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Archived Comments for: The adverse neuro-developmental effects of postnatal steroids in the preterm infant: a systematic review of RCTs

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  1. The problem may be low DHEA...

    James Howard, independent biologist

    16 April 2004

    It is my hypothesis that DHEA was selected by evolution because DHEA may optimize replication and transcription of DNA. (I think an increase in DHEA in evolution produced the mammals and their large brains. "Hormones in Mammalian Evolution," Rivista di Biologia / Biology Forum 2001; 94: 177-184 ) Therefore, I suggest all tissues depend on DHEA for optimal growth.

    Mothers provide DHEA for themselves and their fetuses. When circumstances reduce maternal DHEA or cause interference with the availability of DHEA, the maternal-fetus unit is diminished, usually adversely affecting the fetus more than the mother. I suggest this is the main cause of prematurity or small for gestational age infants.

    A subordinate hypothesis of the foregoing hypothesis is that DHEA use by cells, therefore growth and development, acts in the same manner as addiction. That is, a signal is released from tissues that triggers DHEA production and subsequent use by the signalling tissues. (In fact, I suggest this is the mechanism triggered by all drugs of abuse in adults and results in recruitment of DHEA.) I suggest this is the mechanism which postnatal steroids trigger to provide benefit when they "work."

    If an infant can produce a trigger or signal response to a postnatal steroid, then the postnatal steroid will recruit DHEA and the stimulated DHEA will aid growth and development. However, if the infant cannot produce, or produces an insignificant, rebound of DHEA, then the infant cannot respond sufficiently to overcome the negative effects of the postnatal steroid. This results in adverse effects on the part of the body which I think is most sensitive to DHEA levels, the brain.

    I suggest this explains why some infants are adversely affected by postnatal steroids while some benefit. Perhaps DHEA should be substituted as a treatment for growth-deficient syndromes in infants so affected.

    Competing interests

    None declared

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