism.

Post delivery DHEAS was strongly and significantly correlated with just about every mood symptom measured by the SCL-90R including anxiety, phobia, paranoia, somatization, and the GSI. Recall that DHEAS levels increased an average of 34% and increased for all but of 6 of the women postpartum. In some women, those who had the most severe postpartum difficulties, DHEAS levels increased 2-4X pre-delivery levels.

Moreover, the fourth major finding from this research showed that pre-delivery testosterone was correlated not only with pre-delivery negative mood (phobia, psychoticism, somatization and GSI), but was correlated strongly and significantly with almost every negative mood symptom measured by the SCL-90R post-delivery as well, including anxiety, hostility, psychoticism, somatization, OCD, interpersonal sensitivity, depression and GS. And the correlation was negative. That means that diminished testosterone (amidst the presumably elevated levels of pregnancy) were correlated with increased negative symptoms. This is important for a number of reasons, not the least of which is its predictive possibilities, but it suggests that the adrenal androgens of which DHEAS and testosterone are key component are implicated in perinatal mood.

This is groundbreaking. It has never been addressed before in the literature. If we look at the biosynthesis of steroid hormones during pregnancy, we see that DHEAS is produced both by the fetal and maternal adrenals and is intra-converted in the placenta as well. Biologically, DHEAS is considered inactive, meaning that it must be converted to DHEA before other downstream hormones can be metabolized. DHEAS is storage component for DHEA. If more DHEA is converted to DHEAS, for whatever reason, then less downstream hormones-testosterone are synthesized. These are the results I found. Since I didn’t measure DHEA, I can only speculate, but these two factors in hormone synthesis appear to be altered and these alterations are related to the mood perinatal mood dysfunction. Future studies are needed to confirm these findings and determine their etiology but preliminarily these results open up an entirely different direction for future research that has yet to be addressed, the implications of which will be far-reaching.

Perinatal Cognitive Changes

The cognitive results from this study were no less impressive but not as easily interpreted because cognitive ability was not consistently linked to either mood or hormone data but was obviously impaired.

As a group, these women were educated with many having graduate degrees. The average estimated IQ was approximately 1 SD above the mean and might have been higher if complete testing had been performed. Most of these women worked outside the home in a professional capacity for the duration of their pregnancies, and yet when tested, showed significant memory and executive function deficits when compared to age and education matched normative data. The degree of impairment was striking, and quite frankly, unexpected.

In verbal memory measured by the CVLT-II, many percentile rankings were below the 20th percentile. When testing these women, it became apparent how important semantic memory was, with those women recognizing the categories of words having little difficulty completing the task and probably skewing the data somewhat. However, for a large percentage of the women, there was absolutely no recognition of the categories inherent in the task and their ability to recall even a fraction of the words was hindered tremendously. The women also repeated words, in some cases 2 and 3 times during the course of a trial and recalled words that were not part the trial list.

On spatial memory tasks the deficits were no less obvious. As is exemplified by the CFT tasks, shown in the appendix of my thesis, the impairment was at least in part related to an inability to see the drawing as an entirety. If we look at these drawings closely, we see that in the copy phase, the core of the drawing, the rectangle is missing. That is, each section of the figure is drawn separately. This presents difficulties in encoding that will ultimately limit performance of the recall portion of the task. Again notice the piece meal quality of the figures in the recall task, with large portions of the figure completely missing. The examples illustrated here are representative of performance across participants.

The mood to cognition relationship was interesting if not paradoxical. Conventional wisdom would suggests that negative mood, particularly depression and anxiety would impair cognitive performance. This was not the case. Indeed depression actually improved performance.

The hormones to cognition relationships were no less confusing except that changes in DHEAS were correlated with poorer performance on the CVLT-II. Given the magnitude and direction of change in DHEAS levels this was consistent with the earlier results. Progesterone, was not correlated with mood symptoms but was correlated to both aspects of the design fluency task and the estrogens were correlated with a variety of task both pre and postpartum.

What was particularly interesting about this aspect of the research was that cognitive ability declined in many areas postpartum, but participants perceived themselves as having improved. The disconnect between perception and performance was clear almost across the board.

Finally, it may be that as in the case of other mental illnesses, cognitive functioning is not correlated with severity of symptoms but is associated with measures of therapeutic outcome such that higher premorbid functioning predicts one’s ability to function during and after an episode.

This possibility begs the question that if another group of women was tested having lower premorbid cognitive function and lower socio-economic status, would they have fared as well as the women in this study. That is, would their ability to withstand the physiological and consequent emotional/behavioral change associated with pregnancy and postpartum be comparable to the abilities of this group?

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter and like it, please help support it. Contribute now.

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The studies addressed here were published in 2007 as part of my PhD dissertation. This post was published on HM on November 29, 2018.

Mommy Brain: Pregnancy and Postpartum Memory Deficits

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Pregnancy and postpartum memory problems are common complaints amongst new moms. Are they real? Some research says yes, other research says no.

In graduate school I studied this issue and completed several studies on pregnancy and postpartum mood and memory changes. In one such study, I ran a full battery neuropsychological tests on a group (n = 28) of highly educated, healthy, medication free, first-time moms. We tested in late pregnancy and within 10 days following the delivery of the child. We also measured a range of hormones (progesterone, DHEAS, testosterone, estrone, estradiol and estriol) to determine what relationship the radical hormone changes of pregnancy and childbirth had on a woman’s cognitive ability. We knew from animal research that steroid hormones could affect learning in very significant ways. It wasn’t that difficult to suspect the same would be true of human women.

The study was never published, rejected from at least three, maybe four journals and has been sitting in a file ever since (along with a number of other studies). With the open access and open science movements growing, I decided it was time for this research to see the light of day. I will be self-publishing much of my research over the coming weeks and months. Here is the first study. Understanding Maternal Cognitive Changes: Associations between Hormones and Memory.

Is the Mommy Brain Real?

More importantly, are hormones to blame?  The answer is yes on both counts. We found that pregnant and postpartum women exhibited detectable cognitive deficits across multiple domains. The deficits were worse in late pregnancy and mostly improved postpartum. These memory problems were linked to both the excessively high hormones of late pregnancy, the low hormones following delivery, and the large changes in hormone concentration from pregnancy to postpartum.

What Types of Cognitive Deficits?

Pregnant and to a lesser degree, postpartum women had difficulty sustaining focus – this may be the mommy brain fog that many women complain of. We also found that during pregnancy especially, women were unable to manipulate and organize incoming information effectively. This presented as poor performance across a number of tests that assessed both short and long term memory.

In the case of verbal memory, these highly intelligent (estimated average IQ was 114 – 119) and educated (average years of education was 16 years) women tested in the low single digit to the 20th percentiles across multiple IQ-adjusted verbal recall measures. Even when estimates of IQ were not used to adjust scores, the participants performed poorly compared to normative standards. This was surprising given that many of these women had advanced degrees and were working in professional capacities.

The verbal tests involved remembering lists of words; words that could be grouped into meaningful categories that would improve memory significantly. Most of the study participants had difficulty grouping the words into categories. Instead, they would attempt to remember by rote sequence, which is always much more difficult. They also exhibited high numbers of intrusions – recalling words that were not in the original lists and repetitions – repeating words.

Similarly, and more strikingly visible, visual- spatial memory was marred by the inability to group bits of information and perhaps even to see the groupings in the first place. In this test, the study participants were given a complex figure to copy (shown below). They were not told that they would be asked to recall and redraw the picture later. When asked to redraw the figure, the inability to see the totality of the picture, to group bits of information was apparent.

Visual – spatial memory deficits as assessed by the Rey Complex Figure Test. Marrs et al. 2013, © 2013 Lucine Health Sciences, Inc. All rights reserved.

Does Memory Improve Postpartum?

Interestingly, while spatial memory improved significantly from pregnancy to postpartum, verbal memory did not. And this is probably what troubles women the most, the perceived deficits in verbal memory. Most of us think in words, when our ability to find words, retain words, organize information effectively is compromised, we notice.

Hormones and Memory

Both high levels of late pregnancy estrogens, (estrone, estradiol and estriol – we measured all three) and the low levels these estrogens postpartum were correlated with multiple measures of diminished memory, attention and processing. Additionally, the larger the change in the circulating levels of estrogens from late pregnancy to early postpartum was associated with poor memory postpartum. Indeed, women who had higher postpartum estradiol and estriol specifically, performed better on measures of verbal memory than those who did not.

Progesterone, long thought to be associated with cognitive function, primarily because of its sedative properties, was not associated with any measure of cognitive function at either test time, although large changes in progesterone were associated with some performance measures. DHEAS and testosterone, not often measured in pregnancy, postpartum or even in women’s health in general, were also associated with a few measures of cognitive functioning.

What This Means

Ladies, you are not imagining the pregnancy memory problems. They exist and they are related to the hormones. Most women knew this already, but it took a while for science to catch up. Not to worry though, the memory problems do resolve as the hormones stabilize (my next study to be self-published – a long term follow-up). Read the full study for all the details: Understanding Maternal Cognitive Changes: Associations between Hormones and Memory.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter. 

This article was originally published on Hormones Matter on March 26, 2013.

Maternal Psychiatric Disturbances and Hormones

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As a mom of young children, I was very much affected by the Andrea Yates case. If you recall she experienced successive bouts of psychosis and pursued multiple attempts at suicide following the delivery of each of her children. After her fifth child, she drowned her children, killing them all. The case was a heartbreaking, and I believe, a totally preventable tragedy had her psychosis been taken seriously by medical professionals, family and others in the community. In spite of her psychosis and suicide attempts she was sent home to care for her children, as if a woman with postpartum psychosis is somehow less ill than a man or than a woman whose psychosis develops unrelated to her pregnancies. Raising young children is difficult, even under the best of circumstances, but sending a severely depressed and psychotic woman home to care for young children is just downright negligent. Although there was blame to go around among the doctors, her family and community, I couldn’t but shake the feeling that this tragedy could have been averted if her illness had been taken more seriously.

Identifying the Biological Underpinnings of Maternal Psychiatric Disturbances

The Andrea Yates tragedy inspired me to research and identify the clinical and biological components of perinatal mental illness. My goal was to identify early warning markers; biological tests, that would give women, their physicians and family members a way to predict the possibility of illness and confirm that illness once it had arrived. I thought that if we could predict and identify the risk for this illness, then the families could prepare and maybe even lessen the severity the disease process. At the very least, tragedies like the Andrea Yates case could be prevented.

I knew hormones would be key to the onset and maintenance of perinatal psychiatric symptoms. What I didn’t know is which hormones, when, and related to which symptoms. It seems that no one else did either. Despite years of research and a clear temporal association between the onset of psychiatric distress and childbirth, only tenuous connections between maternal hormone concentrations and varying degrees of postpartum depression had ever been established. This was primarily because the research was focused so narrowly upon the relationships among what are often referred to as the female hormones, progesterone and estradiol, and depressive symptoms. Very little research had examined associations between a broader range of steroid hormones and the full spectrum of potential psychiatric symptoms. This didn’t make sense to me. Certainly, other hormones affected by pregnancy, might also impact brain chemistry; certainly, the range of clinical symptoms that women might experience would go beyond the blues and depression. Even when psychosis appeared, I wasn’t convinced that the psychosis of pregnancy and postpartum was clinically similar to the psychoses that developed irrespective of the vast biochemical changes that took place across pregnancy, parturition and in the weeks and months that followed. If the biochemistry was different, as it most necessarily had to be, wouldn’t everything else about maternal psychiatric disturbances be different as well?

Looking Beyond the Boundaries

And so began my research. For the first study: Beyond Progesterone and Estrogen: Maternal Psychiatric Disturbances Linked to Adrenal Androgens, I recruited healthy, medication free, first time moms, with no previous history of mental illness. This was no easy feat. I soon realized that many women, even pregnant women, were using antidepressants and anxiolytics and many other medications. It seems the old adage that pregnant women should not take medications lest it cross the placental barrier and affect the developing fetus, had fallen by the wayside.

To assess the psychiatric distress, I abandoned the singular blues, depression and anxiety scales used so often in this research and found a broad-based, standardized assessment of psychiatric distress called the Symptom Check List 90R (SCL90R). SCL-90R is a 90-item psychiatric self-report inventory designed to measure the severity and intensity of psychiatric symptoms in both inpatient and outpatient populations. Participants rate the severity of distress experienced during the prior seven-day period using a 0-4 Likert-type scale (0=no distress-“not at all” to 4=extreme). Symptoms measured included: anxiety, hostility (aggression, irritability, etc.) phobic anxiety, paranoid ideation, psychoticism, somatization (perceptions of pain or other physical disturbances), obsessive-compulsive behavior, interpersonal sensitivity (feelings of personal inadequacy), depression and the global severity index (GSI), which reflects the overall symptom severity.

Along with the clinical symptoms, I measured five hormones, progesterone, DHEAS, testosterone, estrone, estradiol and estradiol, using saliva based testing. Symptoms and hormones were assessed twice, first in late pregnancy at 37 weeks (n =32) and again within 10 days following the delivery of their children (n=28, four were lost to attrition). I also conducted a year long follow up of those same participants and will report those data soon.

It’s Not Just Depression and It’s Not Just Postpartum

As I suspected, symptoms were present in late pregnancy and in some cases, increased in severity postpartum, but in other cases, decreased in severity. For some women, pregnancy was more problematic than postpartum, especially those with obsessive compulsive symptoms.

Fully 50% of the women tested experienced symptoms during pregnancy and 57% postpartum. This means maternal psychiatric distress is far more common than generally ascribed. As a group the anxiety related symptom scales, particularly the anxiety and obsessive compulsive scales, had the highest individual scores at each test time and when combined with hostility, phobia and psychoticism contributed the largest increase in symptom severity from pregnancy to postpartum. So it wasn’t the blues and depressive type symptoms that were most troubling, but the agitated, anxiety and even psychotic type symptoms that were the most severe.

Current research suggests that for only 1-2 per 1000 pregnancies psychosis will develop. What I found with this research and from another study,  is that psychotic symptoms were far more prevalent than recognized and may be the symptoms that drive the depression. In this study, we found sub-threshold, but clinically relevant, psychotic symptoms present in several of the women postpartum. Their symptoms were absent concurrent elevations in paranoia (paranoia and psychosis often go hand in hand). The most frequently ascribed to symptoms within this cluster included fears of serious illness (n=8), loss of mind (n=7) and isolation (n=12). Surprisingly, three women showed mild to moderate distress about thought insertion and thought broadcasting, two were concerned about thought control and one woman indicated distress about auditory hallucinations. Interestingly, it was these very same women who had the most dysregulated hormone profiles.

In speaking with the women who indicated these symptoms, the visual hallucinations, involved their children suffering; usually graphic intrusive thoughts, seeing images of their children being burned, thrown out windows, cut with a butcher knife, strangled with the breast pump tubing and the like. When auditory hallucinations were present they berated the women for their weakness, bad mothering etc., inducing guilt and one can only assume, depression. We confirmed the prevalence of these types of symptoms in two subsequent studies, the first published here: Dimensions of postpartum psychiatric distress: preliminary evidence for broadening clinical scope, the second unpublished as of yet.

Aberrant  Androgen Metabolism may be to Blame for Maternal Psychiatric Symptoms

As I suspected and as much research had shown, no symptom clusters were correlated with progesterone, estrone or estriol either pre- or postpartum.  While expected to be a close correlate of postpartum psychiatric symptoms, estradiol was associated with very few symptom clusters in the present study. Instead, it was the androgens that were linked to the symptoms at both time periods and not in a way that might be expected.

Low late pregnancy testosterone was not only related to late pregnancy psychiatric symptoms, but significantly predicted postpartum symptom severity. In conjunction, and this is where the endocrinology gets interesting, elevated late pregnancy DHEAS and supra-elevated postpartum DHEAS were associated with pre – and postpartum symptoms, respectively. This was exciting, because in theory these two hormones should not be aligned. That is, high DHEAS should correlate with high testosterone and it didn’t. So somewhere between DHEAS>DHEA>androstenedione> testosterone there was a problem and I had pretty good idea where.

For now though, we had a pilot study that ripped open the notions that maternal psychiatric distress occurred only during postpartum, was depressive in nature, was rare and was related to the normal or expected hormone changes of pregnancy. It was none of these things. The psychiatric distress was present at both test points, was more agitated, included a spectrum of symptoms, and most importantly, was related to aberrant changes in hormones that were likely exacerbated by the normal or expected hormone disruptions of pregnancy.  I was very excited. If we could identify the problem, then we could fix it right?

Not so fast. I could never get the research published and though I carried on with research I could do without funding, including a long term follow-up of the same participants (to be self-published soon) and an online study of the symptoms of psychiatric distress, the hormone work was routinely and summarily rejected. I learned very quickly how controversial studying hormones in women’s health was. So there it stands, the work was good, it pointed to a biomarker that could be used to identify and then treat a group of women who suffer horribly, but the study needs to be replicated with a much larger and more diverse population of women. It is likely that this is but one of many potential markers along this hormone pathway that could be used to predict and prevent perinatal psychiatric distress. It is also likely that this pattern of metabolism is linked to a host of other mental health and physical health issues. It was because of this research that I began Hormones Matter and have worked so arduously to increase awareness about the need for more research in women’s health. Hormones ought to be measured consistently across a woman’s life span, they aren’t and we need to change that.

Here are the full study details and the article, now officially self-published: Beyond Progesterone and Estrogen: Maternal Psychiatric Disturbances Linked to Adrenal Androgens.

Another portion of this study included assessing cognitive changes: Mommy Brain: Pregnancy and Postpartum Memory Deficits.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.