Number of Americans living with HPV: 79,100,000 (M and F about equally)
Number of new HPV infections annually: 14,100,000
(for 2008, cited in CDC Fact Sheet “Incidence, Prevalence, and Cost of Sexually Transmitted Infections in the United States”, February 2013)
In 2010 (the most recent year numbers are available) —
11,818 women in the United States were diagnosed with cervical cancer.
So the risk of developing cervical cancer if infected with HPV is roughly 12,000 out of ~40 million (only women get cervical cancer)
In what sense can it be said meaningfully that HPV causes cervical cancer, if that happens to one HPV-infected woman in every 3000?
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Not only is the incidence of cervical cancer low compared to most other cancers, it has also declined steadily for many decades: from 14.79 per 100,000 in 1975 to 6.71 in 2010 (SEER Cancer Statistics Review 1975-2010). Between 2001 and 2010, incidence decreased steadily at 1.9% per year (Gynecologic Cancers).
Despite the steady decrease in incidence of cervical cancer, official recommendations are that pre-puberty girls be vaccinated — a practice that carries more risks of harm than possible benefit:
CDC mongers fear and hawks deadly vaccine; Gardasil and Cervarix: Vaccination insanity
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“HIV” may be a role model for wrong inferences based on mistaken confusion of correlation with causation. (Refresher: Correlation never proves causation.)
Because “HIV-positive” is found in a great variety of conditions, “HIV” is being blamed for an increasing range of ailments, many of which are actually caused by antiretroviral drugs, for example heart failure — see The Case against HIV, sections 3.2, 4.3, 5, 6.1
So HPV too is being credited with causing more and more things.
First there was a campaign to treat boys as well as girls with anti-HPV vaccine so that they would be less likely to suffer from genital warts, a practice whose risk/benefit ratio is even less desirable than for women and cervical cancer. Bear in mind that, once again, all that’s known is that there appears to be a correlation between some strains of HPV and genital warts.
Then “studies” have found that “HPV also has been associated with . . . vaginal, vulvar, penile, anal, and some head and neck cancers” (The Link Between HPV and Non-Cervical Cancers).
Here’s another pertinent fact about statistics and correlations. The typical criterion of significance used by sociologists and medical researchers is p < 0.05, meaning that there is a 5% chance or less that the apparent correlation has no significance. Very roughly speaking, that means 5 of every 100 apparent correlations are purely random, chance occurrences.
Look at that another way. Assume there are a number of variables, and each is tested against each of the others to see whether there is a correlation. Purely by chance, 5% of all the tests will appear to show a correlation that is, however, spurious.
In other words: If a study tests 100 possible correlations and finds 5 statistically significant correlations, then all 5 are most probably spurious.
One trouble is that research articles report their “statistically significant” correlations, but don’t alert the reader to how many possible correlations were considered.
“HPV is a group of more than 100 related viruses” but only 2 — HPV 16 and 18 — are said to cause cervical cancer, or rather “about 70 percent of all cervical cancers”.
If just 40 strains of HPV had been tested for possible correlation with cervical cancer, purely by chance there would appear to be 2 correlations, spurious correlations.
Once an unwarranted theory has become mainstream, further research will turn up any number of intriguing things — intriguing because they make no sense. With HPV, for example, because there are so many strains one can come up with really mind-boggling results clearly demanding further research and research grants (HPV vaccines may be less effective in African American women, researchers find):
“Among women with mild cervical dysplasia, or early precancerous cells:
African American women: HPV types 33, 35, 58, 68
White women: HPV 16, 18, 56, 39, 66
Among women with moderate to severe cervical dysplasia, or advanced precancerous cells:
African American women: HPV types 31, 35, 45, 56, 58, 66, 68
White women: HPV 16, 18, 33, 39, 59”.
Since the presumption is that “mild cervical dysplasia, or early precancerous cells” lead to “moderate to severe cervical dysplasia, or advanced precancerous cells” on the way to actual cervical cancer, isn’t it intriguing (= makes no sense) that not the same sets of strains are “associated” with the first conditions as with the second?
What are the odds that these findings will be repeatable?
More likely, later studies will find equally spurious correlations with other strains.
And by the way: What inspiration was behind the hypothesis that cervical cancers would be caused by different strains of HPV in white women and in African-American women?
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I had been stimulated into this sidetrack into HPV and associated vaccines by something that popped up on my Goggle HIV Alert:
This seemed so bizarre that I followed the suggestion that “For further information, please contact Alison Barbuti, Media Relations Officer | Faculty of Medical and Human Sciences | The University of Manchester Tel: +44(0)161 275 8383 Email: email@example.com”
An immediate response came that since I was not a journalist, my request had been forwarded to the authors. One of them e-mailed immediately that the material would be sent as soon as they were back home. That was a month ago. My paranoia is showing again: maybe they looked at my website and didn’t like my attitude toward HIV and antiretroviral drugs?
After all, for lopinavir (LPV) — the “HIV drug” of the title of the press release —one finds in the literature that all protease inhibitors have the following “side” effects (Table 13 in Treatment Guidelines, updated 12 February 2013):
(Associated with MI and stroke in some cohort studies. . . .) . . . LPV/r: PR interval prolongation. Risks include structural heart disease, conduction system abnormalities, cardiomyopathy, ischemic heart disease, and coadministration with drugs that prolong PR interval.
Gastrointestinal (GI) effects
GI intolerance (e.g., diarrhea, nausea, vomiting); Diarrhea: . . . LPV/r > DRV/r and ATV/r
All PIs: Drug-induced hepatitis and hepatic decompensation (and rare cases of fatalities) have been reported with all PIs to varying degrees
Trunk fat increase . . . ; however, causal relationship has not been established.
Stevens-Johnson syndrome (SJS)/ toxic epidermal necrosis (TEN)
. . . LPV/r . . . : Reported cases
For LPV specifically (Lopinavir + Ritonavir LPV/r)/Kaletra:
“GI intolerance, nausea, vomiting, diarrhea; Pancreatitis; Asthenia [weakness]; Hyperlipidemia (especially hypertriglyceridemia); Serum transaminase elevation; Hyperglycemia; Insulin resistance/diabetes mellitus; Fat maldistribution; Possible increased bleeding episodes in patients with hemophilia; PR interval prolongation; QT interval prolongation and torsades de pointes have been reported; however, causality could not be established”.
Again with “HIV” as role model, the idea appears to be to administer dangerous drugs in absence of any substantial and proven risk.