"Adverse Obstetric Outcomes" due to short interval following first pregnancy possibly explained...

"Interpregnancy Interval and Risk of Preterm Birth and Neonatal Death"
(Smith, et al., BMJ 2003; 327: 313 )

Explanation May be Due to Reduced DHEA Postpartum Following a First
Pregnancy

(Copyright 2003, James Michael Howard, Fayetteville, U.S.A., At bottom of:
www.anthropogeny.com/research.html )

Smith, et al., conclude in their report in the British Medical Journal that:
"A short interpregnancy interval is an independent risk factor for preterm
delivery and neonatal death in the second birth." (The abstract is available
below.) I suggest these "adverse obstetric outcomes" result from a single
phenomenon which should not go unacknowledged vis-à-vis the tremendous
burdens in emotional suffering and medical costs. These conditions may be
ameliorated by monitoring low levels of, and supplementation with,
dehydroepiandrosterone (DHEA) in women who become pregnant again, soon after
a first pregnancy.

DHEA has been determined to decline in women "only after a first pregnancy"
for remain low sometimes up to 150 months (J Clin Endocrinol Metab. 1987;
64: 111-8). This finding was repeated: "A previous paper in this journal
reported that first pregnancy was followed by a marked decrease in
dehydroepiandrosterone sulfate (DH[E]AS) and dehydroepiandrosterone (DH[E]A)
levels. We report here confirmatory observations from cross-sectional
measurements in 460 women. In premenopausal subjects (n = 306), the mean
DH[E]AS level was 21% lower (P = 0.005) and the mean DH[E]A level was 32%
lower (P less than 0.001) in parous than in nulliparous women." (J Clin
Endocrinol Metab. 1990; 70: 1651-3). I suggest these low levels of DHEA are
directly connected with "adverse obstetric outcomes" in pregnancies of short
intervals following a first pregnancy.

In order to understand the connection of this low DHEA with "adverse
obstetric outcomes," in pregnancies following first pregnancies without
sufficient time for DHEA to rebound, I have to explain two ideas about DHEA.
In 1985, I copyrighted my explanation of the "fight or flight" mechanism. I
suggested that the major adrenal steroid, dehydroepiandrosterone (DHEA), was
"selected" by evolution because it "optimizes" replication and transcription
of DNA. Therefore, DHEA is involved in every tissue, especially nervous
tissue, the brain. It follows that DHEA in sufficiently available levels
will be involved in increasing, or optimizing, aggression between
combatants. Combatants who fight to death or maiming reduce the probability
of continuance of a species. DHEA levels would be positively involved in
"impulses" or "motivation." I suggest the other major adrenal steroid,
cortisol, was selected by evolution to counteract the effects of DHEA. As
you may know, cortisol is the "stress" hormone, produced when we experience
stress. I suggest cortisol levels are negatively involved in impulses or
motivation. The ratio of cortisol to DHEA will be directly tied to our
personalities as well as actions. When cortisol is high, we flee, when DHEA
is high, we fight. Cortisol antagonizes the effects of DHEA and the ratio of
cortisol to DHEA is important in many physiological phenomena, including
obstetric outcomes. Too much cortisol for extended periods, especially in
low DHEA conditions, may produce very negative effects in all tissues.

Also, one should know that the very abundant source of DHEA in our blood
exists as a "sulfated" form. This is known as DHEAS or DHEAsulfate. The
active molecule, DHEA, is derived from DHEAS. Now, this is not well known.
Therefore, sometimes, when DHEAS levels are measured and found to be high,
this literally indicates that abundant DHEA is readily available. However,
sometimes when DHEAS levels are measured as high, this also may mean that
DHEA is not being produced from DHEAS. Since this is not well known, one has
to look at the pattern of this ratio and interpret it in terms of potential
pathology. So, sometimes high DHEAS may indicate negative or adverse
conditions. I suggest this is the case in the following citations which
connect high levels of DHEAS with preterm delivery.

Mazor, et al., reported that "Maternal plasma DHEA-S concentrations were
significantly higher in women with preterm labor who delivered preterm than
in those who delivered at term." (Arch Gynecol Obstet. 1996; 259: 7-12).
Now, if DHEAS is working normally, the relationship of cortisol ratio
becomes important as an indication that cortisol is too high and
antagonizing the effects of DHEA. (Remember the connection of cortisol to
DHEA above.) Yoon, et al., found this in 1998: "An elevation in fetal plasma
cortisol but not dehydroepiandrosterone sulfate was followed by the onset of
spontaneous preterm labor in patients with preterm premature rupture of the
membranes." (Am J Obstet Gynecol. 1998; 179: 1107-14).

I suggest the "adverse obstetric outcomes" connected with a short interval
between a first pregnancy and a subsequent pregnancy may result from
insufficient DHEA in the mother. These conditions may be ameliorated by
monitoring low levels of, and supplementation with, dehydroepiandrosterone
(DHEA) in women who become pregnant again, soon after a first pregnancy.



British Medical Journal 2003; 327: 313.

 Interpregnancy interval and risk of preterm birth and neonatal death:
retrospective cohort study.

Smith GC, Pell JP, Dobbie R.


OBJECTIVE: To determine whether a short interval between pregnancies is an
independent risk factor for adverse obstetric outcome. DESIGN: Retrospective
cohort study. SETTING: Scotland. SUBJECTS: 89 143 women having second births
in 1992-8 who conceived within five years of their first birth. MAIN OUTCOME
MEASURES: Intrauterine growth restriction (birth weight less than the 5th
centile for gestational age), extremely preterm birth (24-32 weeks),
moderately preterm birth (33-36 weeks), and perinatal death. RESULTS: Women
whose subsequent interpregnancy interval was less than six months were more
likely than other women to have had a first birth complicated by
intrauterine growth restriction (odds ratio 1.3, 95% confidence interval 1.1
to 1.5), extremely preterm birth (4.1, 3.2 to 5.3), moderately preterm birth
(1.5, 1.3 to 1.7), or perinatal death (24.4, 18.9 to 31.5). They were also
shorter, less likely to be married, and more likely to be aged less than 20
years at the time of the second birth, to smoke, and to live in an area of
high socioeconomic deprivation. When the outcome of the second birth was
analysed in relation to the preceding interpregnancy interval and the
analysis confined to women whose first birth was a term live birth (n = 69
055), no significant association occurred (adjusted for age, marital status,
height, socioeconomic deprivation, smoking, previous birth weight vigesimal,
and previous caesarean delivery) between interpregnancy interval and
intrauterine growth restriction or stillbirth. However, a short
interpregnancy interval (< 6 months) was an independent risk factor for
extremely preterm birth (adjusted odds ratio 2.2, 1.3 to 3.6), moderately
preterm birth (1.6, 1.3 to 2.0), and neonatal death unrelated to congenital
abnormality (3.6, 1.2 to 10.7). The adjusted attributable fractions for
these associations were 6.1%, 3.9%, and 13.8%. The associations were very
similar when the analysis was confined to married non-smokers aged 25 and
above. CONCLUSIONS: A short interpregnancy interval is an independent risk
factor for preterm delivery and neonatal death in the second birth.