Intended for healthcare professionals

Rapid response to:

Papers

Birth weight of offspring and insulin resistance in late adulthood: cross sectional survey

BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7360.359 (Published 17 August 2002) Cite this as: BMJ 2002;325:359

Rapid Response:

Re: Transgenerational link with maternal insulin resistance may not be 'genetic'

In my third response to Lawlor, et al., above, I point out my
hypothesis that testosterone reduces overall availability of DHEA,
regarding preeclampsia. Now, my work also suggests that levels of
testosterone affect abilities usually attributed to “the environment.”
More specifically, I think early puberty and increased testosterone
adversely affect final development of the brain. This suggests that the
ability to learn is adversely affected by high levels of testosterone.
This is supported: “The presence of learning disabilities was
significantly associated with higher salivary testosterone.” (Physiol
Behav 1993 Mar;53(3):583-6). Therefore, individuals who exhibit these
qualities, i.e., higher testosterone, may lack the abilities necessary to
compete in a job market increasingly dependent upon advanced learning;
they will be increased in percentage in low socioeconomic levels.

In 1985, I developed my hypothesis that the “stress hormone,”
cortisol, evolved to counteract the effects of DHEA. This has just
recently been supported: “We have demonstrated that each steroid has its
distinct gene expression profile, although DHEA and testosterone co-
regulated most genes in a similar direction while glucocorticoids
frequently regulated the same genes in an opposite direction.” (Horm
Metab Res 2001; 33: 691-5) Therefore, stress may affect birth outcome; it
would simply be worse in a woman of higher testosterone.

(I apologize for my delayed response; I have been on vacation.)

Competing interests: No competing interests

26 August 2002
James M. Howard
1037 Woolsey Avenue, Fayetteville, Arkansas 72701-2046, U.S.A.