REGULAR AS CLOCKWORK: HIV, THE TRULY UNIQUE “INFECTION”

Astonishment, disbelief, incredulity would merely begin to describe my feelings when I began collecting published data about HIV a few years ago.

I got started because I couldn’t believe the assertion, in Harvey Bialy’s book about Peter Duesberg’s work, that (in the mid-1980s, no less) teenage females from every part of the United States were as likely as teenage males to be “HIV”-positive. But I verified the correctness of the assertion in the original source; whereupon I expected to find contradictions in other studies, and so I kept looking. I jotted notes on how rates of testing positive varied with all the factors mentioned in the various reports. And my head swam, or spun, or rebelled, because it made no sense: testing “HIV”-positive seemed to be as regular as clockwork, not at all like the incidence of something infectious or contagious, which sweeps back and forth, here and there, as the opportunity offers itself.

—“HIV”-positive was always greater among men than among women: except in the teenage years, where it was often higher among females.
—“HIV”-positive always increased with age from the teens into the 30s or 40s, and then declined again.
—Most extraordinary of all, so far as age was concerned: children below teenage tested “HIV”-positive more than teenagers did, and increasingly so, the younger they were! The rate of testing positive among newborns rivaled the highest rates among adults in their 30s and 40s!

I was looking at the wealth of data based on tests in the United States, but also came across some reports from elsewhere, published by the same reliable researchers. That strange variation with age, including young children, had been reported also from Africa!

US data of all sorts are typically reported by racial category. Regular as clockwork, rates of testing “HIV”-positive always increased from among Asians to among white Americans to among Hispanic Americans to among black Americans. Whether it was blood donors or gay men, injecting drug users or newborns or their mothers; whether it was military personnel or prisoners, people at STD clinics or women at pre-natal clinics—there were simply no reports that did not fit into that progression of testing “HIV”-positive according to racial category. What sort of infection is it that discriminates consistently and regularly by race?

Whenever there’s discussion of racial disparities between blacks and whites in the USA, the first resort is to explanations based on slavery, Jim Crow laws, racial discrimination in general and their lingering after-effects: high rates of poverty, unemployment, drug abuse, criminality, and so on. But analogous circumstances have been the lot of Native Americans, displaced from their homelands, traditional practices disrupted, never integrated into the American mainstream. So one would expect that Native Americans might test “HIV”-positive about as often as African Americans. But they don’t. Every published study finds that Native Americans test “HIV”-positive at rates closer to those of white Americans than to those of any other group; somewhere between the rates of whites and those for Hispanics, but generally closer to those of whites. HIV is very race-sensitive indeed, and it discriminates by broad racial genetic category as no other infection does.

In South Africa, the same racial disparities in testing “HIV”-positive were reported as in the United States. Whites always much lower than blacks, and coloreds—mulattos—tested in between. “HIV”-positive rates even reflect miscegenation!

Similarly, within the United States, the ethnic category of Hispanic delivers “HIV”-positive rates that are distinctly higher in the East than in the West—in the same manner as the racial proportions among Hispanics differ, higher proportion of Caribbean and African descent in the East than in the West. HIV is adept at recognizing human racial genetics.

HIV is regular as clockwork in other respects, too. The same number of Americans has been “HIV”-positive from when testing began in the mid-1980s right up to the present; about 1 million, give or take whatever uncertainty the Centers for Disease Control and Prevention (CDC) is prepared to admit at any give time.

Who dies of “HIV disease”, the latest obfuscating term devised by CDC? Always the highest rate is among adults in their 30s and 40s, steadily from 1987 to date; no sign of any change in the distribution of deaths by age, no sign that treatments have had any effect, that they have shifted deaths to later ages (“HIV DISEASE” IS NOT AN ILLNESS, 19 March 2008). HIV is regular as clockwork. You can bet on it.

HIV is distributed in the United States in a pattern that hasn’t changed in two decades. Just as the total number of “HIV”-positive Americans has remained the same, so their geographic location hasn’t changed. It’s highest in the Northeast, next highest in the Southeast, and lowest in the North Central and Midwest. That applies to military personnel, new mothers and their infants, members of the Job Corps, blood donors—every tested group shows that same geographic distribution. Like no other infectious agent, HIV knows its place and sticks to it. Regular as clockwork. You can bet on it.

I put one and one together. Constant geographic distribution, constant racial disparities—maybe the geographic distribution merely reflects the racial proportions of the American population in the different parts of the country?
Yes. Calculate what the geographic distribution of HIV would be if it depended only on the racial make-up of the population and the relative rates at which the different races test positive, and you get a very good fit with the maps of “HIV”-positive rates.

There was one regularity in the data I collected that was, if possible, even more puzzling than the others. Quite a few reports made a point of noting that “HIV”-positive rates were higher in urban areas than in rural regions; always that same progression, and always higher, too, in the large urban areas than in the smaller ones. So regular was this that it seemed quantitative: in the largest metropolitan areas, rates of testing “HIV”-positive were about 4 times as high as in rural areas, and in “semi-urban” regions the rates were about half those in the largest cities.
Leave aside “why”, I thought. Clearly, the calculation of geographic distribution should be modified by taking also this factor into account. Doing that, the fit between the calculated and the actual geographic distributions of HIV is even better.

So HIV is this unique, unprecedented, even magical infection that hides itself not only in human bodies (because none of it has never been isolated in live form from an “HIV”-positive person), it hides itself also in its demographic characteristics, by behaving just like something endemic! It doesn’t go up and down in incidence like other infections or contagions. It doesn’t skip, hop, and jump around regions and countries and the world like other viruses or bacteria. It’s just there. It mimics DNA, in fact, because it distributes itself according to racial category. It mimics physiology: it varies according to the age of its host— regular as clockwork, it’s lowest in the teens and highest at birth and in middle age. You can bet on it.

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I’ve mentioned before, on this blog (for instance, HIV DEMOGRAPHICS FURTHER CONFIRMED…, 26 February 2008), how reassuring it has been to find that these regularities, described and documented in my 2007 book (The Origin, Persistence and Failings of HIV/AIDS Theory), continue to be reported in newer studies. Reassuring because it emphasizes that the regularities I had discerned were not artefacts of those particular samples—which was unlikely a priori, in any case, given that those “samples” included just about all the published data and represented upwards of 60 million tests; including some, like blood donors and military cohorts, in which all members of those groups were tested, not just sampled; and moreover tested regularly throughout the era of AIDS.

The present little essay was stimulated by finding confirmation of that most puzzling of the regularities, the variation of “HIV”-positive rates with population density. In gathering data for my book, I had not come across a piece in the Journal of Rural Health by Steinberg and Fleming of the CDC, “The geographic distribution of AIDS in the United States: Is there a rural epidemic?” (16 [2000] 11-19). Maybe I had missed it because I focused my searches on “HIV”, not “AIDS”.

Despite its title, that paper is about the distribution of “HIV”. CDC has added to its many sins by conflating, since the late 1990s, HIV and AIDS in such a manner as to make it difficult if not impossible to know what their statistics refer to. In this instance, “AIDS” is said to include “HIV-related severe immunodeficiency”—healthy, asymptomatic people who test “HIV”-positive and have low CD4 counts. So the numbers given in this publication represent “HIV”-positive rates. The article reports specifically on data for 1996; and it confirms rather strikingly the regular trends, including the variation with population density, that are published in my book, for data collated from the mid-1980s to the later 1990s.

Geographic distribution:
Northeast > South > West > Midwest  (49.4 to 34.2 to 28.6 to 13.5 per 100,000)

Black-to-white ratio, 7.2 (in my book, 5.5 ± 3.4)
Hispanic-to-white ratio, 3.4 (in my book, 2.7 ± 2.1)

Variation with population density:
Metropolitan statistical area (MSA) >500,000, 41.6;  50,000 - 500,000, 17.7; non-MSA, 10.1
In my book, 4 to 2 to 1

Regular as a clock that keeps good time.

“HIV DISEASE” IS NOT AN ILLNESS

This post is longer than I prefer, but I saw no good way to split it into parts. It explains that the way “HIV infections” and deaths from “HIV disease” vary with age and with race and over time constitutes a resounding disproof of HIV/AIDS theory.

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A couple of years ago, I had come to the conclusion that the demographics of positive “HIV”-tests, data published largely by the Centers for Disease Control and Prevention (CDC), represent definitive proof that “HIV” is not an infection. Icing on that cake is the fact that “HIV” and “AIDS” are not correlated—again, in officially published statistics—, as became clear to me while writing The Origin, Persistence and Failings of HIV/AIDS Theory (see chapter 9). Now I’ve found that a more direct line of proof lies in comparing the data on deaths from “HIV disease”—as the CDC has come to call it—with data from “HIV” tests.

In earlier blogs, I had argued that “HIV disease” is not an illness, citing among other things Table A below (see WORLD AIDS DAY . . ., 22 December 2007; “HIV DISEASE”, 28 December 2007; HOW TO TEST THEORIES . . ., 7 January 2008).

TABLE A (click in table for full size)

There I had waffled about how the racial disparities and sex differences in “HIV” deaths parallel those found on “HIV” tests, and how strange it is that blacks and Hispanics are more susceptible to “catching” HIV and yet survive to later ages than do whites or Asians or Native Americans equally suffering from “HIV disease”, and how all this supports the hypothesis that testing “HIV”-positive is a non-specific indication of some sort of physiological stress. But I had failed to grasp the significance of the fact that the age distribution of deaths from “HIV disease” reaches a maximum in people in the prime years of life, mid-thirties to early forties. That is the very opposite of how people react to infectious diseases, where everyone is about equally at risk of infection, but the young and the old are most at risk of succumbing to the infection, from pneumonia, say, or influenza; so the variation with age of “HIV” deaths is the very opposite of how death rates from infectious diseases vary with age; and for the same reason, it’s the very opposite of how all-cause death rates vary with age (Table B).

TABLE B (click in table for full size)

Even death rates from chronic diseases—diabetes, say—or “diseases of old age”—heart and cardiovascular, say, or cancer—show the same trend, though the death rates at very young ages are much less prominent:

TABLE C (click in table for full size)

The all-cause death rates of people in their thirties or forties are comparatively low, between ¼ and ½ of the age-adjusted overall death-rate (Table B, 193.5 or 427 compared to 800.8). Nowhere have I found mention of an illness that is most life-threatening for people aged 35-44 or 45-54—except, of course, “HIV disease”.

One might quibble that the numbers in Table A are not rates for each of the given age-groups; but adjusting for the age distribution in the population makes little difference, as shown by the age distribution of reported death-rates from “HIV disease” (Table D, which is Table 42, p. 236, in “National Center for Health Statistics: Health, United States, 2007 with Chartbook on Trends in the Health of Americans”, Hyattsville, MD, 2007) : for males as for females and in every calendar year, the highest rate of death from “HIV disease” comes at ages 35-44 with the single exception of females in 1987 when it came at 25-34.

TABLE D (click in table for full size)

 * in table D means rates based on fewer than 20 deaths, considered unreliable

The failure of HIV/AIDS theory is demonstrated not only by this incongruous age-dependence of death rates. Note how constant over the years is the shape of this age distribution. While the magnitudes of the rates go up from 1987 to 1995 and then down, they do so in similar fashion in each age group. By contrast, HIV/AIDS theory would have predicted high death-rates at relatively early ages in 1987 and before, when there were no treatments for AIDS and victims were dying within months, or at most a year or two, after diagnosis; then—HIV/AIDS theory would have it—the highest death-rates would have moved steadily to older ages as treatments were introduced, and particularly after the supposedly revolutionary introduction of “life-saving” HAART in the mid-1990s and the development of continually better individual drugs. But there is no such trend; the actual data show no change at all, over the years, in the age range within which people are most at risk of dying of “HIV disease”. For two decades, the greatest risk of dying from “HIV disease” has been experienced by people between 35 and 44years of age.

Also to be noted is that from 1987 into the mid-1990s, every age-group saw a great increase in death rates. That was the era of AZT monotherapy, initially deploying doses so high that even the mainstream acknowledged their toxicity by cutting them back drastically. Discontinuation of monotherapy in favor of “cocktails” then allowed the death rates to fall back again; but, as mentioned above, there is no indication at all that years of survival were increased by introduction of HAART as monotherapy was phased out.

(After writing this I was struck by a sinking feeling that, like increasing arrays of HIV/AIDS numbers issued by the CDC, Table D might have been drawn from computer models, which would explain their astonishing regularity. Then I noticed the phrase in fine print just below the Table’s header, “Data are based on death certificates”, and I was reassured —at least provisionally.)

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That “HIV”-positive” is not an illness is, of course, the reason that African Americans survive “HIV disease” to later ages than do white, Asian, and Native Americans (Table A), one of the points to which I had drawn attention earlier (7 January). Black people test “HIV”-positive more often than others under all circumstances and in both sexes and at all ages (The Origin, Persistence and Failings of HIV/AIDS Theory, Figures 13-17, pp. 53-6), so when they die they still test positive more often at every age, even to an appreciable extent at ages where others test positive so rarely as not to show up in the statistics (above 55 for men and above 45 for women, Table A).

These variations with age of death rates from “HIV disease” run exactly as would be expected on the hypothesis that testing “HIV”-positive is a non-specific response by the immune system to some sort of physiological stress and that, for a given challenge to health, the strength of that immune response varies according to the capacity of the individual’s immune system (The Origin, Persistence and Failings of HIV/AIDS Theory).

From the teens into the “golden years”, external health challenges do not (on average, overall) vary systematically with age, so on average the variation with age of the tendency to test “HIV”-positive reflects the capabilities of the immune system, which tend to be at their best in the middle years of life:

FIGURE 1

Health challenges are considerably higher, though, at very early ages, because newborns experience the stress of birth and because young children meet many health challenges for the first time as their immune systems are just learning to cope with them. So the graph rises to the left not because the immune system is fully capable, as in the middle years, but because the stresses and health challenges encountered in those years are exceptionally great.

But why should deaths from “HIV disease” parallel the tendency to test “HIV”-positive in the middle years if that tendency represents a capable immune-system response?

Because of the manner in which the CDC defines “HIV disease”.

After “HIV” had become accepted as the cause of “AIDS”, an increasing number of diseases were included by the CDC as “AIDS-defining” just because a significant number of people with those diseases were reported as testing “HIV”-positive. As Rebecca Culshaw noted, this led to the extraordinary situation that the death from any cause of a person known to be “HIV”-positive would be reported as a death from “HIV disease”—even when the immediate cause of death was heart attack, liver failure, CMV infection, or even suicide, a car accident, or drowning (“Science Sold Out”, 2007, p. 30, citing Massachusetts Department of Health, 2002). (There may be a financial incentive to do this: federal funds to “fight HIV/AIDS” are apportioned to states and cities according to the perceived relative impacts of HIV/AIDS.)

Now: illness and death are in and of themselves often associated with positive “HIV”-tests (after all, they represent extreme challenges to health). Hospital patients (admitted for reasons not connected with HIV/AIDS) test “HIV”-positive at between 0.1 and 7.6% (The Origin, Persistence and Failings of HIV/AIDS Theory, Table 3 p. 25; Table 23 p. 81); and moreover the tests vary with age as in the diagram above (ibid., Table 26 p. 98); emergency-room patients tested at 5-6% (ibid., pp. 48, 85); “HIV”-positive rates in autopsies were reported in one instance as between 1.9 and 3.7% and increasing in proportion to the degree of death-causing trauma, and in another instance at 18% with no indications of AIDS (ibid., p. 85). Since even accident and trauma victims tend to test “HIV”-positive, as well as people ill for a wide variety of other reasons, there is then a definite probability that anyone who is seriously ill will test “HIV”-positive, and so anyone who dies for any reason may well have tested “HIV”-positive while in hospital, or may well do so in autopsy, with a probability of a few percent or more; that’s much higher than the “normal” rate in the US population as a whole, which is an order of magnitude lower at a few per thousand or less.

The maximum death-rates from “HIV disease” in 2004 (Table D) were 10.9 (per 100,000) at ages 35-44 and 10.6 at ages 45-54. The all-cause death-rates for those age groups were (Table B) 194 and 427 respectively. Thus deaths from “HIV disease” represented respectively 5.5% (10.9/194) and 2.5% (10.6/427) of all deaths in those age groups, quite comparable to the frequency of positive “HIV”-tests among non-AIDS hospital patients and emergency-room patients and in autopsies. Thus deaths from “HIV disease” are merely that fraction of all deaths in which the non-specific “HIV”-positive reaction happened to turn up in response to the health challenge that had caused the death.

So death rates from “HIV disease” parallel the age variation of “HIV” tests simply because all deaths of “HIV”-positives are called deaths from “HIV disease”, and because “HIV” tests are so highly non-specific as to react to many life-threatening conditions. And that is also why the age variation of death rates ascribed to “HIV disease” is (for chronic diseases) unlike or (for infectious diseases) opposite to the variation with age of death rates from every other malady.

Figure 1 is schematic, not quantitative. I had mentioned in connection with its first appearance (ibid., p. 26) that the actual “middle” age of the peak appears to vary somewhat with sex and with race. To compare the actual years of that peak on “HIV” tests with the peak years of “HIV” deaths, I wanted “HIV”-test data for the population as a whole, since the death-data in Table A are also for the population as a whole. The most appropriate data-sets are those, totaling nearly 10,000,000 tests, published in 1995-8 by CDC for all public testing-sites (clinics for TB, HIV, STD, drugs, family planning, prenatal care, and more, as well as prisons and colleges and some reports from private medical practices). Pooling the actual numbers for each of those four years and making the appropriate calculations delivers the following results:

TABLE E (click in table for full size)

The highlighted cells and the “XXX” overlap or straddle in 12 of 13 cases; there is a good quantitative correspondence between the ages of maximum probability of testing “HIV”-positive and the ages of maximum rate of dying from “HIV disease”. But under HIV/AIDS theory, infection by HIV is supposed to be followed by a “latent period” of about 10 years: the peak ages for deaths from “HIV disease” should be a decade or more later than the peak ages for “HIV” infection, rather than overlapping in the same age-ranges. Furthermore, the difference between age of “infection” and age of death should have increased during the years—from the mid-1990s on—when “life-saving” antiretroviral treatments supposedly extended the life spans of “HIV”-positive people by a significant amount. Yet in 2002-4 (Tables A and D), the peak ages for “HIV” infection and for deaths from “HIV disease” are virtually the same as the ages where infections were most common in 1995-8, even though most people “infected” in 1995-98 should have survived well beyond 2005-8!

All this is inexplicable under HIV/AIDS theory, whereas it comports perfectly with the alternative theory that testing “HIV”-positive denotes physiological stress.

HIV/AIDS theory lacks substantive legs to stand on. “HIV” is not any cause of illness. Testing “HIV”-positive signals the presence of some sort of challenge to health. The tendency to test “HIV”-positive depends on what the health challenge is, and on how strongly an individual tends to respond.

UNRAVELING HIV/AIDS

I had described Tony Lance’s article on intestinal dysbiosis as “slicing through the Gordian knot” [20 February 2008] because it offers coherent and plausible answers to the most vexing specific mysteries about “AIDS”. It appeared around 1980 among gay men in a few large cities: Why then? Why there? Why in the form of those particular diseases—KS, PCP, candidiasis? In addition, Lance’s explanation offers a satisfactory resolution to what has been a salient conundrum for HIV/AIDS dissidents: Why does antiretroviral treatment sometimes bring tangible, almost immediate health benefits?

Some of the responses to Tony’s article have brought home to me the need to put this keystone solution into perspective, because “HIV/AIDS” nowadays encompasses such an enormous range of disparate things. It’s an exceedingly complicated mess, with many threads needing to be unraveled even after the central knot has been sliced.

To begin with, one must recognize that

1. “HIV” and “AIDS” are distinctly separate things.
2. Neither “HIV” nor “AIDS” is definitively defined by universally agreed, substantive and objective criteria.
3. That second point is illustrated by the way in which the definitions of “HIV” and of “AIDS” have been changed or augmented over time.
4. To muddy the waters even further, in some circumstances—but not in others—there is an indirect correlation between some claimed measures of “HIV” and the claimed incidence of some forms of “AIDS”.

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1. “HIV” and “AIDS” are two separate things

Chapter 9 in The Origin, Persistence and Failings of HIV/AIDS Theory summarizes the many facts which show that “HIV” and “AIDS” are not correlated:
— “HIV”-negative AIDS cases
— “HIV”-positive people who never come down with an “AIDS-defining” illness
— male-to-female ratios for “AIDS” and for “HIV” are quite different; and the difference has changed over the years
— black-to-white ratios for “AIDS” and for “HIV” are quite different; and the difference has changed over the years
— the overall incidence and prevalence of “AIDS” and of “HIV” have changed quite differently over the years
— the geographic distributions of “AIDS” and of “HIV” are not the same

2 & 3. “HIV” and “AIDS” have not been defined definitively; definitions have changed over time

“AIDS”, when first recognized as a distinct entity, was defined as an immunedeficiency marked by rare opportunistic infections and having no obvious cause (i.e., no cancer, malnutrition, or other condition known to suppress immune function).
After the claimed discovery of “HIV” as its cause, “AIDS” was re-defined to require a positive “HIV”-test. That made it necessary, some years later, to invent the new phenomenon of idiopathic CD4-T-cell lymphopenia—pathogenic immunedeficiency without obvious cause—to describe cases where the clinical diagnosis would have been “AIDS” except that “HIV”-tests were negative.
The inclusion of hemophiliacs under “AIDS” broke the initial definition of immunedeficiency for no known reason.
Further re-definitions over the years added to the list of “AIDS-defining” conditions a number of illnesses where patients often tested “HIV”-positive. This had such bizarre consequences as including tuberculosis as AIDS-defining just because TB patients often test positive for “HIV”, and including cervical cancer as “AIDS-defining” even though its incidence had been declining steadily throughout the period during which “HIV” and “AIDS” were supposedly spreading.
Then the Centers for Disease Control and Prevention decided that “HIV”-positive people with CD4-cell counts of less than 200 in the blood were to be classed as “having AIDS” even when they displayed and felt no symptoms of ill health. That criterion has not been accepted in certain other countries, however, with the result that some “AIDS” patients from the USA may cross the border into Canada and no longer have AIDS; indeed, in 1993 fully half of all newly diagnosed AIDS patients in the United States, more than 20,000 of them, could have been cured just by crossing the border.

“HIV” is variously defined as what is detected by antibody tests (ELISA or Western Blot) or by PCR detection of genetic material. ELISA and Western Blot do not always agree over whether a given sample is “positive”. The criteria for whether a Western Blot is positive are not the same in different countries nor in different laboratories. Counts of immune-system cells (CD4+) and of “viral load” (supposed amount of virus) do not correlate with one another.
Dissidents know, on the basis of any amount of documented evidence, that “HIV” tests are not specific: they react positive under many physiological conditions, and they have never been validated against pure virus, because no pure virus has ever been isolated direct from an “HIV”-positive individual.
Nevertheless, countless published articles have described “HIV” in extraordinary detail of genetic sequence and physical structure—all postulated on the basis of highly indirect inferences, since, to repeat, no single authentic particle of the virus has ever been obtained from an “AIDS” patient. All the so-called “viral isolates” stem from work with cultures; and even those are revealed by electron microscopy as motley mixtures of bits and pieces of various sizes and shapes.
An empirical and natural way of defining “HIV” is: “what HIV tests have been held to detect”. Under that view, published data from tens of millions of “HIV” tests in the United States show that “HIV” is not a sexually transmitted agent, indeed is not an infection at all, because it has been present at about the same level and in the same geographic distribution for more than two decades. The manner in which “HIV” depends on age, sex, and race indicates that it is a very non-specific physiological response to some sort of stress or health challenge. In other words, HIV/AIDS theory contradicts itself; the evidence gained by applying HIV/AIDS theory is incompatible with the theory.

4. Occasional correlations between “HIV” and “AIDS”

What makes things so exceedingly complicated and messy is that even though “HIV” and “AIDS” are not correlated in general and certainly not inevitably, as they would have to be if one were the cause of the other, there are circumstances where there is an indirect or apparent correlation between them.
Since “HIV” tests often react quite non-specifically to health stresses, people test “HIV”-positive when palpably unwell from any one of a large variety of causes; for example, “HIV”-positive rates are relatively high in hospital patients, especially those seen in emergency rooms, and among people whose deaths were such as to call for autopsies. Consequently, “HIV”-positive rates do show some sort of correlation with degree of illness in the so-called high-risk groups: drug abusers, hemophiliacs, and gay men, and this happenstance lends some apparent yet misleading support to the mainstream view.
Not acknowledged by the mainstream, but evident from mountains of data, is the fact that TB patients are another group at high risk of testing “HIV”-positive, and of course at high risk of dying as well.
Hemophiliacs suffer from a chronic, life-threatening disorder. No other explanation is required for why they test “HIV”-positive at high rates and why that sometimes appears to correlate with the severity of their illness.
Drug abusers are unhealthy or ill to varying degrees, depending on the types and amounts of drugs consumed. Addicts test “HIV”-positive because that is a response to physiological stress, and there is a consequent correlation between the degree of that drug-induced stress, that is the severity of the drug-induced ill-health, and the tendency to test “HIV”-positive. The observation that reformed drug addicts are less prone to test “HIV”-positive, in proportion to how long they have been clean, underscores that testing “HIV”-positive is in these cases an indicator of the degree of health stress, and as such it is reversible, just like a fever.
Lance’s intestinal dysbiosis article explains convincingly why gay men often test “HIV”-positive, and why that is associated with the whole spectrum of health and illness, so that there is often a correlation between the severity of the dysbiosis, the probability of testing “HIV”-positive, and the likelihood of developing “AIDS”. The intestinal-dysbiosis hypothesis also affords an explanation for the fact that the most severely ill gay men, those who experience full-blown AIDS, tend to be older rather than younger, in their thirties or forties rather than—as would be expected with a sexually transmitted disease—in their teens or twenties. Figure 10 in The Origin, Persistence and Failings of HIV/AIDS Theory shows “HIV”-positive rates among gay men aged more than 25 as higher than among younger gay men. Michelle Cochrane’s re-examination of medical records of early AIDS cases in San Francisco found that their average age was in the mid- to late thirties. The average age of the first 5 victims in Los Angeles was 31. The first 159 AIDS patients identified by the Centers for Disease Control and Prevention had an average age of 35 (pp. 187-8 in The Origin, Persistence and Failings of HIV/AIDS Theory).
Quite recently I came across yet more evidence of this correlation. A British study of “HIV”-positive gay men found that the average age of those who had no symptoms of illness was 32.4 years; those who had swollen lymph glands or other signs of what used to be called “AIDS-related complex” had an average age of 34.8; those with full-blown AIDS averaged 43.3 years of age (Batman et al., Journal of Clinical Pathology, 42 [1989] 275-81). This is precisely what the dysbiosis theory would predict: the longer one continues doing whatever causes the dysbiosis, the more likely one is to become ill.
In the same vein, a longitudinal study of gay men found that the average age of seroconverting (becoming “HIV”-positive) was 35.3 (Page-Shafer et al., American Journal of Epidemiology, 146 [1997] 531-42).
“Why are so many mid-life gay men getting HIV?”, asked Spencer Cox and Bruce Kellerhouse on GayCityNews© (15 March 2007). That’s a real conundrum under HIV/AIDS theory, but it is to be expected under intestinal-dysbiosis theory. A comment to that piece added anecdotal evidence: “… I was in my 20s and early 30s back in the 1980s and early 1990s. Although there were certainly men my age who were infected, most of the men I knew who succumbed to the epidemic in those years were 10-15 years older than I was. Most of my gay male friends in their 20s-30s were HIV negative and have remained so. I’ve spoken to several other men my age who have seroconverted later in life, and none of us lost close friends in the epidemic. But we did feel that we missed out on the ‘wild’ sex and drugs of the late 70s and early 80’s” (Gary Higo, Jacksonville, FL, Added: Tuesday March 20, 2007 at 05:47 PM EST).

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In sum: Tony Lance’s discussion solves the main puzzles about “HIV” and “AIDS” insofar as they affect gay men, including why they have affected only a small subset of gay men. These insights are also applicable to a variety of other circumstances where disturbances of the intestinal flora have come about for one reason or another in heterosexual men and in women.
But “HIV” and “AIDS” nowadays are so different from their original connotations that many of the observations can only be explained by taking into account the continual changes in definition of both, which has enmeshed the topic of “HIV/AIDS” in a host of complications and contradictions .

HIV DEMOGRAPHICS FURTHER CONFIRMED: HIV IS NOT SEXUALLY TRANSMITTED

The rates at which people in the United States test HIV-positive have remained at about the same level, and have remained distributed geographically in the same manner, for two decades. The rates also vary with age, sex, and race in the same manner in all social groups. Those demographics are characteristic of something endemic, not of something contagious that causes epidemics; thus “HIV” is not something that’s sexually transmitted (see also WHAT “HIV” IS NOT: IT’S NOT SEXUALLY TRANSMITTED, 6 January 2008).

That demographics-based argument, detailed in The Origins, Persistence and Failings of HIV/AIDS Theory (McFarland 2007), is strongly confirmed by finding similar demographic characteristics in Africa as in the United States.

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Consider how testing HIV-positive varies with age and sex:

Sexually transmitted diseases tend to strike adolescents and young adults more than others; by contrast, rates of HIV-positive are highest in newborns and in middle-aged people.

Resistance to infections and illnesses is greatest among adults in the prime and middle years of life; old people are at particular risk for flu, pneumonia, etc. The very opposite applies with HIV: the risk of testing HIV-positive is greatest in middle age.

The above diagram describes general trends. As noted in the source (The Origins, Persistence and Failings of HIV/AIDS Theoryhttp://failingsofhivaidstheory.homestead.com/), there are some variations: “The only major variation between groups is in the precise ‘middle’ age at which F(HIV) peaks, anywhere from 30s to 50s; and that precise age is not always the same for males and females. . . . There are also hints . . . that the peak ages and the male-to-female ratios may be somewhat different in the various racial categories” (pp. 26-7); “black women test positive relatively frequently under some sort of not-necessarily-serious physiological stress, such as pregnancy or childbirth” (p. 247).

Those very same trends can be seen in the Demographic and Health Survey for Rwanda (2005 edition, published July 2006; available at http://www.measuredhs.com/pubs/pub_details.cfm?ID=594&srchTp=).

The data from the United States contained hints that black women are particularly prone to test HIV-positive; the Rwanda data confirm that strongly—women there test HIV-positive more often than men up to age 40, whereas in the United States women test positive more often than men only up to the later teens.

Then there’s the variation with marital status (from Table 15.6, Rwanda Demographic and Health Survey, 2005):

As earlier remarked (TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November 2007), this illustrates the usual variation with age: the widowed are likely to be on average older than the divorced, who are likely to be on average older than those currently married or in a stable relationship, who are likely to be older than those who never had sex. Note, too, that 2 per 1000 men, and 8 per 1000 women, have contracted this supposed STD without ever having had sex.

Yet another confirmation of this variation of HIV-positive with age is reported by Brewer et al., Annals of Epidemiology, 17 (2007) 217-26. The following rates of testing HIV-positive (as percentages) are extracted from their Table 5:

All show the increase with age from teens into “middle age” (which is in the 30s except with Tanzanian males and uncircumcised Kenyan males). Only 1 cell out of 32 (18-24-year-old circumcised Kenyan males) does not fit the pattern, a remarkably consistent, reproducible result for such a demographic variable.

In the Kenya data, note that uncircumcised females test positive more often than males only up to the late teens, which is more like the US data than the Rwandan; whereas in the circumcised group, females test positive more often than males into the thirties, which is more like the Rwandan data than the US data.

Note too how irreproducible is the variation of HIV-positive rate with circumcision status; in 6 cases, circumcised corresponds to a greater HIV-positive rate, in the other 10 cases it is the opposite.

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Among the surprises in the US demographic data was the consistent increase of HIV-positive rates with increasing population density (which is again not characteristic of sexually transmitted diseases). Such a correlation is, however, consistent with an explanation of HIV-positive as a non-specific physiological response to a variety of minor and major insults such as environmental pollution (see p. 89 in The Origins, Persistence and Failings of HIV/AIDS Theory).http://failingsofhivaidstheory.homestead.com/

Remarkably, the same trend with population density is found in Rwanda:
“in 1986 . . . [rates of HIV-positive] were 17.8 percent in urban areas and 1.3 percent in rural areas. . . . In . . . 1991 . . . 27 percent in urban areas, 8.5 percent in semi-urban areas, and 2.2 percent in rural areas. . . . in 1996 . . . 27 percent among urban residents, 13 percent among semi-urban residents, and 6.9 percent among rural residents”; in 2002, 7.0-8.5% in urban areas and 2.6-3.6% in rural areas; in 2003, 6.9-8.3% urban, 2.7-3.6% rural.

The overall rates in 2005 were reported as 2.6 rural and 8.6 urban for women, and 1.6 rural and 5.8 urban for women. This makes the urban-to-rural ratio 3.3 for women and 3.6 for men, so similar that it speaks against any interpretation in terms of different sexual behavior by men and women. Moreover, these ratios are uncannily similar to the approximate ratio of 4 found in the United States (p. 67 in The Origins, Persistence and Failings of HIV/AIDS Theory).

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Religion:
I didn’t come across reports in the United States for how HIV-positive rates vary with religion, but the Rwanda report does include this information:

HIV/AIDS dogma explains rates of testing HIV-positive by sexual and drug-abusing behavior. That provides a dubious basis, to say the least, for understanding how these rates vary with religious affiliation in Rwanda: are we to infer that Muslim women are particularly prone to unsafe promiscuity or drug injecting, while Muslim men are least likely to indulge?

Under the alternative explanation of what HIV-positive means, however—namely, non-specific physiological stress* —, this wouldn’t be at all puzzling if the proportion of Muslim women who are black—of Negroid racial type—is greater than in the other religious groups, since black women are particularly prone to test HIV-positive.
[* see posts of 12 & 25 November 2007, 22 & 29 December, 4, 7, 8 & 12 January 2008]

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It’s often said that scientific theories can be disproved by data that contradict them whereas theories are confirmed when they make successful predictions. Sexually transmitted diseases do not infect middle-aged people more than others in all social groups on disparate continents.
HIV/AIDS theory is disproved because “HIV” is not sexually transmitted.

The theory that HIV-positive reflects a non-specific physiological response was based (in part) on demographic data for the United States, see The Origins, Persistence and Failings of HIV/AIDS Theory. The trends published there and taken as universal constitute effectively predictions that the same trends as to age, sex, and population density would be found elsewhere. They have been found in Africa. The theory is thereby confirmed.

HOW TO TEST THEORIES (HIV/AIDS THEORY FLUNKS)

Here’s another puzzler for HIV/AIDS theory:

Why do blacks and Hispanics suffering from “HIV disease” live longer than Asians, Native Americans, or whites suffering from “HIV disease”?
— Among American women, between 2002 and 2004, all deaths from “HIV disease” among Asians, Native Americans, and whites occurred before age 45; but one third of black and Hispanic women with “HIV disease” lived past 45.
— Among American men, between 2002 and 2004, all deaths from “HIV disease” among Asians, Native Americans, and whites occurred before age 55; but more than 10% of black and Hispanic men with “HIV disease” lived past 55.

It’s generally believed that black and Hispanic Americans do not enjoy as high a level of medical care as do white Americans. So why do they stave off this disease better?

Could it be because they are not being treated with “life-saving” or “life-prolonging” antiretroviral drugs?

* * * * * *

A good theory can make predictions that turn out to be accurate, and it can explain new results as they come in.

HIV/AIDS theory fails on both counts.
— The first prediction was made already as the theory was being announced in 1984: a vaccine against the virus would likely be available within two or three years.
Not only is there no vaccine: scores of attempts have all failed, and we have yet to discover what physiological properties of a vaccine would protect against “HIV infection”.
— A second prediction was that AIDS would spread into the general population since its cause was a sexually transmitted agent.
There has been no spread into the general population. There has been no breaking out geographically either—Sub-Saharan Africa remains the only region with an HIV-positive rate ≥5%; the Caribbean remains the only other region with an HIV-positive rate ≥1%.

— New results, far from being explained by HIV/AIDS theory, have brought conundrum after conundrum: the epidemiology of “HIV” is unlike that of any other sexually transmitted agent, indeed of any infectious agent (The Origins, Persistence and Failings of HIV/AIDS Theory); married women are a high-risk group (TO AVOID HIV INFECTION, DON’T GET MARRIED, 18 November); more exposure results in less infection (MORE HIV, LESS INFECTION…, 21 November); “infection” rates from this incurable illness have declined dramatically without the inevitably required increase in deaths (NOTEWORTHY SUCCESSES AGAINST AIDS IN AFRICA, 4 December 2007); and more.

By contrast, an alternative theory—I’ll call it the “stress theory”—successfully predicts demographic characteristics of “HIV infection” and has remained able to explain new results as they come in.

The stress theory holds that testing HIV-positive is analogous to running a fever. The Perth Group has written copiously about the evidence that positive HIV-tests signify oxidative stress. My book shows that the epidemiology of “HIV” supports the similar, possibly identical view that testing HIV-positive is a rather non-specific physiological response to some sort of challenge or stress.

This evidence-based stress theory predicts that whenever HIV tests are carried out on some group of people matched for other variables, the rate of testing positive will increase from the teen years into middle age before declining again at higher ages. Below the teens, the rate of testing positive will increase with decreasing age, reaching a high among newborns. Males will always test positive more often than females, except in the lower teen years when the reverse is often observed.

The stress theory further predicts that among any group of people matched for other variables, the rate of testing positive will go in the sequence
Asian ≤ White ≤ Native American ≤ Hispanic ≤ Black

This theory has sufficed to explain every significant new result since the book was published.

Take the variation with age. That females test positive more often than males in the early teen years seems difficult to explain if testing positive means infection by a venereal disease whose chief carriers are gay and bisexual men: one would expect teenaged boys to be at greater risk than girls. On the other hand, this phenomenon fits the notion of physiological stress, since menarche (the onset of menstruation) is more physiologically stressful than what boys experience at puberty. At any rate, that female teens test positive more often than male teens was noted already in the mid-1980s among applicants for military service, in the Job Corps, and in a two-decade survey of military cohorts, all in the United States.

I was recently led to look at data from various African countries in quite another connection, and—lo and behold—came across the statement that in Zambia, “The HIV prevalence among girls 14-19 years old is six times that of boys in the same age group” (Summary Country Profile for HIV/AIDS Treatment Scale-Up, World Health Organization, 2005).

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Earlier, a ludicrously mistaken assertion by Sharon Stone (WORLD AIDS DAY…, 22 December 2007) had caused me to look up data about deaths from “HIV disease” in the United States. The following tables show some of the numbers I found. (The trends were the same for each individual year—2002, 2003, 2004—so I aggregated them to lessen the effect of stochastic (chance, random) variations in the smaller numbers. The reports are available at http://www.cdc.gov/nchs/products/pubs/pubd/nvsr/nvsr.htm.)

For both males and females, the numbers vary with age as predicted by the stress theory, reaching a peak in middle age. The numbers for males are significantly higher than for females—except for that teenage phenomenon of females affected more than males: among the only groups where there were significant numbers of deaths among young teens—African Americans and Hispanics—the numbers for females are greater than those for males in the years 10-14 and 15-19.

And, too, the relative mortality rates vary with race precisely as predicted by the stress theory,
Asian ≤ White ≤ Native American ≤ Hispanic ≤ Black

Further: I mentioned in the book (especially p. 246 ff.) that black women seem particularly prone to test HIV-positive. The black-to-white ratio for “HIV” deaths among women, 24, is more than 3 times that for men, 7.4.

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The very fact that these numbers reflect deaths is in itself consonant with the stress theory. Hospital patients and trauma victims test positive at relatively high rates, higher the more critically ill they are (pp. 84-5 in The Origins, Persistence and Failings of HIV/AIDS Theory) . Therefore, among people who die from any one of a number of possible causes, one expects a certain proportion to test HIV-positive. The Centers for Disease Control and Prevention ascribes deaths to “HIV disease” whenever the person was HIV-positive, no matter what the real cause of death was, the manifest cause: cervical cancer, tuberculosis, unexplained weight loss, or just about anything else. So one would expect deaths from “HIV disease” to show the same demographic characteristics as “HIV infection” among living people, and the mortality statistics bear that out.

* * * * * *

It would be interesting to hear from defenders of HIV/AIDS theory their explanation for the age and racial distribution of these deaths on the basis of a supposedly sexually transmitted disease which, untreated, is supposed to bring death within a dozen or so years after infection: How is it that black and Hispanic females manage to survive to age 45-54 before succumbing to this disease whereas Asians, Native Americans, and whites don’t get beyond 44? How is it that black and Hispanic males manage to survive to age 55-64 before succumbing to this disease whereas Asians, Native Americans, and whites don’t get beyond 54?