"(1)The demographics of positive HIV tests are unlike those of any infectious agent, and
(2) frequency of positive tests does not correlate with incidence of AIDS;
set out fully in The Origin, Persistence and Failings of HIV/AIDS Theory (McFarland 2007). Since writing the book I have found further supporting data in the US data on deaths from ‘HIV disease’, see posts on my blog, hivskeptic.wordpress.com:
(3) the age distribution of positive HIV tests superposes on the age distribution of deaths;
(4) the risk of death alleged to be from HIV disease does not increase exponentially with age in the manner found in all other diseases and in all-cause mortality.
(5) The HIV tests do not detect specifically a retrovirus."
(numbers added)
Each of these claims - the five pillars of Henry's thesis - is utter nonsense. But like Tolstoy's unhappy families each of Henry's five central claims is ridiculous in its own way. I'll look at each in turn in the next few posts.
------------------------------------------------------------------------
(1) “The demographics of positive HIV tests are unlike those of any infectious agent”
ACTUALLY, HENRY, THEY'RE A LOT LIKE the demographics of numerous other infectious agents.
No two infectious agents have exactly the same demographic pattern, and a even single pathogen will vary in its demographic patterns from time to time and place to place.
The demographics of different infectious diseases vary according to transmissibility and the relative importance of different transmission modes, the natural history of each infection, and the impact of human efforts to control them at different times and places: preventive public health interventions and, where available, treatments. The commonalities and the differences between patterns of age, sex, geography, racial and other social groups - and also rates of change in these parameters - shed light on the unique epidemiology of each pathogen. HIV is no different to any other bug in this regard.
Even before the discovery of HIV, the earliest epidemiological studies of AIDS strongly suggested an infectious rather than a non-infectious cause, because of the striking similarities between the demographics of AIDS and those of an already known infectious disease, hepatitis B. Like hep B, AIDS and ARC disproportionately struck gay men, injecting drug users, blood product recipients (prior to screening), the sexual partners of people with the condition and babies born to mothers either with, or at risk of the condition.
IT IS EASY TO FIND examples for most of the demographic indices of HIV in the US that have parallels in other infectious diseases. For example, Henry tries to claim that AIDS cannot be the result of a sexually transmissible infection because the median age of diagnoses was around the mid 30s, while the commonest STIs (chlamydia, HPV and HSV) have their highest rates of incident infections in the teenage years to early 20s.
"When first named in the early 1980s, AIDS was diagnosed in people (largely men) whose average age was in the mid-30s (A). That already throws into serious doubt the notion that AIDS is brought about by a sexually transmitted agent, because it’s teenagers and people in their early twenties who are most prone to incur sexually transmitted diseases (STDs) or infections (STIs) (B). "
Elsewhere he claims:
"That first positive tests come at a median age in the mid-30s or somewhat later is not compatible with the hypothesis that a positive “HIV”-test signifies a sexually transmitted infection."In fact, the age distribution of incident HIV diagnoses in the US just happens to be very similar to that of another sexually transmissible infection, syphilis: this table shows incident primary and secondary syphilis by age: the median age of diagnosis from 2003 to 2007 was in the mid to late 30s (largely men). By Henry’s reasoning this “throws into serious doubt the notion” that syphilis is brought about by a sexually transmitted agent!
HENRY ALSO TRIES TO USE the relatively high seroprevalence of HIV among US blacks compared whites to argue that that what is detected by HIV antibody tests cannot be a sexually transmissible entity: he argues that for this to be possible there would have to be commensurate differences in sexual and drug using behavior between races, a proposition he dismisses as too “racist” to even countenance, as if having sexual intercourse or taking intoxicants are behaviors that inherently place people beyond the pale of decent human society.
In fact the reasons why HIV seroprevalence has grown more rapidly in black communities than in white (from a baseline of virtually zero in both groups around 1977) are more complex than simply reflecting in a directly proportional manner overall rates of unprotected sex or needle sharing.
But there is a much simpler test to take to Bauer’s claim that the racial distribution of HIV seroprevalence indicates that it cannot reflect an infectious entity:
Here are the syphilis rates by race, 1998 - 2007 :
And the gonorrhea rates by race :
Both display a fairly similar pattern of racial distribution to that of HIV - although there is no reason why they necessarily should: while sexual transmissibility is a shared characteristic there are also major differences in factors like chronicity, curability, per-contact transmission and even the types of contacts that typically result in transmission.
Nonetheless, if Henry claims to be an HIV/AIDS “Rethinker” on the basis of the age distribution of HIV diagnoses or the racial distribution of HIV seroprevalence in the US, then he also needs to be a Syphilis “Rethinker” and a Gonorrhea “Rethinker”!
Can we expect Henry to soon claim that Treponema pallidum and Neisseria gonorrhoeae have never been proven to exist, cannot be infectious entities, let alone sexually transmissible? And that doctors who treat these conditions are nothing more than dupes of a corrupt scientific faction who are exploiting gays, blacks, thirty-somethings and other minorities to push their fiendishly evil treatments?
3 comments:
Hi Snout
That is pretty much a killer argument against Bauer's misconceptions and I assume that he is aware of it. Has he, or any of his followers, ever tried to answer it, as far as you are aware?
SteveN
Not that I know of, Steve.
If you try to raise problems with his "theory" like this his usual response is to ignore and delete, or to dismiss them as "trivial nit picking". Or to Gish-gallop off on to another tangent. Or to move the goalposts. Standard denialist rhetorical practice.
A constantly recurring problem with Henry's "theory" is that his arguments often rest on patently false or only very vaguely defined assumptions, and he goes to extraordinary lengths to avoid being pinned down on these.
Like other denialists he invents supposed "rules" for fields of science he's proudly and openly ignorant of, and his followers rarely challenge him on this because they are just as clueless about the basics as he is. He poses as an educator, but in fact it's a con.
In this case the assumption he's trying to get you to swallow is that infectious diseases (and STIs specifically) as a class have a single and predictable pattern of demographics - including a predictable degree of irregularity over time and place - and that HIV doesn't conform to this. It's just nonsense.
As for his followers, well I have yet to see any defence of his assertions mounted here, which is a little disappointing, but not surprising.
What is more interesting is that the age distribution for syphilis is distinctly bi-modal. There is actually a dip in the 30-35 age group.
How does Bauer explain this?
It should be obvious that any simplistic notions of how an STI "should" spread are hopelessly inadequate.
The same pattern of argumentation is seen with other Denialists. They come up with a "killer" argument against HIV put fail to test the same argument on other pathogens.
At least those lunatics who deny the whole germ theory of disease are consistent
Post a Comment