"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.