Wednesday, August 02, 2006


Math Professor Explains Why HIV/AIDS Model Doesn’t Add Up


Originally published in Zenger's Newsmagazine, July 2006

Copyright © 2006 by Mark Gabrish Conlan for Zenger's Newsmagazine

In 1997, Rebecca Culshaw was a graduate student in mathematics with an interest in pursuing “mathematical biology,” the application of mathematical models to biological problems. Her thesis advisor steered her to HIV research because it was a hot field, and Culshaw won both her Master’s degree and her Ph.D. with modeling work aimed at predicting the rate at which HIV would replicate in the human body. But by the time she received her Ph.D. in 2002, she no longer believed in her own work because she no longer accepted the central premise that HIV or any other single virus could cause AIDS.

Today Dr. Culshaw is a math professor at the University of Texas’s Tyler campus, and her apostasy on the HIV/AIDS question has pushed her out of the mathematical biology field and towards more theoretical branches of mathematical modeling. Early this year she published two articles on the Libertarian Web site, one called “Why I Quit HIV” — discussing how she encountered the alternative scientific perspective that AIDS is a long-term toxic condition rather than an infectious disease — and a follow-up called “Why I Quit HIV: The Aftermath,” detailing the responses she got to her first piece. While some of them bore the nastiness and personal attacks frequently leveled by defenders of the HIV/AIDS model against its critics, many were surprisingly supportive, including one from a social worker who works with “HIV-positive” women prisoners and told Culshaw “they always seemed more scared than sick.”

Zenger’s: Why don’t you start by telling me a little of your background, and what field of science you’re involved in, and how you got interested in it.

Rebecca V. Culshaw, Ph.D.: I’m actually a mathematician, and specifically a mathematical biologist. When I got to university I actually wanted to do medical research, but I gradually got less interested in that and I started taking more math classes. I got a math degree, and then when I finished my math degree I went to do a Master’s. I had to do a thesis, and I discovered that there are people that were doing mathematical models of infectious diseases. I thought this would be a perfect thing for me. I discovered that I could make and analyze models of infectious diseases, and the really big field at the time was HIV modeling. I’d been interested in this anyway because I thought it was an interesting disease, and I wanted to learn more.

So I started working on immunological models, not to analyze data or do epidemiology, but to use differential equations to analyze the evolution of a disease and its interaction within a single person’s body. This was a really big field at the time, and I started working on that in 1997. I wrote a thesis and we got a paper out of it. I wasn’t sure if I wanted to go on, so I took two years off and I worked as an actuary for a while. I was over in England for a while, working in a pub and that kind of stuff. After I worked with the insurance company, I decided that I wanted to go back and do more research. So I started in a Ph.D. program in the beginning of 1999.

I knew I wanted to do mathematical biology, but I wasn’t really sure that I wanted to work on HIV anymore. I wasn’t convinced that was where I wanted to go, but my advisor convinced me that I’d already started on this, and so I might as well continue. I started looking at some models of the interaction of HIV with the immune system and the natural immune response. At the time, the big thing was natural killer cells and their role in disease progression. I also started looking at treatment models. For my doctoral work, I started looking at using a different branch of mathematics, called control theory, to investigate what would happen if we tried to implement different kinds of treatments.

The hope with these models is they’ll help to streamline the process of designing clinical trials, for example, by showing what kinds of effects various treatments would have on the different surrogate markers. Instead of just picking things randomly, the idea is to establish some theoretical basis for saying this is more likely to work, so this is what we’re going to use. I finished my Ph.D. in 2002.

Zenger’s: When did you start having doubts about the HIV/AIDS model, and why?

Culshaw: That’s sort of a complicated question, because when I think about it objectively, I’d been having doubts about it for a lot longer than I have saidthe two papers that I wrote. Early on, during the AIDS era, I remember, even as a teenager, thinking that there was a big rush to judgment; people saying basically, “HIV equals AIDS.” I remember when Magic Johnson came out and said he was HIV-positive and all these people were saying, “Oh, Magic Johnson has AIDS.” I remember thinking, “This is ridiculous. He doesn’t have AIDS. He’s perfectly healthy. He’s HIV-positive. This is not the same thing.”

At the time, I didn’t think there was any doubt that this was the causative agent, but I remember thinking there’s something wrong here when people are saying that two different things are the same thing. I remember when I was working on my Masters’ thesis, and I’d been reading a lot of the biological papers for background, some things just weren’t adding up. I was thinking, at the time, that science was not perfect, we don’t understand everything yet, and I really bought into this whole “mysterious virus” thing.

I was on my way to a conference to present a talk, and for some reason I had picked up Spin magazine. I never read that magazine, so it was weird that I had picked it up, but there was an article by David Rasnick called “Blinded by Science.” This was the first time I’d seen that anybody ever had any doubts about HIV, and that actually scientists were having doubts about this. I thought, “Wow, this really makes sense. I had no idea there were doubts. This is really interesting.”

Then I kind of forgot about it for a while, because I had left academia, and it just wasn’t really at the forefront of my mind. When I went back to do my Ph.D., I still had some lingering doubts, like I — at the time I was still kind of in the co-factor camp. I thought, “Well, there are just too many things that don’t add up. There must be some sort of co-factors involved here.” But it would be interesting to work on mathematical models, and maybe understand more how that might work. So that was where I was with that for a long time. To be honest, after I finished my Ph.D. I felt, “I’m going to work on something else now,” and I sort of stopped thinking about it for a while. It’s only been in the last couple of years that my doubts were just really solidified from reading more of the information, basically.

Zenger’s: What were the factors that actually decided you that what we have been told about AIDS cannot be true and that HIV cannot be the cause of it, certainly not the way the mainstream says it is?

Culshaw: There were a lot of different deciding factors, to be honest with you. It was more an accumulation of information, some of it scientific but some of it political and sociological. I’ll start with the scientific evidence first. When I read some of Peter Duesberg’s stuff, I had never known what the difference was, really, between a virus and a retrovirus. I didn’t realize, for example, that our cells can produce retroviruses but they can’t produce real viruses — well, not “real viruses,” I don’t mean.

Zenger’s: Meaning the difference between an endogenous and an exogenous virus.

Culshaw: Yes, thank you. Good. So I read his 1989 Proceedings paper, “Correlation but Not Causation,” and also the paper about “Retroviruses as Carcinogens and Pathogens,” and thought, “This man obviously understands how retroviruses work, and if he’s going to say that there’s just no way they can kill cells the way people are saying that they’re going to. I have to take that seriously.”

Also, it seemed like the scientists were always changing their minds about things. This is something I experienced very directly, as somebody that was doing research in the field. It takes a long time to write a math paper. Not to mean any disrespect to biologists, but if you’re a biologist you can run your experiments, you can get some results, and even if it doesn’t do what you think it’s going to do, you can usually publish it pretty quickly. But if you’re a mathematician, if you propose some sort of theory or something and you can’t prove it, then you have nothing.

As a consequence, it will usually take several years from the start of a paper to getting it finished, refereed and back, and actually published. It will be up to three to four years at times. It happened to me on more than one occasion that I would cite some sort of reference on the dynamics of T-cell killing, for example, and as I worked the authors of the references I was citing kept changing their minds. That was a red flag that kind of came up for me, was why do they keep changing their minds? Do they not know how the T-cells are dying?

The reviewers would come back and they’d say, “Oh, this reference, it’s three years old, it’s out of date.” This would happen more and more, and I would think, “How can they just keep changing their minds?” Obviously, there’s something wrong here. This is not an accumulating body of secure knowledge that they’re building on. It’s more like they’re knocking the whole thing down a few years and just starting over with something else, all the while maintaining that this virus is at the center of it all. That just didn’t add up to me. So I guess, scientifically, those were the main things.

And also, the fact that there never was any agreed-upon mechanism of how the T-cells actually died. I thought that was suspicious. I thought, “How can they possibly spend this many billions of dollars and still not know how this virus works? It’s ridiculous. If we’ve got great brains working it out and they cannot figure out this problem, this virus cannot be that mysterious.”

I became more aware of what was happening within the scientific community to people who would question the hypothesis. Obviously, Peter Duesberg is the biggest example of somebody whose career has just been ruined by just the fact that he expresses doubts. I get very suspicious whenever I see this sort of massive consensus and belief. To me, it doesn’t guarantee that the people are wrong on their consensus is over, but it’s certainly a big red flag that there’s something. Why are they protesting so much? I thought that was a little strange. So I guess those are the main things that made me doubt.

Zenger’s: You said there were not only scientific reasons but also what you called political and sociological reasons.

Culshaw: O.K., so I’m not sure how to put this so that it really makes sense, but I read a lot of John Lauritsen’s work, and a lot of the things that he said made sense to me, about AIDS is really used as a social weapon. I don’t think that the government came up with this in order to try to oppress certain groups of people in society, at least not consciously, but it seems like there’s so much blame being thrown around. It’s disguised as political correctness and compassion and everything like that. There is a large proportion of society that is very bigoted, I think. I see it a lot of the time, especially living in East Texas, and people who are very uncomfortable with people who live lifestyles that are different from their own. Somewhere around the 1970’s and 1980’s it became much less popular — I hate this term, but I’m going to use it — to Gay-bash.

Then it seemed all of a sudden like AIDS sprung up. Boom! Then people could just say, “Oh, no, we’re not actually being homophobic at all, or racist, or whatever” — because there’s a very big racist component to AIDS as well. “We’re being compassionate. We really care.” To me it just stinks. I don’t understand how some of these government researchers can say that they’re being so “compassionate” when they have all of these programs in place to take away the civil liberties of anybody who’s just diagnosed HIV-positive. I mean, that’s just completely outrageous to me. Also, I think the religious Right just jumped on it. A lot of people were talking about “God’s wrath” at the time, and I think that a lot of people still think that way on some level, but it’s so internalized that they don’t even know it.

Zenger’s: I’ve raised the question, as a Gay man, of why does my community believe in HIV so totally and come down so hard on other Gays who dissent. It wasn’t just the predictable enemies of the Gay community who adopted that, it was Gays themselves who initially just leaped on to the HIV model as saying, “Oh, no. It’s not us. We’re not to blame. It’s not our lifestyle. It’s a virus.”

Culshaw: But, ironically, the whole virus thing has been turned around and now is used to place blame on people anyways. If somebody becomes HIV-positive, there’s this kind of blame that says, “You were irresponsible. You did things that you shouldn’t have done. You were bad, you were promiscuous, you did drugs,” or whatever it is. Even though it’s supposed to be this virus that doesn’t discriminate, people still use it to discriminate.

And everything is just moralizing. The line is, “If you don’t use a condom you’re an idiot.” basically. The amount of moralizing that goes on about this disease —from every aspect of it, from prevention campaigns to if you dare express a doubt that there’s a virus causing it — is crazy. I mean, there’s no rational discussion happening here, as far as I can see.

The average person on the street has a very distorted idea of what AIDS is, or what HIV is, or how effectively it’s spread. People just don’t know. And even if the HIV model of AIDS turned out to be correct, there’s still all sorts of misinformation. Most people think, for example, that “viral load” is actually measuring viruses. Nobody in the medical community is ever going to say that that’s not what they’re doing.

Zenger’s: Something you said earlier, it reminded me of a comment [pioneering New York AIDS physician and researcher] Joseph Sonnabend made when I interviewed him. He said it’s perfectly possible that HIV does cause AIDS, but that it causes it in the normal way viruses cause disease, which is that most people exposed to the virus don’t get an active infection; most people who get an active infection don’t get sick; and most people who get sick don’t die. Yet, as you pointed out, one of the basic principles of the HIV/AIDS model is that everyone who comes in contact with HIV will develop an active infection, will get AIDS and will die.

Culshaw: That leads into another thing that really bothers me about about the way the orthodoxy approaches this whole thing, and this would be a problem even if HIV is a real virus and even if it causes AIDS. There’s just no hope. They like to give lip service to the idea that they have these great new drugs and you can live a normal life for a long time,” blah blah blah, but the whole thing is marketed as this campaign of doom.

To me, that’s criminal. It’s just a horrible thing to do. I was reading something on some orthodox Web site — and they were discussing these “Four Stages of Disease.” I think there were four; I can’t remember exactly. They were based on T-cell counts. Stage IV was, I think, with less than 200 T-cells, and the Web site said something like, “Well, once you’re in Stage IV, you can never go back into any of the other stages even if your T-cells increase.” I thought that was ridiculous.

They’ve written it into the definition that you can’t recover, even if you do. People are just given absolutely no hope. There’s no other disease I can think of for which people are given no hope. Even the most horrible types of cancer, there’s an optimistic hope offered to patients that “cancer can be beaten.” There’s this sign in one of the parks around the town where I live, this big “cancer bell,” and it says, “Hope rings eternal. Cancer can be beaten.” I thought, “Well, nobody would ever say that about AIDS.”

I know other people have said this before, but it’s like a death cult. You can’t ever hope to get better. You cannot ever hope to recover, and if you get infected by this thing that might be a virus, then you can never clear it. This idea may have worked to some extent in modifying people’s behavior a little bit in the early days, but ultimately it’s a self-fulfilling prophecy, because if you think that you’re doomed, you’re very likely going to get sick, even if there’s nothing wrong in your body at all.

Zenger’s: Was there anything specifically relating to your area of scientific expertise that you could cite as a reason to question the HIV/AIDS model?

Culshaw: It wasn’t so much what I did find as what I didn’t find. Everybody that would create a model would make all these assumptions. They would assume that HIV was killing T-cells in this way, and that it was happening at all these different rates, and they’d have all these parameter estimates. You’d look at one paper and it’d have these parameter estimates, like this is the rate of T-cell clearance in the body, and they wouldn’t agree necessarily from paper to paper. Sometimes I actually came across some models where they just made up some parameters. They didn’t actually get these parameters from anything, you know, any real-life people or anything. They just made them up in order to make their model work. That was suspicious in and of itself.

As mathematicians, we’re trained to be very, very skeptical of our own theories. If you come up with some model or some idea that works for basically everything you’ve observed, you state it as a conjecture and then you try to prove it. But you never, ever, ever say, “Well, I’ve seen all these examples, and it works for all these examples, therefore it must be true.” You can’t do that. You would never finish your course, let alone get anything published.

Another thing is that if you have a theory, and you come across one counter-example that flies in the face of that theory, then you have to throw it out. You cannot use it again. It seemed to me, like with the HIV theory, not only were they using a bunch of examples but they were throwing away every counter-example that they found. I understand that medicine and biology are not as rigorous as mathematics, and there might be a little bit more room to move when it comes to proving things, but it seemed that they came up with this theory, and when it didn’t fit the observations, it wasn’t the theory that’s wrong, it was the observations. That’s counter-natural. That’s not the way science should work.

Zenger’s: Just one final question: what are you doing professionally right now?

Culshaw: I’m working on theoretical mathematics. As I mentioned before, I was using optimal control theory to work on these treatment models, and so I’m working on some more theoretical problems on control theory. I’ve distanced myself, at this point, from mathematical biology because, even though I haven’t had a whole lot of response from the mathematical biology community, I have the sense that referees in that field would not be terribly friendly to me. So I’m going to stay away from that field for a little while and concentrate on the theoretical aspects of mathematics.

Web references for the articles referred to above:

By Rebecca Culshaw:
“Why I Quit HIV”:
“Why I Quit HIV: The Aftermath”:

By AIDS dissidents:
Peter Duesberg: “Retroviruses as Carcinogens and Pathogens: Expectations and Reality” (1987):
Peter Duesberg: “HIV and AIDS: Correlation but Not Causation” (1989):
Peter Duesberg and David Rasnick: “The AIDS Dilemma: Drug Diseases Blamed on a Passenger Virus” (1999):
David Rasnick: “Blinded by Science” (1997):