Questioning authority

From a book I’m reading just now:

“when confronted by perfectly valid reasons  for considering an alternative . . . , the need to save face governs intellectual honesty, and refuge is sought in censorship, ridicule and a blatant disregard for conflicting evidence”

“in their own personal realities, . . . [HIV/AIDS theory has] everything they wish for, and they protect their creation against disbelievers with the only armaments available — invective and ridicule”

“’I agree that antagonism to the . . . debate from within the profession is so great that it would be as difficult for a professed . . . [HIV/AIDS skeptic] to be hired in the first place, much less gain tenure, as for a professed creationist to be hired to gain tenure in a graduate-level department of biology’. . . . Truth, it would seem, is sometimes barred from the universities when it threatens to replace the dominant paradigm”

My insertions [in square brackets] acknowledge that the book isn’t about HIV/AIDS, but the expressed sentiments illustrate how similar are the experiences of people in any field who question a mainstream consensus. Nor need there be the vast array of vested financial and other outside interests connected with HIV/AIDS to make disagreement over an intellectual issue just as viciously ad hominem; as the saying goes, disputes in academe are so bitter because there’s so little at stake — not that prestige, status, a career invested in a certain belief, seem “little” to the individuals concerned.

In physics, similar quotes could have been taken from Lee Smolin’s “The Trouble with Physics”, which describes the stranglehold that “string theory” has despite lacking a single tangible actual accomplished result or application. The experience is quite similar in astrophysics, where those who point to the inadequacies of Big-Bang theory are banished from grants and appointments — read, for instance, Halton Arp’s “Seeing Red”; so too in geological science with those who point so annoyingly to phenomena that continental drift (or plate tectonics) cannot explain; read, for example, “Tectonic Globaloney” by N. Christian Smoot.

People who doubted that the Clovis culture represented the earliest human presence in the Western Hemisphere were denigrated and ridiculed for decades, until the persistence of Tom Dillehay (“The settlement of the Americas: a new prehistory”) and a few others prevailed and the actual evidence was grudgingly acknowledged of much earlier habitation in South America. It was a dogma that the Mayan picture-script could never be deciphered, until Michael D. Coe showed that it could be,  once the possibility was admitted that the present-day natives speak much the same language as their ancestors did (read Coe’s “Breaking the Maya Code”). All the experts knew that the Linear B script was not an ancient form of Greek, until the architect and amateur philologist Michael Ventris showed that it is in fact an ancient Greek language (John Chadwick, “The decipherment of linear B”). Perhaps even more remarkable: the experts all knew that one could not decipher an unknown script if the language it recorded was also unknown, yet Steven Roger Fischer did just that, not only once but twice, with the Phaistos Minoan disk and the Easter Island Rongorongo script (Glyphbreaker).

So there are no end of subjects where, as with HIV/AIDS, outsiders and an unfortunate but courageous few insiders keep pointing out that the evidence for the mainstream consensus is as lacking as were the Emperor’s New Clothes.

At any rate, if you want to take a break from thinking about HIV/AIDS theory, which affects and has affected in so many drastic, harmful, indeed lethal ways so many people, you might enjoy reading “Proving Shakespeare — The Looming Identity Crisis” by David L Roper, from which I took the quotes at the beginning of this post. There is far less evidence to support the notion that the Stratford man (Shaxpere, Shaksper, there are all sorts of other versions as well) wrote the “Shakespeare” plays than there is to support HIV/AIDS theory. Roper, as is rather typical for us dissenters from orthodoxy, is not always judicious and doesn’t always make the case most likely to appeal to naïve observers, but he does marshal the case comprehensively and quite logically, most particularly that all the sparse tangible evidence left by the Stratfordian concerns his business dealings, which were often a bit shady and had nothing to do with literature or writing; everything else is speculation and imagination based on the belief that he wrote those plays and therefore “must” have . . . been educated (despite a lack of school or other pertinent records), etc., etc. My reservations are chiefly Roper’s exposition of the deciphering of alleged codes, where I simply don’t know enough about either Elizabethan practices or cryptography in general to venture a guess. My conviction that the Stratfordian wasn’t “Shakespeare” is owing to Diana Price’s impeccably argued and documented “Shakespeare’s unorthodox biography” which details, for example, that there are no pertinent references to Shakespeare by contemporary playwrights and writers whereas there are innumerable such references among those contemporaries about one another. I had earlier enjoyed “Alias Shakespeare: Solving the Greatest Literary Mystery of All Time” by Joseph Sobran, which first suggested to me that those who question the Stratfordian’s authorship aren’t crazy.

If you become interested in the authorship question, you can keep up with some of the latest discussions at www.shakespeare-oxford.com . It’s a fascinating exercise in assessing evidence without the spiritual burden that accompanies thinking about what HIV/AIDS theory has wrought. And there’s even a very plausible solution already at hand to the mystery of who was the real author of “Shakespeare’s” works.

Dr. Frankenstein turns to CCR5

It was once imagined that Europeans are protected from “HIV” by the CCR5Δ32 gene (CCR5 with deletion 32). However, comparison of the geographic distributions of CCR5Δ32 and of “HIV” disproves that suggestion [Mainstream duffers clutch at Duffy straws: African ancestry and HIV, 26 July 2008]. No sooner had we posted that information than HIV/AIDS “researchers” publish a brilliant scheme for mimicking the  Δ32 deletion via genetic engineering, as “an attractive approach for the treatment of HIV-1 infection”:

“Homozygosity for the naturally occurring 32 deletion in the HIV co-receptor CCR5 confers resistance to HIV-1 infection. We generated an HIV-resistant genotype de novo using engineered zinc-finger nucleases (ZFNs) to disrupt endogenous CCR5. Transient expression of CCR5 ZFNs permanently and specifically disrupted 50% of CCR5 alleles in a pool of primary human CD4+ T cells. Genetic disruption of CCR5 provided robust, stable and heritable protection against HIV-1 infection in vitro and in vivo . . . . HIV-1-infected mice engrafted with ZFN-modified CD4+ T cells had lower viral loads and higher CD4+ T-cell counts than mice engrafted with wild-type CD4+ T cells, consistent with the potential to reconstitute immune function in individuals with HIV/AIDS by maintenance of an HIV-resistant CD4+ T-cell population. Thus adoptive transfer of ex vivo expanded CCR5 ZFN–modified autologous CD4+ T cells in HIV patients is an attractive approach for the treatment of HIV-1 infection” (Perez et al. [23 authors, correspondence to C. H. June], “Establishment of HIV-1 resistance in CD4+ T cells by genome editing using zinc-finger nucleases”, Nature Biotechnology 26 [2008] 808-16).

This brings out in force the Luddite that has been growing in me, fertilized by the copious manure that emanates non-stop from the drug industry and its academic henchpeople. (Luddites are named after the machine-destroying protesters in 19th-century Birmingham whose jobs were lost to mechanization during the Industrial Revolution. It’s come to be applied to antagonism against things that are widely applauded as scientific or technological “improvements” or “advances”.)

There are at least two immediately obvious things very wrong with this sort of anti-HIV approach, irrespective whether HIV has anything to do with AIDS. First, gene therapy remains an idea, not a reality—moreover, an idea whose time has passed because its basis has been found to be incorrect. Second, does not the CCR5 gene perform any functions apart from its possible connection to “HIV”? What are those functions? What happens to them if CCR5 is disrupted in a manner that natural selection (or the Creator, makes no difference) never invented or intended?

The idea of gene therapy stemmed from the initial interpretations of DNA as the carrier of hereditary information. It was thought at first that specific sequences of DNA form distinct and separate genes, individual units of hereditary information, each of them responsible only for the production of one particular protein. That has turned out to be not the case. Genomes are dynamic systems and not linear arrays of fixed genes. At various times, different sub-units of what are still called “genes” work together with sub-units of other “genes” to generate the proteins needed at any given time and place. The sophistication of these precisely scheduled interactions is such that genomes can produce many more proteins than they have “genes”: humans have fewer “genes” than corn and only 25% more than flatworms, even though humans are somewhat more complex creatures; see the fairly recent review by Ast, “The alternative genome”, Scientific American, April 2005, 58-65.

Given that current understanding, any notion of replacing a “defective gene” with a non-defective one presupposes that we know everything about which bits of which genes are needed for what, and at which times, in the development and life of the organism. Our knowledge is very far from that.

Official websites describe the problems quite well:

“Although gene therapy is a promising treatment option for a number of diseases (including inherited disorders, some types of cancer, and certain viral infections), the technique remains risky and is still under study to make sure that it will be safe and effective. Gene therapy is currently only being tested for the treatment of diseases that have no other cures” [published 18 July 2008]

“The Food and Drug Administration (FDA) has not yet approved any human gene therapy . . . . Current gene therapy is experimental and has not proven very successful in clinical trials. Little progress has been made since the first gene therapy clinical trial began in 1990. In 1999, gene therapy suffered a major setback with the death of 18-year-old Jesse Gelsinger. . . . [who] died from multiple organ failures 4 days after starting the treatment. . . .  Another major blow came in January 2003, when the FDA placed a temporary halt on all gene therapy trials using retroviral vectors in blood stem cells. . . .  after . . . a second child treated in a French gene therapy trial had developed a leukemia-like condition. . . . Before gene therapy can become a permanent cure for any condition, the therapeutic DNA introduced into target cells must remain functional and the cells containing the therapeutic DNA must be long-lived and stable. Problems with integrating therapeutic DNA into the genome and the rapidly dividing nature of many cells prevent gene therapy from achieving any long-term benefits. Patients will have to undergo multiple rounds of gene therapy. . . . Anytime a foreign object is introduced into human tissues, the immune system is designed to attack the invader. The risk of stimulating the immune system in a way that reduces gene therapy effectiveness is always a potential risk. Furthermore, the immune system’s enhanced response to invaders it has seen before makes it difficult for gene therapy to be repeated in patients. . . . Viruses, while the carrier of choice in most gene therapy studies, present a variety of potential problems to the patient—toxicity, immune and inflammatory responses, and gene control and targeting issues. In addition, there is always the fear that the viral vector, once inside the patient, may recover its ability to cause disease. . . . Conditions or disorders that arise from mutations in a single gene are the best candidates for gene therapy. Unfortunately, some the most commonly occurring disorders, such as heart disease, high blood pressure, Alzheimer’s disease, arthritis, and diabetes, are caused by the combined effects of variations in many genes. Multigene or multifactorial disorders such as these would be especially difficult to treat effectively using gene therapy. . . .” [last modified 13  May].

Perez et al. ingeniously avoided some of those problems, but the basic lack of knowledge remains. The disruption of CCR5 also disrupted the genome at other sites, chiefly at the neighboring CCR2: “Loss of CCR2 in CD4+ T cells is predicted to be well tolerated as CCR2-/- mice display phenotypes that are not disabling . . . . Mutant alleles of CCR2 have been correlated with delayed progression to AIDS in HIV-infected individuals, although no influence on the incidence of HIV-1 infection was observed . . . . Thus, parallel mutation of a small proportion of CCR2 in CD4+ T cells ex vivo is unlikely to be deleterious . . . . ”; and there was also disruption at “an intron of ABLIM2 on chromosome 4”. “Thus, except for CCR2 (5.39%), and rare (~1/20,000) events at ABLIM2, all the remaining sites showed no evidence of . . . [disruption], given a threshold level of detection of ~1 in 10,000 sequences”.

In other words, the engineering of the CCR5 gene is not 100% specific, other parts of the genome are affected. That no deleterious “side”-effects were observed in the experimental mice is hardly persuasive that the procedure could do in human beings only the one thing we want done and nothing else. Above all, Perez et al. say nothing about why CCR5 exists at all, what functions natural selection intended for it, and whether the CCR5Δ32 that supposedly protects against “HIV”—but doesn’t, according to epidemiological comparisons—is associated with any undesirable conditions.

So, I suggest, Perez et al. are tinkering with things they don’t understand and that are better left alone, hence my reference to Dr. Frankenstein. Incidentally: if you think “Frankenstein” was written by Mary Wollstonecraft Shelley, you should read John Lauritsen’s “The Man Who Wrote Frankenstein”, an illustration that it’s not only in medical science that the mainstream consensus can be wrong for long periods of time. The dogma that the Clovis people were the first Americans was maintained for more than half-a-century in the face of contradicting evidence as well as the implausibility of the idea that the earliest discovered habitation sites would correspond with the earliest actual sites. Back to literary scholarship: it is also not the case that William Shakspere of Stratford-on-Avon wrote Shakespeare’s works, see Diana Price, “Shakespeare’s Unorthodox Biography: New Evidence of an Authorship Problem” ).