The U.S. is contributing to the spread of HIV/AIDS among African women by its reckless distribution of hormonal contraceptives of all kinds in so-called “reproductive health” programs.
Vol. 12/No. 11
The world’s deadliest killer, HIV/AIDS, and the Birth Control Pill have been carrying on a secret and deadly “love affair” for decades. While women swallowed their “freedom” with the morning orange juice, studies that should have made global headlines yellowed in medical journals, unknown to the general public. Only doctors learned about the pills deadly affair with HIV/AIDS, and they were too busy writing prescriptions for hormonal contraceptives to talk.
More than 50 medical studies, to date, have investigated the association of hormonal contraceptive use and HIV/AIDS infection. The studies show that hormonal contraceptives—the oral pill and Depo-Provera—increase almost all known risk factors for HIV, from upping a woman’s risk of infection, to increasing the replication of the HIV virus, to speeding the debilitating and deadly progression of the disease.1
A medical trial published in the journal AIDS in 2009—monitoring HIV progression by the need for antiretroviral drugs (ART)—saw “the risk of becoming eligible for ART was almost 70% higher in women taking the pills and more than 50% higher in women using DMPA [Depo-Provera] than in women using IUDS.”2
Studies aside, it is well known that HIV/AIDS strikes more women than men. Some would argue that this is a result of the desire of men for young—and presumably uninfected, sexual partners. Few are willing to discuss a more obvious explanation, namely, that the Pill and Injectables render women particularly vulnerable to HIV/AIDS.
How serious is the problem? Oral contraceptives and Depo-Provera
are among the world’s most popular and prevalent contraceptive
methods. According to one study, “Globally, at least 150 million women
currently use hormonal contraceptive methods.”3 In America,
hormonal contraceptive rates are over 52% in unmarried
women—those at greatest risk of HIV/AIDS. Moreover, in the
interest of lowering the birth rate, the UNFPA and USAID continue
unloading boatloads of hormonal contraceptives on Africa, Haiti and
other AIDS-ravaged developing nations.
The best meta-analysis done to date, done by Dr. Chia Wang and her colleagues, surveyed the consensus results of the 28 best published studies since 1985. They found that the “significant association between oral contraceptive use and HIV-1 seroprevalence or seroincidence … increased as study quality increased.” In fact, “Of the best studies, 6 of 8 detected an increased risk of HIV infection associated with OC [oral contraceptive] use.”4
On the National Scale
Moreover, Wang’s results showed even more of a Pill/HIV link when they limited studies to those conducted on African populations. This is significant for two reasons:
First, sub-Saharan Africa is home to the world’s earliest and largest heterosexual HIV/AIDS epidemic, which to date has infected an estimated 22.4 million5 people. This is two-thirds of the total number of infections worldwide.
Second, sub-Saharan Africa has endured decades of contraception-focused population control programs and countless hormonal-contraceptive trials. “Among the six [African] countries hardest hit by the HIV/AIDS epidemic … two in three users in the six countries rely on the OC (oral contraceptives) or injectables,”6 said Iqbal Shah of the World Health Organization.
Likewise, Thailand, praised for a contraceptive prevalence of 79.2% in 2000 and upwards of 70% today, is a land where, “More than one-in-100 adults in this country of 65 million people is infected with HIV.”7 Among Thai women, “Oral contraception is the most popular method.”8, 9
On the other hand, Japan’s HIV rate is, at 0.01%, one of the lowest in the world.10 In this context, it is important to note that the birth control pill was illegal in Japan until 1999, and even today only 1% of Japanese women use oral contraception. Similarly, the predominantly Catholic Philippines, with a longstanding popular resistance to contraception, boasts an HIV “prevalence rate of only 0.02%.”11
Hormonal Changes Heighten HIV Risk
The studies that demonstrate a connection between hormonal contraceptives and HIV/AIDS infection postulate a number of mechanisms at work.
First, let’s review the basics. The Human Immunodeficiency Virus (HIV), is carried in warm blood or sexual fluids. It infects through fragile, inflamed, bleeding or needle-pricked tissue, attacks specific T-cells in the immune system, and causes the incurable, debilitating condition known as AIDS (Acquired Immunodeficiency Syndrome).
Hormonal contraceptives increase almost all known risk factors for HIV infection.
Studies have found that hormonal contraceptives “alter the microenvironment of the female”12 and boost the cell count of those specific cells that HIV uses to infect and proliferate (HIV co-receptor CCR5 in cervical CD4+ T lymphocytes).
What is more, a progesterone side effect known to American women as “breakthrough bleeding,” is caused when hormonal contraceptives excessively thicken the uterine lining. The large, bleeding surface of the uterus creates an ideal site for HIV infection.
Progesterone also has an immunosuppressant effect, which means that women using hormonal contraceptives have less in the way of natural defenses against HIV and other STDs, such as chlamydial infection or genital herpes (HSV-2).13, 14 In one study, “HSV-2 infection itself more than tripled the risk of HIV infection.”15
In the vagina, increased blood and the independent hormonal effects of the Pill eliminate the natural pH acid protection against infection. What is more, a famous study of rhesus macaques found that hormonal contraceptives thin the vaginal walls and markedly increase SIV infection (the monkey equivalent of HIV).16 Vaginal dryness, another side effect of hormonal contraceptives, is not only painful but also makes one prone to tears and abrasions—fertile sites for infection.
One study points out, “On a cellular level, hormonal contraceptives have been associated with cervical and vaginal inflammation.”17
Further, hormonal birth control causes the fragile cervical tissue to grow beyond its natural bounds and replace what would normally be thick, protective membrane. This “cervical ectopy” is dangerous because the cervix’s thin surface is the main site of HIV infection.18
Given all these different ways that hormonal contraception promotes HIV/AIDS infection, it is not at all surprising that several studies show women on the pill, Depo-Provera, etc., are more likely to be infected with not just one, but several variants or strains of HIV. This “in turn leads to higher levels of viral replication and more rapid HIV-1 disease progression.”19, 20, 21
Women on hormonal contraceptives are not only more likely to contract HIV/AIDS, they are also more likely to pass it along to their sexual partners. The three studies which focused on “the impact of hormonal contraception on cervical shedding of the cell-associated virus”22 all found that HIV-positive women on hormonal contraceptives are far more likely shed HIV in their body fluids. High-dose pill users were over 12 times more likely to shed the HIV virus than women not using contraception, low-dose users were almost 4 times more likely, and Depo-Provera users were 3 times more likely.23
The Pill Pushers Push Back
Some dismiss out of hand the impressive body of scientific research demonstrating a Pill/HIV link. They quote from the handful of studies and highly selective trials which claim to find “no increase in HIV risk among users of oral contraceptives and Depo-Provera.”24
The problem with many of these studies, such as Mati et al. 1995, Kapiga et al. 1998, and Sinei et al. 1996 is that they were conducted with and through “family planning clinics.” Since the chief business of these clinics is the promotion, sale, and distribution of contraceptives, the possibility of bias is undeniable. Who would trust Marlboro to monitor a study on the link between cigarettes and cancer?
Moreover, the handful of studies that deny a link between
hormonal contraception and increased risk of contracting HIV are
dwarfed by the many studies that have not only found such a link, but
convincingly explained precisely what it is about such contraception
that contributes to the spread of the disease.
Yet population control groups continue to lobby for more contraception, not less. Take Dr. Willard Cates, president of the Institute for Family Health of Family Health International (FHI), one of the major purveyors of hormonal contraception to the developing world. Wrote Cates to the Journal of American Medical Association, “Preventing unintended pregnancies among HIV-infected women who do not currently wish to become pregnant is an important and cost effective way of preventing new HIV infections of infants. … More must be done to ensure access to safe and effective contraception for HIV-infected women.”25
Obviously, FHI’s concern here is less to prevent the infection of preborn infants, than to continue to contracept as many women as possible with your tax dollars and mine. What the organization refuses to admit, however, is that by doing so it is arguably contributing to the spread of the HIV virus.
How many lives are being lost because we continue to ship boatloads of hormonal contraceptives to a continent and to countries laboring under an HIV/AIDS pandemic? Isn’t it time that we stopped?
See the full report in the upcoming May/June Issue of the PRI Review.
1 Baeten et al. 2003, “Hormonal Influences on HIV Disease and Co-Morbidites.” J Acquir Immune Def Syndr. 2005, Vol 38, Suppl 1: S19
2 http://www.iasociety.org/Article.aspx?elementId=11977; Stringer et al, AIDS. 2009, 23:1377-1382
3 Morrison et al., 2009, Best Practice & Research Clinical Obstetrics and Gynaecology 23 (2009) 264
4 Wang et al., 1999, JAIDS
6 Shah, I. 2003, J Acquir Immune Def Syndr, 2005
10 http://apps.who.int/globalatlas/predefinedReports/EFS2006/EFS_PDFs/EFS2006_JP.pdf. (Homosexual men account for just over half of Japan’s domestic HIV cases.)
12 Prakash et al. 2004; Prakash et al. 2002; Furth et al., 1990
13 Baeten et al. 2001; Cottingham et al. 1992; Avonts et al. 1990; Louv et al. 1989
14 Hunt et al. 1998; Zang et al. 2002; Gillgrass et al; 2003
15 http://www.iasociety.org/Article.aspx?elementId=10470; Baeten et al. 2007
16 Marx et al. 1996; Abel et al. 2004; Veazey et al. 2005
17 Baeten et al. 2001; Ghanem et al. 2005
18 Baeten et al. 2007; Critchlow et al. 1995; Louv et al. 1989; Plourde et al. 1994
19 Beaten et al. 2003; Poss et al. 1995; Long et al. 2000
20 Furth et al. 1990
21 Baeten et al. 2007, Clinical and Infectious Diseases, 360-361
22 Stringer et al. 2008
23 Wang et al. 2004; Mostad et al. 1997; Clemetson et al. 1993
24 Mauck, C. 2005, S11; Studies noted: Mati et al. 1995; Kapiga et al. 1998
25 JAMA. 2006; 296:2802