The article "Shock Waves" by Carolyn Lochhead (Jan.) is simply the best analysis of the bushwhacking that occurred on November 8 throughout this great country. You do not need to read any more articles to get the complete picture. Only two pages long, it should be inserted into every new history book published in the next century. Bravo, Lochhead!
C. Russell Farmer
Rick Henderson ("Sobriety Test," Jan.) offers several issues the Republicans must confront if they are serious about cutting government. All good thoughts. But I'll believe all this talk about giving government back to the people only when I read that Washington-area real-estate prices are in free fall. And when I see angry government employees marching on the Capitol to protest massive layoffs. Yes, Virginia, this is no time to be responsible or polite ("Washington Traps," Jan.). We need insurgents, guerrillas. Are these new Republicans up to the job? My optimism is leavened with skepticism. History shows us that few can resist the siren song of power.
Palm Desert, CA
AIDS Causes, Cont.
As a physician and medical researcher who is not a part of the AIDS-research establishment, but who has made a study of the HIV/AIDS controversy, I was pleased to see REASON tackle the issue ("What Causes AIDS?," June 1994 and "What Causes AIDS: The Debate Continues," Dec.). Let me add a few points:
1) The idea that AIDS in gay men is caused by illicit drug use rather than a virus can be tested by examining the statistical effect of drug use on AIDS risk after HIV infection. For AIDS risk to be associated with drug use before HIV infection but then become independent of drug use after HIV infection suggests that HIV is the critical element, and drug use is simply a marker for behaviors that transmit HIV. We have at least six studies which find exactly such results (for non-IV drugs). Also, the 1993 study discussed in REASON found that immune decline over time in groups of San Francisco men is purely a function of HIV status and has no association with drug use after HIV status is taken into account. This pattern held for the years before AZT became available in 1987, so HIV status was not merely a marker for AZT use, as critics occasionally suggest.
2) Many AIDS risk groups such as hemophiliacs and transfusion recipients and their spouses are not heavy drug users. To explain hemophilia-associated AIDS, authors Thomas, Mullis, and Johnson abandon Occam's razor and postulate that the hemophilia AIDS epidemic results from a second mechanism (this time, gross immune failure due to clotting-factor treatment), which is supposed to have begun to operate at significant levels in hemophiliacs just as the new epidemic of immune deaths exploded among gay men. Even though AIDS appeared epidemically in hemophiliacs and homosexuals a few years after we know a silent epidemic of HIV infection hit both groups almost simultaneously, skeptics nevertheless reject the simple body-fluid borne infection hypothesis in favor of a complicated one, in which the new epidemic of AIDS has as many separate causes as risk groups, and appears at the same time in each coincidentally.
Can we test the clotting-factor causation idea? Just as is the case with drugs, at least two studies find that hemophiliacs who become HIV-positive go on to develop AIDS, years later, independently of how much clotting factor they use after becoming HIV-positive. This again implies that any association between AIDS and clotting-factor consumption prior to HIV infection results simply from the increased probability of contracting HIV the more infected clotting factor is used. After the virus is in the body, clotting-factor use becomes statistically irrelevant, as a viral hypothesis would predict.
Nor does AIDS look toxin-mediated to the epidemiologists, who know that exponentially rising rates of disease are typical of beginning infectious disease epidemics. Ten to 15 years of previous drug use in gay men, even if immunotoxic in ways that cannot be seen in animals, hardly explains the exponential increase in AIDS cases noted in the first four years of AIDS. Similarly, the crude death rate in hemophiliacs during the first quarter of 1984 was nine times what it had been for each of the two preceding years--an abrupt phenomenon not explainable on the basis of a treatment which had first been introduced into this population with wide time variability, more than a decade before. The AIDS plague in hemophiliacs was both real and sudden.
Which brings us to a factual correction: Thomas et al., following Peter Duesberg and Robert Root-Bernstein, have absurdly claimed that "hemophiliacs in the age of AIDS are living longer than they ever did in the past," a myth apparently universal among HIV/AIDS skeptics. In fact, due to clotting-factor treatment, life expectancy in hemophiliacs had risen to nearly normal by 1979, just before the era of AIDS, but fell for the first time in the later 1980s and now has fallen to a figure less than it was before World War II. About half of all clotting-factor-using hemophiliacs were infected with HIV in the seven years before factor concentrate was purified of virus in 1985; since then, between one-fourth and one-third of these infected people have died of AIDS.
3) Hemophilia is not the only problem for HIV/AIDS critics, for data from transfusion AIDS victims also needs explaining. In 1984, even before a commercial HIV-virus test had appeared, a landmark study was published which compared people who developed AIDS after blood bank transfusion with people who had been transfused equally from the same blood bank but remained well. It was found that AIDS victims were far more likely than healthy transfusion control cases to have gotten blood which came from "high-risk activity" donors, such as self-injecting drug users or promiscuous gay men. Only a hypothesis involving infectious microbe(s) plausibly explains a firm statistical link between disease development in blood recipients years after transfusion and the lifestyles of blood donors they had never met.