A New Explanation of Postpartum Depression and Postpartum Psychosis
At the MSNBC Health Bulletin Board, I was asked if my work could explain
postpartum depression and postpartum psychosis. I was able to generate
an explanation of these phenomena, and my explanation was posted there
in "Frontal Lobe and Violence." Since I think my answer may explain
these phenomena, I thought it should be posted here, in case anyone is
interested. The following contains the question posed to me and my
"Dawn Baynes wrote:
'I do research on woman who go through postpartum depression\psychosis
and some of the infanticide cases I have studied. Most of these women
were either very atletic or had male babies. The majority had to be
induced with pitocin in order to deliver. I would think that the culprit
could be that these women carry more androgen or testosteron and in
return lower their progesterone and estrogen --and that would be the
cause of a lack of oxytocin. These women also had lactation problems-
again pointing to oxytocin. Could this be why some mothers go through a
severe postpartum and have trouble bonding with their child? And could
this be why they have aggressive thoughts and feelings towards their
newborns. And quite a few women who get infections of some kind seem to
experience this illness to. Most of the mothers I talk to--suffer from
Postpartum Obsessive Thought Disorder- and I would think that the
intrusive thoughts would be due to a lack of serotonin- and the presence
of infection and possibly a decrease in estrogen/progesterone and
increase of androgen\testosterone or a combination of something.
Unexplained hirsuitism is another symptom. I'm sure that the hundreds
of women who commit neonaticide and infanticide are not cold blooded
murderers! When I say this I get clobbered by the general public and
I'm not trying to defend or excuse their behavior but considering a lot
of these mothers are religious and pro-life--this is the only thing
that would make sense to me! I belong to an organization-Postpartum
Support International- are you familiar with this group?'
James Howard responds:
I will try to answer your questions. However, as I do this, it should
occur to you, or someone else reading this, that my "work" covers so
many things. I think you should have a brief explanation of this to
avoid confusion, and this will help you understand my answers. My
principle hypothesis is that DHEA acts to optimize transcription and
replication of DNA. Therefore, my theory suggests that DHEA is involved
in the functions of every cell, tissue, organ, body, and can be seen in
populations. With that in mind, I will now try to answer your
questions. This will be difficult to do, briefly; so, read carefully
and then put it together.
DHEA is provided for the mother and the fetus from the adrenal glands of
the mother. The adrenal glands of the infant do not start producing
DHEA until birth. This means that the DHEA provided by the mother must
provide for all of her tissues and the fetus. (Since your questions
refer to the mother, I will not mention the infant again.) At the first
pregnancy, DHEA decreases significantly in the mother (J. Clin.
Endocrin. Metab. 1987; 64: 111). In 1985, because of my principle
hypothesis, I proposed that low DHEA will result in depression and
Alzheimer's disease (copyrighted, 1985). In 1997, DHEA was used in "six
middle-aged and elderly patients with major depression and low basal
plasma DHEA." These investigators found that: "In both studies,
improvements in depression ratings and memory performance were directly
related to increases in plasma levels of DHEA and DHEA-S and to
increases in their ratios with plasma cortisol levels. These
preliminary data suggest that DHEA may have antidepressant and promemory
effects and should encourage double-blind trials in depressed patients."
(Biol. Psychiatry 1997; 41: 311).
So, just in mothers of low DHEA who give birth, according to my theory,
one would expect to find depression. I suggest this is the explanation
of postpartum depression. Since you mentioned a number of women who
required oxytocin (pitocin)for birth, exhibited postpartum depression,
and infanticide, my explanation is further supported. Consider this:
"RESULTS: Oxytocin augmentation followed standard indications in 29 of
the 55 patients. The mean maternal DHEA sulfate level was significantly
lower in these patients than in the remaining 26 who progressed
spontaneously through labor. CONCLUSION: Among term nulliparous women,
maternal serum levels of DHEA sulfate are significantly lower in those
clinically requiring pharmacologic augmentation than in those
progressing spontaneously through labor. Dehydroepiandrosterone sulfate
may be an important factor in efficient labor." (Obstet. Gynecol. 1996;
Furthermore, my theory suggests that reduced DHEA may result in
psychosis. At my website, you may read my theory of schizophrenia, a
developmental problem, I think, is caused by low DHEA. Schizophrenia is
known to exhibit significantly reduced DHEA
(http://www.naples.net/~nfn03605). According to my work, this low DHEA
results in the reduced cerebral hemispheres found in schizophrenia.
Now, it is known that schizophrenia usually occurs in late teens or
early twenties. My work suggests that the "availability" of DHEA can be
affected by two major hormones, cortisol and testosterone. I think
cortisol evolved to directly counter the effects of DHEA. (The
explanation of this is too lengthy for this post.) I think testosterone
causes DHEA to increase the use of DHEA for testosterone target tissues.
So, I think that stress (cortisol) and puberty (testosterone in both
sexes) causes the availability of DHEA to decrease. In some
individuals, whose cerebral hemispheres have not fully developed due to
low DHEA, this is a time for the appearance of schizophrenia. (It is
known that, while stress does not cause schizophrenia, stress (cortisol)
often triggers it.
Now, in some women who have low DHEA affecting the development of their
cerebral hemispheres, the decline of DHEA, postpartum, may induce
psychosis. In schizophrenics and people with AIDS, both of which
exhibit low DHEA, the basal glanglia exhibit increased activity, along
with reduced prefrontal lobe activity (Am. J. Psychiatry 1985; 142: 564
and Science 1988; 239: 587). The prefrontal lobes control the impulses
of the lower areas of the brain, in which one finds the basal ganglia.
If women whose prefrontal lobes are underdeveloped give birth, I think
it quite possible that they could loose control and harm or even murder
their infants. The midbrain contains more receptors for testosterone
than the cerebral hemispheres (which include the prefrontal cortex).
This means to me that "athletic" women may produce more testosterone and
this effect may cause their midbrains to be more active relative to
their frontal lobes. I think it is possible that this may explain what
you report, above. These women may loose control and act on it, rather
than simply show less aggressive symptoms of psychosis. This could also
explain lack of bonding.
My work suggests that people, who are prone to infections, are low DHEA.
The decline in DHEA of the first birth could result in increased
infections. Since the immune system will compete with the brain for the
available DHEA, the infections could aggrevate already low DHEA and
possibly induce postpartum depression or psychosis.
I hope this answers this set of questions."