February 27, at the 9th Annual Retrovirus Conference in Seattle, researchers
reported that "In a study of 115 female commercial sex workers with HIV, those
who were on hormonal contraceptives - primarily birth control pills or
injectable progesterone - at the time of infection had a five- to seven-fold
higher risk of becoming infected with multiple strains of the virus than those
not on hormones." One author of the study suggested this may be due to "birth
control pills [causing] thinning of the vaginal lining," while another author
says it may be "the hormones may change the cell population in the genital
tract, possibly increasing the number of cells that are targets for HIV."
Another hypothesis, directly tied to known effects of the estrogenic
components of oral contraceptives, ethinyl estradiol and mestranol, as well as
"injectable progesterone," may explain the report. In 1985, I first connected
low levels of the adrenal androgen, dehydroepiandrosterone (DHEA), with AIDS.
It is my hypothesis that DHEA optimizes transcription and replication of DNA,
therefore, all tissues are negatively affected by low DHEA. I suggest low
DHEA results in reduced immune response to HIV infection and that the symptoms
of AIDS actually represent further loss of DHEA during disease progression.
A study of "oral contraceptives" found a significant decrease in DHEA in all
groups using different oral contraceptives (Contraception 1996; 53: 171-6).
Ethinyl estradiol, predominantly, and mestranol, secondarily, are the
estrogenic components of various mono-, bi-, and triphasic, combination oral
contraceptives. Ethinyl estradiol in oral contraceptives reduces DHEA
(Contraception 1998; 58: 75-81 and Eur J Endocrinol 1999; 141:579-84) as does
mestranol (Obstet Gynecol 1984; 63: 12-4). This reduction in DHEA is
attributed to reduced production of DHEA by the adrenal glands, not the
ovaries which are a source of smaller amounts of DHEA (Am J Obstet Gynecol
1978; 132: 380-4). Noristerat and depo-provera (medroxyprogesterone) are the
two injectable progesterone contraceptives. There is no research regarding
the effects of noristerat on DHEA. However, in women using depo-provera as a
contraceptive, DHEA was significantly reduced (Contraception 1986; 33:
503-17).
In animal models, DHEA protects against a number of deadly viruses, including
West Nile, Sindbis, and Semliki Forest viruses (Arch. Virol. 1991; 120: 263).
I suggest that low DHEA increases vulnerability to HIV infection. The fact
that oral and injectable contraceptives reduce DHEA may be the reason that
contraceptive use increases the probability of HIV infection.
James Michael Howard
Fayetteville, Arkansas 72701-2046
U.S.A.
