Wednesday, 23 February 2011

More than BPA in the water in Maine

In a striking example of how a state's proximity to Canada is not directly correlated with levels of political craziness, the Governor of Maine, one Paul LePage, has recently commented that bishpenol A "isn't a problem".

“Quite frankly, the science that I’m looking at says there is no [problem],” LePage said. “There hasn’t been any science that identifies that there is a problem.”

Really, LePage? There hasn't been any science that identifies a danger due to BPA? What about this? Or this? Or this and this and this? I found these papers in about 5 minutes after searching PubMed for "BPA", and there are undoubtedly many more. The biological ramifications of BPA exposure are well documented. The toxicity of BPA, especially to developing children, is irrefutable. Having done research on BPA myself, I know this as a fact.

So just what science have you been looking at, Gov. LePage? Of course, he doesn't cite a single study, but that is unsurprising for a politician. However, LePage recently appointed Patricia Aho - a former lobbyist for BPA-producing chemical companies - as the deputy commissioner for the Maine Department for Environmental Protection. I think that gives us a clue who's science he's been looking at.

This whole issue is eerily reminiscent of the kerfuffle over tetraethyl lead, and over CFCs. Both these chemicals have irrefutable deleterious health and environmental effects, but right-wing politicians fought tooth and nail against regulations on them, claiming that they were harmless when the science plainly said otherwise.

There is one problem with BPA that LePage sees, however:

“The only thing that I’ve heard is if you take a plastic bottle and put it in the microwave and you heat it up, it gives off a chemical similar to estrogen. So the worst case is some women may have little beards.”

Tuesday, 22 February 2011

Deepak Chopwned

Gotta love this video. The most succinct takedown of Chopra I've ever seen.

That confused "I don't get it" look on Chopra's face makes the video all the more great.

Monday, 21 February 2011

Creationists: not so smart and honest.

Browsing Youtube today, I came across a video entitled "Why do SMART AND HONEST people laugh at Darwinsits?". With a title like that, I knew I had to watch it. Here it is, below:

The guy's argument is this: the scenarios used by evolutionary biologists to explain the giraffe's long neck are completely implausible (and smart and honest people, apparently, laugh at them). According to him, biologists claim that the giraffe's neck grew longer to reach leaves higher up on trees, and all the shorter neck giraffes died of starvation because they were "too proud" to bend their necks down and eat the grass on the ground. Why, he asks, did none of the other African animals also grow long necks? Why didn't the giraffes just eat the grass on the ground? This scenario is ridiculously laughable, he says. Silly biologists!

The problem is that he has a less than tenuous grasp on how evolution works and hasn't a clue what evolutionary biologists actually say on the issue.

The currently favoured hypothesis in evolutionary biology is that the giraffe's neck is an example of runaway sexual selection, not natural selection via resource competition. Male giraffes routinely use their neck in "necking" competitions - mating displays that males use to establish dominance and win the fancy of females. Just like the peacock's tail, the giraffe's neck grew longer and longer in response to the ladies' preferences. Shorter neck giraffes did not "die of starvation"; they had a harder time wining mates and this negatively impacted their reproductive fitness. Why don't the other plains animals have long necks?  Because this sexual selection process didn't occur in other animals.

But even in the absence of sexual selection, the giraffe's neck can be explained by ecological selection alone. Those giraffes with longer necks had access to greater resources than those with shorter necks (that is to say, not only could they eat the grass, but they could eat leaves higher up on trees, too). The long neck giraffes, then, had greater reproductive fitness than those with shorter necks. The alleles for longer necks became more and more prevalent in the population; the alleles for shorter necks became less and less frequent. The short neck giraffes did not "die from starvation", the short neck alleles were weeded out over time. The video's creator asks "why didn't the short neck giraffes just eat the grass?", and if he thought about it for a second, he would realize that they did. It was competition from the other grazing animals that prompted giraffes to find resources else where; those that could eat both the grass and the high leaves had an advantage!

So why do smart and honest people laugh at "Darwinists"? They don't. They laugh at fools trotting out tired creationist canards without doing a moment's research.

Saturday, 19 February 2011

AIDS Denialism: Deadly Ignorance Part III: Fuzzy Math and Distorted Reality

In the previous two part of this series (see Part I and Part II), I tackled the forerunners of the AIDS "skeptics" community, and addressed how Koch's Postulates support HIV as the cause of AIDS. In this part, I will assess how some of the deniers distort studies and misinterpret math to support their dangerous ideas.

If you spend any time on AIDS denialist websites, there are likely a few statistics that will show up repeatedly. This is because it is a common practice for AIDS denial websites to copy and paste the same arguments verbatim from one website to the other, no matter how old the information might be, or if the arguments have been debunked already. One such statistic that the deniers constantly toss around is that half – or more - of Africans who qualify as having AIDS test as HIV-negative1. Specifically, they routinely cite three specific studies2:

122 patients with "AIDS": 69% test HIV-negative (Brindle, 1993)
227 patients with "AIDS": 59% test HIV-negative (Hishida, 1992)
913 patients with "AIDS": 71% test HIV-negative (Songok, 1994)

But if one were to take a critical look at each of these studies, they do not support the claims of the AIDS "skeptics" in the least. Let's take a look at each of them.

The first paper by Brindle et al. is entitled "Quantative bacillary response to treatment in HIV-associated pulmonary tuberculosis"3. In this study, the authors looked at 122 patients with "culture-proven pulmonary tuberculosis". These patients were divided into two groups, and each group had their tuberculosis treated with one of two different treatments. They then looked at how the HIV-positive individuals in each group took to their treatments compared to the HIV-negative individuals. The purpose of this was to determine if patients with HIV would respond to chemotherapeutic treatments differently than those without HIV (and they found that there was very little difference).

It should be noted that the 122 patients in the study were NOT patients with AIDS. They were patients with pulmonary tuberculosis. This is a symptom of AIDS, but of course, pulmonary tuberculosis can arise in humans in a variety of ways; it is not exclusive to AIDS patients. Of the 122 patients, only some of them had AIDS. So where did the denialists get their numbers? Of the patients that were given the first treatment, 17 were HIV-positive and 57 were HIV-negative. Of those that were given then second treatment, 20 were HIV-positive and 35 were HIV-negative. In total, 37 of the 122 patients were HIV-positive, so 85 out of 122, or 69%, were HIV-negative. But this is not the number of AIDS patients who were HIV-negative; rather it is the number of tuberculosis patients who were HIV-negative. This is a different thing altogether. The AIDS "skeptics" misrepresent this number to support their case, when in fact, it does not.

The second paper is "Clinically diagnosed AIDS cases without evident association with HIV-1 and 2 infections in Ghana" but Hishida et al4.The authors' aim in this paper was simple: to test patients suspected of having AIDS for HIV. It is important to remember that the patients they looked at were suspected cases of AIDS – the authors state "CD4 cells were not counted [in these patients] because of insufficient facilities". They looked at 227 cases and found the following results : 48 were positive for HIV-1, 17 were positive for HIV-2, 11 were positive for both stains, and 16 were of indeterminate HIV status. The remaining 135 patients were determined to be HIV seronegative. Those 135 of 227 patients amounts to the 59% the AIDS denialists toss about. So at a superficial glance at the numbers might be seen as giving support to the denialist arguments.

But the denialists apparently didn't read any further than the raw numbers, because the authors continue: the 135 seronegative samples were from patients that had "weight loss, prolonged diarrhea, chronic fever" – so is this AIDS? The authors didn't think so. They state "We believe that many patients of this group were perhaps improperly diagnosed or had other unidentified diseases…[t]he existence of other agents causing AIDS-like syndromes might be possible for these so-called HIV-negative cases." In other words, it's likely the HIV-negative cases were from patients who did not have AIDS to start with – remember that these were samples from suspected AIDS cases, and not confirmed cases. The denialists take a quick look at the numbers, point out the 59% HIV-negative cases and ask "How could this be?" without bothering to read further and realize that the authors have answered that very question!

I also feel that I should point out that the authors used serological techniques to detect the presence of HIV antibodies in the samples, rather than using more sensitive PCR techniques. I am confident that if this study was repeated today, using PCR and improved diagnostic techniques, the suspected AIDS cases that test HIV-negative would be quite fewer.

The third study the denialists refer to is Songok et al's paper "Low Prevalence of Human T-Lymphotrophic Virus Type 1 (HTLV-1) in HIV patients in Kenya"5. They claim that this study showed a huge 71% of AIDS patients were HIV-negative; such a bold claim better have a wealth of evidence supporting it. The first thing one might notice when reading it, however, is that it isn't a peer reviewed research study; it's just a letter to the editor. Nevertheless, the authors report on some original research they were doing: they wanted to check to see the prevalence of HTLV-1 infections in HIV infected individuals. They did this by collecting 913 samples from suspected AIDS cases in Kenya. Again – remember that these are not confirmed cases of AIDS. Using these samples, they tested for HIV-1 using both ELISA and western blots. They reported that 265 (or 29%) of these tested positive for HIV-1 on both tests. This is where the denialists get their statistic. However, this number represents the samples that were positive on both the ELISA and the western blot – it excludes those samples that tested positive on one or the other tests. They also tested for HIV-1 alone; they did not test for HIV-2, and this undoubtedly reduced the number of positive results. And again, the researchers did not use more sensitive PCR techniques, so it is entirely plausible that many positive cases were missed.

What all three papers have in common is that the estimates of HIV-positive individuals are underestimated. All three papers were written before sensitive PCR-based methods for detecting HIV were developed and put into common use, and before doctors were able to accurately diagnose AIDS and differentiate it from other immunodeficiency syndromes. And what deniers need to realize that it is impossible to obtain a 100% detection rate. Multiple factors exist that prevent the presence of HIV from being detected 100% of the time. If the AIDS "skeptics" really wish to show that HIV does not cause AIDS, then perhaps they should find a study to cite that isn't two decades old.

So as usual, critical examination of denialist claims shows that they don't have a leg to stand on. Better luck next time, guys. Come back when you have recent research that you can cite without twisting the statistics into misleading conclusions.


  1. See for an example.
  2. These three statistics were also stated by the Youtube user who prompted this series on debunking AIDS denial nonsense.
  3. Brindle et al. Quantative bacillary response to treatment in HIV-associated pulmonary tuberculosis. 1993. American Review of Respiratory Disease
  4. Hishida et al. Clinically diagnosed AIDS cases without evident association with HIV-1 and 2 infections in Ghana. 1992. The Lancet
  5. Songok et al. Low Prevalence of Human T-Lymphotrophic Virus Type 1 (HTLV-1) in HIV patients in Kenya. 1994. Journal of Acquired Immune Deficiency Syndromes

Wednesday, 16 February 2011

AIDS Denialism: Deadly Ignorance Part II: Koch’s Postulates, AIDS and more Wackaloonery

(Click for Part I and Part III of this series)
In my previous post, I wrote about some of the faces of AIDS denialism, and the arguments (and I use that word loosely) that these "skeptics" present. What their arguments revolve around - and indeed the arguments put forth by virtually all members of the AIDS denialism community - is that there is no evidence that AIDS is caused by HIV. Certainly, by all accounts, the medical and scientific communities have demonstrated otherwise. But how do we know that HIV is the causal agent behind AIDS? How do we know what the causal agent is behind any disease? Do we have a standard method of determining causality, and is the HIV/AIDS connection supported by this method? The answer is yes.

In 1884, a Prussian physician by the name of Robert Koch, along with is colleague, the bacteriologist Friedrich Loeffler formulated a set of criteria that they used to establish a causal relationship between an illness and a causative agent. These criteria were published in 1890 by Koch and have since been known as Koch's Postulates. Koch used this set of postulates to determine the etiology of both tuberculosis and anthrax1, and in the 120 years since their first publication, the causes of many other diseases have been determined by successful application of Koch's Postulates. The four tenants of Koch's Postulates are as follows:

  1. The causative agent must be found in all organisms exhibiting the disease, and not in healthy individuals.
  2. The causative agent must be isolated from a diseased individual and grown in culture.
  3. The causative agent, when introduced to a healthy individual, should cause the original disease.
  4. The causative agent must be reisolated from the inoculated, diseased host and shown to be identical to the original agent.
Note that the first postulate is not universally required, as many diseases exhibit asymptomatic carriers (as is the case for HIV). The third postulate is unique in that it states "should" rather than "must" – this is because infection rates are never 100%. The fourth postulate was originally required by Koch, but fulfilling the first three postulates is generally considered to be sufficient to indicate causation. If all four postulates are fulfilled by a particular causative agent, then it can be said that the agent is the likely cause of the disease.

So, when these four postulates are applied to HIV/AIDS, does the result support the claim that HIV causes AIDS? The answer is a resounding "yes". Let's take the postulates one at a time.

The causative agent must be found in all organisms exhibiting the disease, and not in healthy individuals.

As noted above, this first postulate is not universally required, as asymptomatic carriers of HIV appear as healthy individuals. Nevertheless, those with HIV-1 and no symptoms at time of diagnosis, eventually progress to AIDS. And in 95% of cases, individuals suspected to have AIDS test positive for HIV virions, HIV antibodies or positive for HIV viral loads2. This association between HIV and AIDS is supported by a wealth of evidence from countless studies, and cannot be dismissed.

The AIDS denialists, however, will insist that this first postulate has not been fulfilled. They will point out that there are cases of individuals exhibiting AIDS-defining characteristics who have not tested positive for HIV antibodies. This, they are quick to claim, is in violation of the first postulate, since these cases show the disease without the putative causative agent. There is a very straightforward answer to this, though: immune deficiencies can develop in more ways than just being induced by HIV infection. There is a virtual plethora of ways immune deficiencies can arise, and these will exhibit symptoms similar to AIDS – bacteria, genetic conditions, environmental factors, and immune suppressing drugs can all cause symptoms associated with AIDS. In such cases, it is not surprising that patients test HIV negative! But in cases where individuals present all or most of the AIDS-defining characteristics – particularly a depletion of CD4+ lymphocytes – the HIV virus is found3. Koch's first postulate remains fulfilled.

The causative agent must be isolated from a diseased individual and grown in culture.
Culturing the proposed pathogen is not only the second postulate but also, perhaps, the most important step in identifying the suspected pathogen. Viruses can be more difficult to grow in culture than bacterial strains, but this has not prevented HIV from being cultured from samples taken from AIDS patients. Over the years, it has been cultured in T-cells, macrophages as well as in HeLa cells. Furthermore, isolated and cultured strains of HIV have had their genomes sequenced and cloned, with literally thousands of unique sequences added to sequence data bases. Isolation of HIV from samples is not an issue, and there have been multiple4,5 protocols established and published on how to accomplish this. There are even commercially available kits which allow HIV to be isolated from infected samples. Culturing HIV has become a routine practice in HIV research to the point where it is more or less a triviality. Postulate 2 has been fulfilled and continues to be filled on a daily basis.

The causative agent, when introduced to a healthy individual, should cause the original disease.
The third postulate is perhaps the most controversial of the postulates. For one, it cannot be fulfilled solely on the basis of epidemiological data but must rather rely on experimental evidence. When looking at diseases in animals or when using animal models, the third postulate is easy to demonstrate experimentally. When it comes to the transmission of diseases in human subjects, however, the third postulate is tougher to demonstrate. No ethics board would ever allow researchers to experimentally infect healthy people with cultured HIV to see if they progress to AIDS. Nevertheless, this postulate has been fulfilled due to the unfortunate accidental transmission to humans who were doing research on HIV6.

In this case, three lab workers were working with HIV-1, and all became accidentally infected with the virus. None of these workers belonged to any of the high-risk groups; they were not drug users, had not had blood transfusions, and did not engage in homosexual behaviour. All three of the workers exhibited depleted CD4+ cell counts (two of which were low enough to warrant an AIDS diagnosis) and one progressing to pneumonia7. AIDS "skeptics" who insist that HIV does not cause AIDS and that AIDS is caused by drug use are at a loss when it comes to explaining this case study. How else could the infected workers, who were not part of any risk groups, have developed AIDS unless it was due to HIV infection? How do they explain the onset of symptoms in these workers if HIV is, as they claim, pathologically asymptomatic?

Evidence from animal studies has also given support to the third postulate. Studies in which baboons have been infected with HIV-2 have shown these animals to develop AIDS-like symptoms including depletion of CD4+ lymphocytes8 (and I highly doubt these baboons were drug users!). Mouse strains used to model SCID which have been given human peripheral blood lymphocytes (hPBLs)9 also develop severe immunodeficiencies when infected with HIV10. These mice also show depleted CD4+ cell counts.

Studies like this show experimentally that cultured HIV, introduced into healthy individuals, result in the hosts progressing to AIDS. This is sufficient to fulfill the third postulate.

The causative agent must be reisolated from the inoculated, diseased host and shown to be identical to the original agent.
This fourth postulate, as noted above, is now often considered extraneous to suggesting causation by a suspected pathogen. Nevertheless, the example of the infected lab workers cited above is a good case of this postulate also being demonstrated. The virus was reisolated from the infected lab workers, and sequenced11. The divergence between the sequences from the strains isolated from the workers was very small – about the same as the divergence in sequence between HIV-infected infants and their mothers. In other words, it was the same strain that they had been working with. Consider Postulate 4 demonstrated.

So it is plainly obvious that all of Koch's postulates are fulfilled, and HIV can be said to be the likely causative agent behind AIDS. Koch's postulates demonstrate reasonable criteria for determining causation, and provide reasonable evidence that the AIDS "skeptics" are wrong.

I will continue in Part III, where I examine the fuzzy math used by AIDS "skeptics" to distort reality and push their dangerous nonsense.


  1. The infectious agents behind these diseases, Mycobacterium tuberculosis and Bacillus anthracis, respectively, were discovered and first isolated by Koch himself.
  2. See the references in Part I for more on this.
  3. There is an exception to this. A rare condition exists called hypogammaglobulinemia where individuals are unable to mount an immune response to invading pathogens. People with this disorder who are infected with HIV will not show HIV antibodies present when tested.
  4. See
  5. See
  6. Weiss SH, Goedert J J, Gartner S, Popovic M, Waters D, Markham P, Veronese FD, Gall MH, Barkley WE, Gibbons Jet et al: Risk of human immunodeflciency virus (HIV-1) infection among laboratory workers. Science 1988, 239:68-71.
  7. I have been unable to find any information on these three workers more recent than the above referenced article. If anyone has updated information, I would be interested in hearing it!
  8. Barnett SW, Murthy KK, Herndier BG, Levy JA: An AIDS-like condition induced in baboons by HIV-2. Science 1994,266:642-646.
  9. SCID-model mice are unable to produce B and T lymphocytes. Transplanting hPBLs into these mice reconstitutes a functioning immune system.
  10. Mosier DE, Bulizia R J, Baird SM, Wilson DB, Specter DH, Spector SA: Human immunodeficiency virus infection of human PBLSCID mice. Science 1991,251:791-794.
  11. Reitz MS Jr, Hall L, Robert-Gurofl M, Lautenberger .I, Hahn BH,Shaw GM, Kong LI, Weiss SH, Waters D, Gallo RC,Blattner W: Viral variability and serum antibody response in a laboratory worker infected with HIV-1 (HTLV-IIIB). AIDS Res Hum Retroviruses 1994, 10:1143-1155.