Explanation of Postpartum Depression and Postpartum Psychosis

James Howard jmhoward at sprynet.com
Mon Aug 17 08:08:27 EST 1998


Explanation of Postpartum Depression and Postpartum Psychosis

James Michael Howard
Fayetteville, Arkansas, U.S.A.

I first published this idea to a number of internet newsgroups September 15,
1997.  I recently found a new citation (end) that further supports my idea,
so I decided to add the citation and publish my idea again.

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.  Therefore, levels of DHEA will affect such phenomena as labor
and mental function.

DHEA is provided for the mother and 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.  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, in mothers of low DHEA who give birth, according to my theory, one would
expect to find depression.  A posting at a bulletin board mentioned that a
number of women, with whom the person had experience, who required oxytocin
(pitocin) for birth, exhibited postpartum depression and infanticide.  This
area also fits my explanation, because use of oxytocin for labor actually
increases DHEA, in low DHEA women.  “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."

The following quotation, from 1998, adds further support that women who have
difficult labor may have difficulty due to low DHEA.  The conclusion of the
report is that: “Dehydroepiandrosterone sulfate may be an important factor
in successful labor induction.”  Above, I mentioned my explanation of
depression as a result of low DHEA.  One may read my explanation of
schizophrenia, as a result of low DHEA, at my web page,
http://www.naples.net/~nfn03605/.  Psychotic behaviors also may occur in
Alzheimer’s disease and AIDS, both of which exhibit low DHEA.  I suggest
that the coincidence of postpartum depression and psychosis in some women
following birth, especially in those who have difficult labor, is due to low
DHEA in these women.

“OBJECTIVE: To evaluate the maternal serum dehydroepiandrosterone (DHEA)
sulfate level as a factor associated with the outcome of labor induction.
METHODS: Venous blood was collected from 161 women at the initiation of
labor induction. Pregnancies complicated by maternal corticosteroid use,
antepartum chorioamnionitis, or cesarean delivery for indications other than
arrest disorders were excluded from analysis. In 155 women meeting inclusion
criteria, induction followed established protocols. Serum DHEA sulfate
levels were measured by radioimmunoassay and correlated with the outcome of
each induction attempt. A success was defined as progression to active
labor. The Welch approximate t test, Mann-Whitney test, Fisher exact test,
simple regression, and multiple regression were used for statistical
analysis, with P < .05 considered significant. RESULTS: The mean (+/-
standard error) DHEA sulfate level was higher in women who progressed to
active labor (n = 147) than in those with unsuccessful attempts (n = 8),
(109.01 +/- 5.19 microg/dL versus 58.78 +/- 15.83 microg/dL, respectively; P
= .02). Compared with women with DHEA sulfate levels above 70 microg/dL,
women with lower levels had an unsuccessful induction odds ratio (OR) of
4.46 (95% confidence interval, 1.12, 17.67; P = .04). The OR increased as
DHEA sulfate levels decreased. CONCLUSION: Dehydroepiandrosterone sulfate
may be an important factor in successful labor induction.” Obstet Gynecol
1998 May;91(5 Pt 1):771-773








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