Mainstream pseudo-science good, alternative pseudo-science bad

HIV/AIDS vigilantes like to accuse promoters of alternative treatments of threatening lives. In South Africa they have campaigned against Matthias Rath for pointing out the considerable health benefits of vitamin supplements for malnourished people. President Thabo Mbeki has been charged with the needless deaths of hundreds of thousands of people for questioning  the worth of antiretroviral drugs, and his Health Minister, Manto Tshabalala-Msimang, was sarcastically referred to as “Dr. Beetroot” for suggesting the value of some natural remedies.

But when properly “scientific” Westerners discover that naturally occurring substances might make good medicine, of course that’s something else. So the discovery by UCLA’s AIDS Institute was reported reverently, that “the herb Astragalus root may help fight HIV” [UCLA’s AIDS (“Beetroot”) Institute discovers how HIV kills cells, 2 January 2009]. Not to be outdone, Houston researchers have identified an ingredient of green tea as active against “HIV” even at physiological concentrations:

“Thursday, February 5, 2009, 3:15pm CST
Houston researchers cite HIV breakthrough
A chemical that occurs naturally in green tea appears to prevent HIV-1, the virus that causes AIDS, from infecting cells in the immune system and could prove a valuable component of treatment for the disease, according to a report by researchers from Baylor College of Medicine and Texas Children’s Hospital.
After further research, the study could move to human trials, the researchers said Thursday.
In previous studies, Dr. Christina Nance, assistant professor of pediatrics at BCM, and Dr. William Shearer, professor of pediatrics at BCM, had demonstrated that epigallocatechin gallate — EGCG — found in green tea, inhibited infection in a specific HIV-1 strain.
The latest discovery shows EGCG can inhibit infection in multiple HIV-1 strains.
‘This is paramount from a global aspect,’ Nance said. ‘Most initial studies with HIV-1 in the Americas are based on subtype B.’ However, she added, most of the world is infected with other strains.
‘EGCG may represent a potential low-cost inhibitor of global HIV-1 infection that could be used at least as adjunctive anti-HIV therapy,’ said Nance and Shearer in their report.
Previous drugs developed to block the entry of HIV-1 into cells proved ineffective because the virus mutated. Nance hopes that EGCG, derived from a natural product, will be less likely to generate such mutations.
BCM has received a grant from the National Institutes of Health to being a phase 1 trial to study the safety of the compound in HIV-1-infected people.
Funding for the research came from the National Institutes of Health and the Baylor Center for AIDS Research.
The report appears in the current issue of the Journal of Allergy and Clinical Immunology.”

In the true spirit of objective science, the researchers refrained from saying “breakthrough”, that was only the designation in the popular media; the researchers themselves merely titled their article “Preclinical development of the green tea catechin, epigallocatechin gallate, as an HIV-1 therapy” [by Christina L. Nance, Edward B. Siwak, & William T. Shearer, J Allergy Clin Immunol 2009;123:459-65] — though, come to think of it, that’s still making a pretty big claim, “development”, even if only pre-clinical as yet. And the Conclusions carry a tone of certainty: “We conclude that by preventing the attachment of HIV-1–glycoprotein 120 to the CD4 molecule, EGCG inhibits HIV-1 infectivity. Because this inhibition can be achieved at physiologic concentrations, the natural anti-HIVagent EGCG is a candidate as an alternative therapy in HIV-1 therapy.”

Perhaps this discovery explains why Asian-Americans, to whom we owe our introduction to green tea, have been so much less affected by HIV/AIDS than have Caucasian Americans?

At any rate, those of us who believed those unscientific peddlers of traditional remedies who have long touted green tea as health-promoting can feel vindicated as we continue with — indeed increase — our gullible guzzling of that beverage. And those intrepid researchers in Houston are being justly rewarded with continuing grant support from the National Institutes of Health.

Least susceptible = most affected?! More HIV/AIDS nonsense

No one questions that people of African ancestry feature much more frequently in HIV/AIDS statistics than do others, be it in Africa, the United States, the Caribbean, or elsewhere.

Three chapters of my book deal with those facts and their interpretation, as do several posts on this blog. The issue is really quite straightforward: Is the prominence of Africans as to HIV/AIDS a reflection of riskier behavior with respect to sex or drugs?

The Centers for Disease Control and Prevention and other official bodies and activist groups in the United States accept that risky behavior is the culprit; they harp on behavioral change as the way to deal with and ideally to prevent this prominence of blacks in HIV/AIDS statistics. James Chin infers for sub-Saharan Africa an extraordinary degree of promiscuity.

I disagree. This official stance entails that African ancestry determines behavior. That’s wrong because genes don’t determine behavior so simply and directly. It’s also racist, replaying the fear-mongering about oversexed black men.

I’ve argued that the data cannot be legitimately interpreted in this fashion. Behavior varies by social group. If there is a disease that strikes some people more than others, and if its incidence is invariably linked to certain genes in every social group, then that disease is hereditary and not a contagious infection spread by particular behavior — for example, sickle-cell anemia. The racial disparities in prevalence and incidence of “HIV” are the same among blood donors, drug abusers, gay men, military cohorts, pregnant women, university students, and other social sectors, in all countries and cultures. Blacks are “HIV-positive” far more frequently than whites in all those social groups and in all countries for which I’ve seen data: USA, Britain, Germany, the Caribbean, Africa. Clearly, that phenomenon is not the result of a particular kind of sexual behavior that blacks practice more than others, anywhere and everywhere. The great tendency for blacks to acquire “HIV-positive” status is not a result of behavior. “HIV” is not an infection, a fortiori not a sexually transmitted infection.

There have been a few mainstream attempts to make the sexually transmitted hypothesis compatible with the facts which show that “HIV-positive” status is determined by some inherent, i.e. genetic property: suggestions that something in ancestral African genes renders CD4 cells more prone to infection by and killing by “HIV”. Those attempts are less than convincing, to put it mildly  [Racial disparities in testing “HIV-positive”: Is there a non-racist explanation?, 4 May 2008 ; Mainstream duffers clutch at Duffy straws: African ancestry and HIV, 26 July 2008 ; Dr. Frankenstein turns to CCR5, 31 July 2008 ].

In any case, the facts present an inherent contradiction about blacks and HIV/AIDS. On the one hand, blacks are (1) much more likely to test “HIV-positive” and (2) much more likely to die from “HIV disease”. On the other hand, they (3) become “HIV-positive” at older ages than others and (4) die at older ages than others. The first two facts indicate that blacks resist “HIV” less well than others do, the last two facts indicate that blacks resist “HIV” better than others do.

(1) That blacks test “HIV-positive” at far greater rates than others is not controversial. That these differences cut across social groups is documented from official sources and peer-reviewed journals and in great detail in my book and several blog posts.

(2) That blacks die at far greater rates than others from “HIV disease” is shown in the relative mortalities reported, for example, in data from the National Center for Health Statistics. Examples from 1999 and 2004 were given in an earlier post:

(3) That blacks test “HIV-positive” at greater ages than whites was also shown in an earlier post:

(4) The rate data in Table 1 show that the median ages of death are higher for blacks than for whites, especially for males. They are also quite significantly higher than for Asians, Native Americans, or Hispanics:

People of African ancestry don’t contract “HIV” until they are on average older than others, and they survive that “disease” longer than others do — they are less susceptible to it, in other words, better protected against it in some fashion. At the same time, they are far more likely to contract the “disease”, and they die from “it” at a far greater rate than others — they are more susceptible to it, in other words.

Those are blatant mutual contradictions. Strangely enough, a similar contradiction is seen among blood donors:

The highest rates for each group are in bold italics. The maximum rate for testing positive is much lower, and occurs at lower ages, among the repeat donors than among the first-time donors. Repeat donors have been screened more thoroughly than first-time donors, obviously, so it’s hardly surprising that the rate of “HIV-positive” is much higher among first-time than among repeat donors; but why then do those first-time donors who do become “infected” acquire that status at distinctly higher ages? Once again, as with the racial disparities: those who are most likely to have been “infected” by a sexually transmitted agent tend to be infected at older ages than those who are less likely to be infected?! Among both males and females?

This strikes me as one of the more memorable absurdities that HIV/AIDS theorists demand that we swallow. A sexually transmitted agent that infects maximally people in their mid-30s?! In all social groups! Year after year! And the more susceptible you are to this “infection”, the older you are likely to be before you get “infected”?!
And the more susceptible you are to becoming infected, the longer you’re likely to live before being killed by that infection?!

Selling a couple of Brooklyn Bridges ought to have been much easier than selling  HIV/AIDS theory.

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Here’s a PDF of blog posts from 7th to 22nd February inclusive.

AIDS in China

Louis Hissink alerted me to the claim that

“AIDS has become China’s deadliest infectious disease for the first time, the government says. It says figures show that at least one person died every hour, on average, in the first nine months of last year.
AIDS overtook tuberculosis and rabies as the country’s number one disease killer in 2008, the health ministry said in a report released on Tuesday. Although full-year figures were not released, the ministry said the 6,897 people who died from AIDS from January to September made it the deadliest infectious disease. It said 34,864 people had died from AIDS since it was first detected in China in the 1980s. A total of 264,302 people were confirmed to have contracted the HIV virus that leads to AIDS, the report said. However those figures are a vast underestimate of the true picture, as the tally refers only to confirmed incidents of the condition. China actually had an estimated 700,000 HIV/AIDS carriers in 2007, with an estimated 85,000 people infected that year, according to the ministry.”

Not long after that, David Crowe sent a pertinent dispatch that he allows me to post (slightly edited):
“Someone seems to want to make AIDS a big issue in China, as evidenced by this article which has  some interesting numbers and statements. Although this made a big splash in the newspaper (full color covering all of page 7), the article was not mentioned on the home page of the newspaper for that day.
The article claims that ‘one-to-one education…is 100 percent effective’… Yet a team funded by Asia Development Bank, Chinese Preventive Medicine Association, Humana People to People and the Yunnan Poverty Alleviation and Development Office ‘visited about 500,000 households, workplaces and schools’… But only ‘offered advice to an estimated 250,000 people’. Were the people not home? Did they slam the door in their face? And, more important, ‘More than 2,000 have already been persuaded to take VCT [voluntary counselling and testing]’. Maybe the counselling is effective, but it doesn’t seem like most Chinese want to be counselled. And how voluntary is the counselling. One volunteer quoted at the top of the article says that ‘she sometimes had to resort to confrontational tactics to help break down people’s barriers’ … ‘it can take one or two months of visits before someone finally opens up their heart to me’…’Only friends can share their intimate moments, and by becoming their friend and showing them they can trust me I can convince them to take voluntary testing’. This sounds like desperation to me. Weeks of confrontation, begging and pleading before one person can be convinced to get tested. Another interesting number is that this project has 2,000 village volunteers to put on shows in markets, but so far only 10,000 people have seen these shows, that’s 5 people per volunteer.
There are some statistics claiming that HIV is now the leading infectious killer in China, although the statistics are so poorly reported that it is impossible to know if they are cumulative or annual, refer to all of China or just to a region.
I think that somewhere behind this there must be a Chinese CDC report. Obviously they are trying to open up a new front in this war, convincing the Chinese that this is a big health problem.
What are the real health problems in China? Well, clearly air quality (respiratory disease) and contaminants in water and food. For example, in the same issue, was a story about children experiencing kidney stones due to milk previously deemed to be ‘safe’ by authorities. Yet there is an epidemic of kidney stones (or worse) in consumers of one brand of formula. Obviously Chinese parents, experiencing prosperity, are making the disastrous choice to not breastfeed their children. This problem alone has left over 300,000 children with kidney ailments according to the China Daily (which is unlikely to exaggerate the problem).
Yet the supposed 7,000 deaths this year due to ‘AIDS’ get bigger headlines.”

Deaths from “HIV disease”: Why has the median age drifted upwards?

In “HIV, AIDS, and age: HIV/AIDS theory is wrong” [23 January 2009], I pointed to the similarity of median ages for HIV tests, for “new infections”, for AIDS diagnoses, and for deaths from “HIV disease”, arguing that this contradicts the widely accepted theory that, after a “latent period” of about 10 years, HIV causes AIDS and eventual death. Not only that: all those ages are within the range of 35-45 years, whereas the maximum risk of incurring sexually transmitted infections is at ages that are younger by a couple of decades and the maximum risk of death from any illness or disease rises at an exponential rate with increasing age from around 30. Furthermore, the age distributions of deaths are narrower than the others [No HIV “latent period”: dotting i’s and crossing t’s, 21 September 2008], the very opposite of what HIV/AIDS theory demands. That theory is simply wrong, on these several counts as well as others, for example, that “HIV” tests in the United States demonstrate that those tests do not track something infectious [The Origin, Persistence and Failings of HIV/AIDS Theory].

All the mentioned median ages are similar to one another, but all of them (and of course the age distributions) have drifted upward over the years. Defenders of the orthodoxy have claimed that the upward drift in median age of death from “HIV disease” illustrates a life-extending benefit from increasingly better treatment over the years, for example:

“The median age at death due to HIV disease increased almost linearly from 36 years in 1987 to 39 years in 1995, and to 45 years in 2005. This is a reflection of the postponement to older ages of HIV-attributable deaths that were not entirely prevented by improved treatment. The median age at death due to HIV disease varied little by racial/ethnic groups”.

That statement is an annotation to Figure 1:

This suggested explanation for the upward drift of the median age of deaths ignores that the median ages have also drifted upward (1) for first positive “HIV” tests, (2) for new diagnoses of “AIDS”, and therefore, (3) of surviving PWA:

The actual numbers for the data in Figure 2 are given in Table 1:

I don’t know why the CDC graph begins at 1987 rather than 1982, which was the first year for which CDC published deaths by age group. In any case, there is not an “almost linear” increase since 1987, as the numbers in Table 1 show. From 1982 to 1987, the increase was ~0.16 years per year (YPY).  If one chooses the interval from 1982 to ca. 1990, it was a bit bigger, ~0.2 YPY; to the mid-1990s, it was a bit bigger again, approaching 0.3 YPY; for the whole period 1982 to 2004, it was ~0.42 YPY. In other words, the rate of upward drift was increasing over the years; and it was already ~0.16 YPY before there was any antiretroviral therapy. For the pre-HAART, largely AZT period 1987 to 1993, the upward drift was ~0.37; for the HAART era (1996 on), it’s been  ~0.64 YPY.

One might them be tempted to credit AZT with ~0.21 YPY benefit (0.37 – 0.16), and HAART with an additional ~0.27 YPY (0.64 – 0.37) with respect to “deaths that were not entirely prevented by improved treatment”. But even so minimal a claim ignores the fact that the ages at which people were testing positive, and the ages at which they were being diagnosed as having AIDS, had also been drifting upward at somewhat comparable rates. The population of PWA is selected by AIDS diagnoses. As that population ages, deaths among that group will also occur at increasingly older ages (just as among the population at large, life expectancy increases with age among those surviving to any given age).

The upward drift in median age of those testing “HIV-positive” was ~0.4 YPY between 1995 and 2004, among the roughly 2 million people tested annually. That was not significantly owing to any trend to test older people, for the median age of those being tested increased by only ~0.1 YPY in that period, leaving ~0.3 YPY attributable to whatever was contributing to an upward drift in age of those testing “HIV-positive”. That might be owing to changes in the tests themselves or to changes in the nature of the tested population, or of course both.

Now, the tendency to test “HIV-positive” varies somewhat by sex and race, and so does the median age at which positive tests are most likely. As it happens, the median ages at which blacks test “HIV-positive” are about a year higher than the median ages at which whites test “HIV-positive”; and for both blacks and whites, the median age at which men test positive most often is a couple of years higher than the age at which women test positive most often:

Now, the proportions as to sex and race of those being tested changed over the years. In 1995, 1.39 million females were tested and 1.10 million males, a ratio of 1.25, 25% more females than males, whereas in 2004 it was 947,000 females and 933,000 males, a ratio of only 1.02, almost equally males and females. Since the proportion of men among those tested increased significantly, and the median age for testing positive is greater for men than for women (by about 2 years, see Table 2), the overall median age for testing positive drifted upward solely because of the changing composition of PWA in terms of men and women.

Furthermore, the proportion of blacks among those tested increased significantly between 1995 and 2004: in 2004, only 36% of those tested at public sites were white and 39% black, whereas in 1995 it had been 49% white and only 33% black. That change is consistent with and perhaps a consequence of the increasingly pervasive shibboleth that HIV/AIDS has, in the United States, become a disease of the black community, spurring concerted efforts for more comprehensive testing in that community. Since blacks test positive at median ages greater by about a year (Table 2) than the median age at which whites test positive, the changing composition of PWA in terms of race adds a further upward drift in the median age of those testing positive, and thereby of the PWA population as a whole.

The most significant change in the population of PWA, however, was one that began in 1993, when the definition of “AIDS” was broadened to include healthy, asymptomatic individuals if they were “HIV-positive” and had CD4 counts below 200. Thus the average level of health among PWA was improving since 1993, and one would expect to see the median ages of those dying among that group to drift upward at an increasing rate. That’s what the data indeed show: the rate of increase was ~0.3 YPY from 1982 to 1993, and since 1999 it’s been ~0.6 (an international re-definition of “AIDS” in 1998 makes numbers from 1997-99 less comparable to others).

So the median age of death from “HIV disease” experienced an upward drift because the median age of the population of PWA, from which those deaths are drawn, drifted upward owing to the changing composition of the population of PWA in terms of age and sex. In other words, the changing composition of the population of PWA contributed indirectly to an upward drift in median age of death.

In addition to that, however, the changing composition of the population also contributed directly to an increase in the median age of death: “HIV disease” mortality among blacks is greater than among whites, and blacks also die at older ages (Table 3).

Data for intermediate years are quite similar (before 1999, reports were not in the same format). At any rate, compare male whites with male blacks, and white females with black females: in both cases, the maximum rate of death is at an older age among blacks than among whites, and in both cases the maximum rates of death are considerably greater among blacks than among whites — by a factor of ~7 with males and ~12 with females.

Since the proportion of blacks among PWA increased over the years, and since black PWA died at a greater rate than white PWA, and at older ages, the overall median age of deaths “from HIV disease” drifted upward even more than the upward drift predicted solely by the greater proportion of blacks entering the population of PWA.

So: Does the upward drift in age of death reflect some lingering benefit from HAART, as the Centers for Disease Control and Prevention suggested?

Not at all. The changing population of PWA and the different characteristics of blacks and whites suffice to explain the upward drifts of median ages of death as well as of PWA.

Henry Bauer and the Loch Ness monsters

One of the burdens that AIDS Rethinkers and HIV Skeptics impose on one another is that the HIV/AIDS groupies and vigilantes seize every possible opportunity to assert “guilt by association”. I’ve felt apologetic for some time that my fellow Rethinkers and Skeptics have been tarred by the brush of being associated with Henry Bauer, who is a believer in Loch Ness monsters (“Nessies”). Most recently, Seth Kalichman and Richard Wilson have been trying to make hay from this association, so I thought it might be useful if I made a plain statement about the matter — useful, that is to say, for anyone who is interested in actual facts.

But first, some comments on what the real issues are here.

1. Guilt by association is understood by all thinking people to be invalid, whether it’s being held accountable for someone else’s views or actions (e.g., House Un-American Activities Committee, McCarthyism) or whether it asserts that a person who is wrong about one issue is therefore wrong about all other issues — e.g., because Isaac Newton spent most of his time and intellectual energy delving into alchemy and Biblical exegesis, therefore his views on calculus and celestial mechanics are not worthy of consideration.

2. People who seek to counter what I’ve written about HIV/AIDS by pointing out that I’ve written about the Loch Ness mystery reveal thereby their inability to counter the arguments I’ve made about HIV/AIDS. It’s rather like the response that HIV/AIDS defenders always give when they’re asked to cite specific data that prove HIV to be the cause of AIDS: they never give a direct reply, it’s always about “overwhelming evidence”, “virtually unanimous consensus”, “hundreds of thousands of papers over 25 years” — when the argument would be cut short decisively in their favor if only they could cite such specific data. Similarly, if the groupies and vigilantes had conclusive answers to the data and inferences presented in my book, they could just give those answers, and then they wouldn’t have had to spend the considerable effort that they’ve evidently devoted to reading my writings on so many other matters, not only about Loch Ness but even my memoir of academic administration.

The following isn’t directed at those whose interest it is to assassinate characters because they can’t answer my substantive arguments, and it isn’t for those who pull things out of context to serve as innuendos; it is for my fellow Rethinkers and Skeptics who may have felt embarrassed by my Loch Ness connection and who have at times defended me from those sorts of attacks in the many Internet venues that I personally eschew, in which guilt by association, character assassination, bleep-worthy invective, and the like, are standard fare.

A direct question:

Do I believe in the existence of Loch Ness monsters?

A direct answer:

Yes and No     😉
It depends on what the meaning of “believe” is   😉

Flippancy aside: When we say in conversation, “I believe Loch Ness monsters are real animals”, or “I believe the President’s economic stimulus package is the best thing to do”, we’re expressing a strong opinion that’s not the same as saying, “I’m 100% certain that  Loch Ness monsters are real animals and that the President’s economic stimulus package is the best thing to do”.

I believe that the balance of the available evidence is that unidentified animals disport themselves deep under the waters of Loch Ness, but I’m not 100% certain — I wouldn’t bet on it anything that’s important to me.
If you’re interested in what the significant evidence is, read my essay, “The case for the Loch Ness Monster: The scientific evidence”, Journal of Scientific Exploration, 16(2): 225-46 (2002).

My book about the matter, The Enigma of Loch Ness: Making Sense of a Mystery, doesn’t make the case for the existence of Nessies, it is the second of my books to explore the differences between knowledge-seeking within and without the formal scientific community. Though it’s a scholarly monograph published by a university press rather than a popular work, its sales have exceeded 4500 copies plus some unknown number in a British edition and as a “book on tape”. I was delighted by some two dozen reviews of the book (all are listed at my website), overwhelmingly favorable, for example:

“We need more books of this type. Although Bauer personally says that he thinks the creatures do exist in Loch Ness, he is careful not to push his views, or to turn this book into a plea for Nessie. It remains a cautious examination about what is known, what is believed, why it is believed or not believed. The reader is left to make his or her own conclusion, or to make none at all. .  . . Rationalists will be pleased” (Gordon Stein, American Rationalist).

I would no more disown my associations with Loch Ness than Barack Obama would disown his associations with a man who was the preacher at his church for many years. There’s a bit more to me than my associations with Loch Ness, but I have no reason to be ashamed of those associations. Indeed, attempting to satisfy my curiosity about the possible existence of Nessies led to all sorts of good things for me, both personally and professionally.

I was first at Loch Ness during a honeymoon in 1958. I didn’t then take Nessies seriously, made no effort to ask about them, and didn’t buy the recently published book by Constance Whyte, “More than a Legend”. A few years later, I came across Tim Dinsdale’s 1961 book while browsing in the local library. Still photographs in it that were claimed to come from a moving film intrigued me, and I wanted to learn more. During a sabbatical leave in Britain in 1972-73, we encountered Dinsdale, and I arranged lecture tours for him in 1975 in Kentucky and 1979 in Virginia. Whenever there was the opportunity to visit Britain, I would try to include Loch Ness. I took a mini-sabbatical there in 1985, during which time I wrote my memoir about academic administration and made a number of friends. I spent a second honeymoon actually at Loch Ness, and my wife and I took summer vacations there for about 20 years, forming some close and valued friendships and delighting in the scenery across the Highlands; there cannot be many trails or by-ways that we haven’t traversed more than once, and I became quite adept at the maneuverings and the courtesies appropriate to single-track roads with infrequent “passing places”, often unpaved or with only two tire-width strips of asphalt.

So Loch Ness brought me quite powerful and altogether positive personal experiences. The mystery of the possible existence of Nessies brought me stimulating and rewarding intellectual experiences. My first question, naturally, had been, “Could these things really exist?” The second question came from looking in encyclopedias and journals for relevant information, leading me to ask myself, “Why can’t I find an authoritative scientific resource about this?” That led me to explore that question with historians, journalists, and others, and to a recognition that scientific activity is a far more complicated matter than “applying the scientific method”. And that led to my change of academic career from chemistry to science studies, with an interlude in academic administration that was also very instructive about the intellectual differences among academic specialties.

That background of learning about how science works, and about the role of unorthodox views in the progress of science, prepared and enabled me to look for the “beef” in HIV/AIDS theory after I had become aware that some people questioned the mainstream view. What I had learned about the history of science allowed me to contemplate the possibility that a firmly held consensus might be wrong, a realization shared by all too few people outside the academic fields of history of science and science studies or the like.

So there you have it. I “believe” (estimated probability ≥0.9) that Nessies exist, and I believe quite firmly (probability ≥0.999) that studying controversies over such matters can be intellectually rewarding. In the words of the motto adopted by the student newspaper at my alma mater:

Honi soit qui mal y pense