Judy Wilyman

Judy Wilyman is a student at the University of Wollongong pursuing a doctorate in Science and Technology Studies. Her thesis title is "A critical analysis of the Australian government's rationale for its vaccination policy".

Writings on HPV Vaccination

Searching Google Scholar for 'Judy Wilyman HPV "CIN 3"' for papers for which she is the sole author finds two related papers: Here are three key points from the 2013 paper:

Can HPV cause cervical cancer by itself?

One key point repeated several times was that HPV cannot cause cervical cancer by itself:
"It is also observed that the majority of HPV 16/18 infections do not lead to cervical cancer. This indicates that other etiological or "risk" factors are necessary for persistent HPV infection to progress to cancer...
The International Agency for Research on Cancer (IARC) working group also acknowledged in 2005 that there are cofactors that are associated with HPV infection and cancer development [9]. In other words, an HPV infection does not progress to cancer without the co-factors being present....
In 1995 it was known that HPV infection on its own was not sufficient to cause cervical cancer [1,8]"
Ms. Wilyman cited references to support this claim, but do they really support it? Here they are:
  1. "IARC monographs on the evaluation of carcinogenic risks to humans, volume 64, human papillomaviruses", 1995, 279-290. Note that page 280 directly contradicts Wilyman's assertion in two ways:
    "Besides growth promotion, high-risk HPVs induce chromosomal instability and could therefore act as solitary carcinogens. High-risk HPVs immortalize human and rodent cells in vitro, which can subsequently convert to malignant growth either spontaneously or after exposure to other carcinogens"
  2. "Human papillomavirus is a necessary cause of invasive cervical cancer worldwide", Walboomers JM, J Pathol. 1999 Sep;189(1):12-9. (unpaywalled copy). This paper, as far as I can tell, does not support Ms. Wilyman's claim in the slightest.

  3. "Carcinogenicity of human papillomaviruses", The Lancet Oncology - 1 April 2005 ( Vol. 6, Issue 4, Page 204 ). The key bit appears to be
    "Important cofactors in cancer associated with human papillomavirus infection include coinfection with chlamydia or HIV, smoking, and parity (eg, > 3 children)"
    It's not clear why she referenced this short summary rather than the paper it described, "IARC monographs on the evaluation of carcinogenic risks to humans, volume 90, human papillomaviruses", 2005 (an updated version of reference 1), which says in the chapter "Co-factors of HPV in cervical cancer" that smoking (p. 279), parity (p.290), and coinfection with chlamydia (p.319) or HIV (p. 355) increase the risk of cervical cancer -- but nowhere did I see it say that cervical cancer required a co-factor.

Result: three references, three errors.

Can HPV cause cervical cancer at all?

The 2013 paper states
"Infection with HPV 16 and 18 has been stated to be the central and independent cause of cervical cancer. This infers that no other factors are required for pathogenesis to occur. However, epidemiologists observe that an infectious agent is an insufficient cause of disease [16]. This is because pathogenesis of any infectious agent is dependent upon environmental and lifestyle characteristics [16]. ... the global distribution indicates that the 'risk' of infection from HPV 16 and 18 is similar in all countries but the risk of 'disease' (cervical cancer) is higher in lower socioeconomic countries and communities. ... the lifetime risk of developing cervical cancer before the age of 64 is only 0.8% in a developed nation [18]. This risk increases to 1.5% in developing countries [18]. This difference cannot be fully explained by the presence of screening programs in developed countries because it is known that cancer is an uncommon outcome of all high-grade lesions in women [20]."
Let's see if those references support her claim:
  1. Friis RH, Sellers TA: Epidemiology for Public Health Practice. London: Jones and Bartlett Publishers Inc; 2004.

    She may be referring to the Epidemiologic Triangle; according to the CDC, "The mission of an epidemiologist is to break at least one of the sides of the Triangle, disrupting the connection between the environment, the host, and the agent, and stopping the continuation of disease." This does not argue against HPV being the cause of cervical cancer.

  2. Global Cancer Statistics 2002.

  3. Australian Government, Department of Health and Ageing (DHA): Screening to prevent cervical cancer: guidelines for the management of asymptomatic women with screen detected abnormalities. NHMRC, National Screening Program; 2005.
    "Ostor (1993b) calculated ... 12% [of CIN3] progresses from CIN 3 to cancer"
    This directly contradicts Wilyman, unless you consider 12% uncommon.
Result: three references, two errors.

What fraction of CIN3 progresses to cervical cancer?

In her 2013 paper, Ms. Wilyman states
"HPV natural history shows that only 5% of HPV infections progress to CIN 2 or 3 within 3 years [11]. Of this 5% many CIN 3 lesions will regress (80%) and approximately 20% progress to invasive carcinoma within 5 years. Of this 20% only 40% progress to invasive carcinoma within 30 years [11]."
This statement is rather garbled -- it says that, of the 20% of CIN3 that progress to invasive carcinoma in 5 years, 40% progress to invasive carcinoma at 30 years, possibly implying that really only 8% of CIN3 progresses to invasive carcinoma at 30 years.

And Wilyman really does seem to think nearly all CIN3 regresses; she recently wrote

"More than 95% of high-grade lesions (CIN 3) in young women (15-26 years) regress without treatment."
So, what is the real figure for CIN3 -> CC progression? Her reference [11] says:
  1. "Prophylactic HPV Vaccines and Prevention of Cervical Intraepithelial Neoplasia, Heitmann ER, Harper DM, Current Obstetrics and Gynecology Reports September 2012, Volume 1, Issue 3, pp 95-105. Excerpt:
    "Natural history studies of HPV infection show that ... Only 5% of infections progress to a cervical intraepithelial neoplasia (CIN) grade 2 or 3 precancerous stage within 3 years. Of those CIN 3 lesions that do not regress, only 20% progress to invasive carcinoma within 30 years (Fig 3) [23]."
That paper in turn refers to
  1. "Natural history of cervical neoplasia and risk of invasive cancer in women with cervical intraepithelial neoplasia 3: a retrospective cohort study". Excerpt:
    "In 143 women [with CIN3] managed only by punch or wedge biopsy, cumulative incidence of invasive cancer of the cervix or vaginal vault was 31.3% (95% CI 22.7-42.3) at 30 years, and 50.3% (37.3-64.9) in the subset of 92 such women who had persistent disease within 24 months."
In other words, approximately untreated CIN3 progresses to invasive cancer at a rate of 50% at 30 years, not the 20%, 8%, or 5% variously claimed or implied by Wilyman.

Result: one reference, one error.

Accuracy and the Review Process

An unscientific spot check of less than half of the key points of one paper is not a firm foundation for conclusions about an author. Nevertheless, the fact that 7 of 8 references did not support the text does not inspire confidence.

The 2013 paper was peer reviewed, and the review history is open for inspection. There were three reviewers, all very qualified. Two of the reviewers raised substantive issues similar to, but in much greater depth than, those I raised above.

For example, here's one issue that was raised by a reviewer:

"6. Page 8: 'This difference cannot be fully explained by the presence of screening programs in developed countries because it is known that cancer is an uncommon outcome of high-grade lesions in women even in the absence of screening [20 p15].' I do not understand this sentence, the fact that cancer is an uncommon event eve in the absence of screening is demonstrated by the fact that cervical cancer risk in developing countries is 'only' 1.5% despite most of the women have an infection during their life. The difference in risk between risk in screened and unscreened could be much more than 0.8 vs. 1.5, see for example the papers by Quinn, Anttila, and many others."
Wilyman's response to the reviewer's comment:
"I have removed this phrase."
Alas, although Ms. Wilyman removed the words 'even in the absence of screening', it did not render the sentence correct or supported by her reference (see above).

Presumably another round of review might have caught this, but the review process ended after two of the three reviewers had no more objections.

Truth-teller, or true believer?

Ms Wilyman maintains a web site "Vaccination Decisions" dedicated to opposing routine immunization as recommended by mainstream medicine. It accuses doctors, the media, and the Government of spreading misinformation, saying specifically
"Vaccines did not reduce the deaths and illness from infectious diseases...
current scientific evidence suggests [vaccination] is the most likely cause of autism..."

This is a remarkable rejection of the current scientific consensus that vaccination saves millions of lives annually. that no causal link between vaccines and autism has been established, and that Dr. Wakefield's claims that vaccines cause autism were fraudulent.

Given the remarkable decline in prevalence of Diphtheria, Measles, Mumps, Pertussis, Poliomyelitis, Rubella, Smallpox, Tetanus, Hepatitis A, Acute Hepatitis B, Haemophilus influenzae Type b, Pneumococcal Disease, and Varicella since introduction of vaccines against those diseases, and evidence of the effectiveness of individual vaccines such as HiB, there seem to be only two likely ways to account for the wide divergence between Ms. Wilyman's position and the scientific mainstream: either she's right (in which case the government, along with most scientists and journalists, is lying and cannot be trusted), or she's wrong (in which case Wilyman falsely believes, as she has written, that the government, scientists, and journalists are conspiring to promote vaccines against the interests of the people).

How can we distinguish between these two possibilities? Doing this objectively is challenging, since most people are on one or the other side, and suffer from some degree of confirmation bias, but let's try.

Adherents of conspiracy theory believe those theories even in the face of overwhelming contrary evidence. They seem to see the world through what Erich Hoffer called a 'fact-proof screen', i.e. their perceptions are clouded by severe confirmation bias.

How might severe confirmation bias influence how the sufferer reads textual information, and how might traces of these events show up the sufferer's own writings?

Someone reading an article might see support where there simply is none, or might miss a key paragraph that explicitly and strongly refutes it. Or they might trust a demonstrably false article without verifying it.

So to check for confirmation bias, one might find key sections of the person's writing, check the references in those sections to other texts, and see how often those two kinds of errors occur. The frequency of these errors should be higher in text written by people with more confirmation bias.

Endorsement of Wilyman's Errors by University of Wollongong

As shown above, Ms. Wilyman's writings are based on several easily verified factual errors. If widely followed, her writings might hinder the prevention of disease through effective vaccination programs.

Not surprisingly, the University of Wollongong has come under criticism for supporting her research.

The University has replied in 2012

"Any 'conspiracy' theories she may have are independent of her relationship with the University of Wollongong. Her PhD has to meet the rigorous standards set by the university"
and in 2014
"The University of Wollongong wishes to strongly reiterate that articles and associated comments published by Judy Wilyman on the internet, on vaccination issues, are her own personal views and not those of the University. The University has never indicated at any time that it promotes or supports her views regarding vaccination issues."

Do the "rigorous standards" of the University provide for a thesis review committee that has expertise on the science being discussed, and state that factual errors of the sort described above would disqualify a thesis? Let's see.

The UoW's Submission of Postgraduate Thesis - Guidelines for Higher Degree Candidates says

"4.1 Number of Examiners required... Doctoral degrees Two examiners - both external to the University of Wollongong
4.2 Selecting Potential Examiners... the candidate and supervisors should consider the following guidelines: The expertise of the examiners in the field of study ought to be unchallengeable...
4.3 Completing the Nomination of Examiners Form In consultation with their supervisors, candidates should nominate at least four (4) potential examiners on the Nomination of Examiners Form. The supervisors will select two scholars from this list to be examiners. Candidates must not be informed about the final selection of examiners. The supervisors will forward the Nomination of Examiners Form to the HPS (Head of Postgraduate Studies) for final approval."
So the examiners should have unchallengable expertise in the field of study, it's up to the student's supervisor to select the examiners, and up to the HPS to approve them.

In this case, the supervisor is Dr. Brian Martin, and the HPS for the School of Humanities and Social Inquiry is currently Dr. Sarah Sorial.

Neither Dr. Martin nor Dr. Sorial have expertise in biology or medicine, and the field of study is arguably "Science and Technology Studies" rather than biology or medicine. Thus it is likely that the thesis review committee will also lack any expertise in biology or medicine.

Whether that means they will not consider errors of fact in biology or medicine relevant to the quality of the thesis is unknown, but it would mean they might lack the expertise to recognize these errors. A PhD approved by a committee lacking this expertise would leave the University open to charges of supporting pseudoscience.

See Also

David Hawkes' review of Wilyman's 2011 paper

Copyright 2014 Dan Kegel
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