Excursus 18.104.22.168.1. from Noosomatics Vol. V:
The R4 IA: physiology of this prenatal injury
Homeostasis during gravidity is determined by the adequate mixing organization of the hormones. Any immediate influence on the mixing organization by a woman is normally not possible. An
exception to this are women with the cerebro-physiological switch (CPS) (22.214.171.124.1.). Due to its impact on the rostral nerve center region in the TRO, the CPS, if activated, is able to change the hormonal mixing
organization in favor of the androgens and thus to cancel the pregnancy-saving (progestative) effects of estrogen and progesterone. This prenatal IA can have effect between the 4th month of pregnancy (when the myelogeny of the peripheral nerves of the fetus begins; then, the fetus can survive such an IA) and the 6th month when the autonomy of the TRO of the fetus begins.
At the end of the 3rd month, the fetus becomes independent of the maternal production of estrogen and progesterone (the placenta takes on the production to a large extent), the corpus luteum (the yellow body) degenerates, the fetus can build up their peripheral nervous system, with which the fetus buffers the central nervous system (CNS) of the mother. The effect of nervous stimulation enhances the maturation of the organs and brings about the possibility of relative differentiation; as a result, the maternal testosterone can be transformed into 17-ketosteroids (17-KS) in the fetal liver in order to relieve, in this respect, the placenta and the fetal adrenal cortex in their work, as these have to manage some more tasks (otherwise, an abortion would be the consequence due to the overly limiting effect on the placenta). Via the circulation, the 17-KS reach fetal tissue, which is able to transform them into estrogens with the help of enzymes. The estrogens develop a stimulating effect on the metabolism of the fetus; in particular, they increase, at the heart, the heart minute volume (HMV) by stimulating the estrogen receptors in the right atrium (effecting an increase of the sinus node frequency, i.e. the autonomous pacemaker frequency) and increase the CNS perfusion (the blood itself transporting estrogen at an elevated level).
In the kidney, the glomerular filtration rate (GFR) is increased. Estrogens are released into the placenta at an elevated level: they are the “currency”, so to speak, for the
right to exist (the mother with the CPS is suddenly feeling much better). Due to the permanent delivery of testosterone, the estrogen level is kept irregularly elevated, which has a positive effect on the
mother’s mood on the one hand (the CPS lowers the level of female hormones in women), and leads to an increased activity in the amygdaloid body, in the hippocampus, and in the TRO of the fetus on the other
hand. The TRO of the fetus will become autonomous with an elevated “starter standard value”in the 6th month; after birth, there is a permanently elevated requirement for impulses to initiate activities and to inform thinking. If the requirement is not met from outside or inside, information will be missing (”I didn’t notice that one being said,“ would be the comment).
ADH (the antidiuretic hormone originating from the rostral nerve center region in the hypothalamic region of the TRO and effecting an increased back-resorption of water within the kidney) is
secreted at an elevated level, resulting in further increasing the GFR of the kidney. The kidney produces renin, which transforms angiotensin produced in the liver into A I (angiotensin I), which is further broken
down to A II in the blood and the lungs. This prevents the GFR from overshooting, simultaneously the blood pressure from falling, to maintain the compensatory effect (nb. there is now an acute danger for the mother
to develop pyelonephritis since her uptake of A II may result in an inadequate decrease of her GFR).
Merely considering the fact that the half-life of estrone is about 90 minutes and the plasma half-life of testosterone between 10 and 20 minutes, it is conceivable that the effect of the
increased testosterone production varies depending on the sex of the fetus. A female fetus has a longer compensating possibility than a male one. This increase therefore results in a changed liver activity limited
The increased prenatal testosterone production effects a corresponding quantification of liver products: the male fetus produces even more 17-KS, thus less hemoglobin and erythrocytes; in
the same situation, compared to the male fetus, the female fetus requires less 17-KS, so it produces more hemoglobin and erythrocytes. In the male fetus, this blood-forming effect of testosterone is impeded due to
the transformation into female hormones (to ward off the danger of suffocating).
A confusion of the male and the female principle, which was learned during the perinatal injury, becomes apparent in hemoglobin and erythrocytes in that their levels are at the lower limit
or, occasionally, below in women and at the upper limit and above in men. MCV levels are in the reference range of the other sex. If, in addition, men show a reduction in white blood cells (leukocytopenia) and women
a reduction in blood platelets (thrombocytopenia), this indicates the ”traumaphilia” syndrome (126.96.36.199.), which may prevent this prenatal injury from showing in the laboratory.