The Dance of Death

I keep an eye open for reports on HPV, since reading that, while it causes cervical cancer, it’s also linked rather less strongly to genital and anal cancer.  I turned up another couple of links tonight. The first from the Mouth Cancer Foundation relates to oral cancer:

The most dangerous HPV’s, 16 and 18, which are transmitted through sexual contact are known to cause up to 95% of cervical cancers. Now these two HPV’s are also being linked to oral cancer.

A study done by Dr. No-Hee Park showed that the mouth was, at the cellular level, structurally very similar to the vagina and cervix. Both organs have the same type of epithelial cells that are the target of HPV 16 and HPV 18. The majority of oral cancers are cancers of epithelial cells, primarily squamous cell carcinomas, not unlike the cancers that affect the cervix. Dr. Park’s study also showed that smoking and drinking alcohol help promote HPV invasion.. Combine tobacco and alcohol with HPV, and the epithelial cells in the mouth, and you may have the formula for the development of an oral cancer.

A recent study conducted by Dr. Maura Gillison at the Johns Hopkins Oncology Center furthered the premise that HPV is linked with certain types of oral cancer. In 25% of 253 patients diagnosed with head and neck cancers, the tissue taken from tumors was HPV positive and HPV 16 was present in 90% of these positive HPV tissues. This information helps to confirm that there is a strong link between HPV 16 and oral cancer.

What is meant by "combine tobacco and alcohol with HPV"? It sounds like they might physically serve in some manner to enable HPV to enter epithelial cells, with nicotine holding the cells open while the alcohol washes it in or something.

But most likely it doesn’t mean that at all. It probably simply means that people with a history of oral sex are quite likely to also have a history of smoking and drinking.  Let me guess: I bet that they’re quite likely to have a history of listening to loud rock music. dancing, and dressing fashionably smartly. That is they’ll have histories of doing all the things that people do when they go and try to get themselves laid. They get a bit drunk to lose their inhibitions, and they smoke cigarettes to calm their nerves, and then they hope they’ll, well,.. get lucky.

And what counts as oral sex? Is it just oral-genital sex, or does that include mouth-to-mouth snogging? It probably does include the latter, because anything that transfers tissue from mouth to mouth is likely to tranfser HPV from one mouth to another. But so also is sharing someone’s food or cup or fork. There can be all sorts of ways that a virus can be transferred from one person to another. The less material that is transferred, the less likely someone is to get infected.

And in the same token, if all those people smoking and drinking out on the dance floor in a club at night are more likely to get laid and infect each other with HPV, it follows that non-smoking non-drinkers who stay at home at night reading books are less likely to get laid, and contract an HPV infection. 

Second link from WebMD relates to throat cancer:

HPV, the virus that causes cervical cancer, is also linked to throat cancer, and oral sex is a major risk factor for both men and women, new research shows.

Having multiple oral sex partners topped the list of practices associated with an increased risk of developing oropharyngeal cancer, according to the study published in the May 10 issue of The New England Journal of Medicine.

People in the study who reported having a history of six or more oral sex partners were three times as likely to develop the cancer as people who reported that they had never had oral sex.

In looking at patients with tumors that were positive for a particular strain of HPV already well-linked to cervical cancer, six or more oral sex partners increased risk for throat cancer by eightfold.

And those who showed evidence of a prior oral infection with human papillomavirus (HPV) were 32 times more likely to develop the cancer.

Oral sex seemed to be the main mode of transmission for oral HPV, although the researchers note that transmission from mouth to mouth contact couldn’t be excluded. The new study shows that oral HPV infection is linked to head and neck cancer regardless of two other known risk factors: heavy tobacco and alcohol use.

What’s meant by "head and neck cancers"? A neck isn’t quite the same thing as a throat. It seems to be suggesting that cancers on the outside of the neck or head aren’t associated with tobacco and alcohol. Transfer of HPV from mouth to head or neck might not be sexual at all. They might be transferred by coughing or sneezing or a peck on the cheek. No ‘sex’ at all. And so no need for tobacco and alcohol, those two great sexual enablers.

Epithelial cells, which cover the entire surface of the body, inside and outside , are also found in lungs:

Simple epithelium promotes the diffusion of gases, liquids and nutrients. Because they form such a thin lining, they are ideal for the diffusion of gases (eg. walls of capillaries and lungs).

So if HPV 16 and 18 targets epithelial cells, it will most likely target epithelial cells in the lung as well. As I’ve reported before, HPV has been found in 25% of lung cancer cases, and sometimes (in Japan) in as many as 80% of cases.

If HPV is the true cause of many cancers, including lung cancer, then why was there such an upsurge in cancer in the 20th century? And the answer may be that it had nothing to directly do with smoking, but had everything to do with relaxing sexual mores, which may have paradoxically come as a response to improving medical treatments of the more common sexually transmitted diseases – like syphilis and gonorrhea – and also, equally importantly, improving contraception. Once people were having multiple sexual partners and engaging in experimental sex, HPV started jumping from person to person. But why was it lung cancer so often? Perhaps because the surface area of human lungs is very large:

Together, the lungs contain approximately the same length as 1500 miles (2,400 km) of airways and 300 to 500 million alveoli, having a total surface area of about 70 square metres in adults — roughly the same area as one side of a tennis court.

The external surface area of a human is about 2 or 3 square metres.This suggests an airborne HPV transmission route person to person. An airborne stray packet of HPV may have a good probability of ending up in human lungs. But how? Maybe it was because back then people danced cheek-to-cheek on crowded dance floors, changing partners every few dances. While they danced, cheek to cheek, and very often nose by nose, they breathed in airborne HPV. If so, then the reason that lung cancer incidence peaked in the late 20th century (if it has peaked) is because by then people danced separately after dances like the jive and the twist became fashionable. It could be that Chubby Checker single-handedly did far more to cut the incidence of lung cancer than all the doctors in the world laid end to end.

And that the waltz was the dance of death.

POSTSCRIPT: If lung cancer is the consequence, 10 or more years later, of HPV infection, why was there an asymmetry in its incidence between men and women, with women getting it a lot less often? One way this might have happened would have been if lots of men had sex with relatively few women – e.g. prostitutes or ‘loose women’. If there was an asymmetry between men and women’s sexual practices – i.e. a ‘double standard’ – with fewer women becoming sexually liberated, then fewer women would have been infected. And there was indeed a double standard. But as women also became more sexually liberated, HPV would have spread from the red light districts to the wider community, and an epidemic of lung cancer started. If so, to specifically cause lung cancer, it suggests that HPV must have ‘taken off’ and become airborne at some point, perhaps concentrated in a very localised HPV-rich ‘hot spots’, like clubs and bars.

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12 Responses to The Dance of Death

  1. Anonymous says:

    HPV / Lung cancer
    Don’t forget Klein & Petersen:
    The data suggest that HPV is the second most important cause of lung cancer after cigarette smoking and strongly argues for additional research on this issue:

  2. Frank Davis says:

    Re: HPV / Lung cancer
    Yes. I think I probably referenced the Klein and Petersen study in one of my earlier posts. It’s the source of my 25% and 80% HPV incidence in lung cancer. The abstract reads:
    HPV has been identified not only in gynaecological carcinomas but also in tumors of other organs, especially of the oropharynx and upper aero-digestive tract. In this study we focused on the available literature on HPV in lung carcinomas. In total, 53 publications reporting on 4508 cases were reviewed and assessed for the following parameters: continent and region of the study, number of cases, detection method, material type, HPV type, histological subtype and number of the HPV-positive cases. Overall, the mean incidence of HPV in lung cancer was 24.5%. While in Europe and the America the average reported frequencies were 17% and 15%, respectively, the mean number of HPV in asian lung cancer samples was 35.7%. There was a considerable heterogeneity between certain countries and regions. Particular high frequencies of up to 80% were seen in Okinawa (Japan) and Taichung (Taiwan). However, there were also discrepant results within the same region pointing to methodological differences and the need for validation. All lung cancer subtypes were affected and especially the high risk types 16, 18, 31 and 33 as well as the low risk types 6 and 11 were found, the later mainly in association with squamous cell carcinomas. The data suggest that HPV is the second most important cause of lung cancer after cigarette smoking and strongly argues for additional research on this issue.

  3. Anonymous says:

    HPV and Lung Cancer
    That is a compelling hypothesis Frank!
    A couple of additional points:
    1. The Japanese have very low levels of lung cancer (despite high smoking levels).
    2. Lung cancer diagnosis is not reliable. A number of studies have compared death certificates with autopsy examinations and found only about 50% agreement. (smokers tend to be over-diagnosed whereas non-smokers tend to be under-diagnosed) (1)(2)
    Leading to a couple of thoughts:
    1. Maybe low Japanese levels are in part the result of more reliable diagnosis?
    2. The 80% HPV in the Japanese studies may be a better estimate of the total prevalence of HPV in genuine lung cancer.
    1 Professor Eysenck’s book:
    “How many people does smoking actually kill?” – Warning 22MB PDF
    2 Richard White’s book:
    “Smoke Screens – The Truth About Tobacco”

  4. Frank Davis says:

    Re: HPV and Lung Cancer
    Well, it’s an interesting hypothesis.
    You will note, of course, that I had to adjust the hypothesis when I realised that the original hypothesis would have led to equal incidence of cancer in both men and women. But the sexual ‘double standard’ of yesteryear came to my rescue. I won’t be surprised if other objections emerge.
    I know about the inaccurate diagnosis of lung cancer. And about the low incidence of lung cancer in Japan. I read once that the incidence of lung cancer in Yemen was nearly zero, despite children as young as 6 years old there smoking. I’m not sure if lung cancer diagnosis and HPV testing is more accurate in Japan or not.
    To fit into my hypothesis, I’d have to look for cultural differences between West and East – that exist of course – which result in less mixing/proximity between the sexes.

  5. Frank Davis says:

    Re: HPV and Lung Cancer
    In addition my hypothesis more or less requires an airborne virus. I can’t see how a virus can get into lungs if it isn’t airborne. And for the most part HPV isn’t an airborne virus.
    I came across an <a href="
    “>online forum where someone mentioned that her professor said people were looking into the possibility that HPV could be airborne. This suggested once again that it’s not generally regarded as airborne.
    Another 2007 <a href="
    “>article, not specifically about HPV, reported:
    Professor Lidia Morawska, director of QUT’s International Laboratory for Air Quality and Health, said the study dispelled the myth that viruses emitted from humans only travel a metre in the air. [His team has] been studying the way droplets carring viruses are dispersed in the air when people speak, cough, sneeze and breathe.
    As part of the study QUT designed and built a machine to measure the distance a droplet travels in the air prior to drying.
    “This droplet could potentially be carrying a virus,” she said.
    “The significant part of our research has found that rather than the droplet falling directly to the ground after leaving the mouth, the liquid component of the droplet dries in the air and the dry residue travels large distances.
    “When a droplet dries in the air the residue is carried in the air, and therefore there is a risk that people can inhale that air and become infected.”
    Professor Morawska said a droplet drying on a surface could be infectious but the greater danger was droplets drying in the air.
    “A droplet can travel for 10cm before it dries in the air, it doesn’t immediately fall to the ground.”

    She’s shown how a SARS infection case where 300 people had been infected could have been spread by one person just breathing.
    Elsewhere, in 1936 Wells and Brown reported that inluenza virus was infective for ferrets for at least one hour after spraying. And survived best in dry air (RH<50%).

  6. Frank Davis says:

    An additional report
    May 10, 2007
    HPV infection linked to throat cancers
    Researchers at the Johns Hopkins Kimmel Cancer Center have conclusive evidence that human papillomavirus (HPV) causes some throat cancers in both men and women. Reporting in the May 10 issue of the New England Journal of Medicine, the researchers found that oral HPV infection is the strongest risk factor for the disease, regardless of tobacco and alcohol use, and having multiple oral sex partners tops the list of sex practices that boost risk for the HPV-linked cancer. Study author and cancer virus expert Maura Gillison, M.D., Ph.D., first reported the connection between HPV and specific throat cancers in 2000, supporting previous work by other investigators. “We believed the links were strong, but needed to understand which behaviors put people at higher risk,” said Gillison. Gillison added that “people should be reassured that oropharyngeal cancer is relatively uncommon, and the overwhelming majority of people with an oral HPV infection probably will not get throat cancer,” said Gillison. Consistent condom use may reduce risk.
    In Gillison’s study of 100 men and women newly diagnosed with oropharyngeal cancer (located in the tonsils, back of the tongue, and throat), those who had evidence of prior HPV infection were 32 times more likely to develop the cancer. This was much higher than the rate increase of threefold for smokers and 2 ― -fold for drinkers. Study participants who reported having more than six oral sex partners in their lifetime were 8.6 times more likely to develop the HPV-linked cancer. In a surprising twist, Gillison said their data show no added risk for HPV carriers who smoke and drink alcohol. “It’s the virus that drives the cancer,” explains Gillison, an assistant professor of oncology and epidemiology at Johns Hopkins. “Since HPV has already disrupted the cell enough to steer its change to cancer, then tobacco and alcohol use may have no further impact.” “It is important for health care providers to know that people without the traditional risk factors of tobacco and alcohol use can nevertheless be at risk for oropharyngeal cancer,” said Gypsyamber D’Souza, Ph.D., a co-author and assistant scientist at the Johns Hopkins Bloomberg School of Public Health. Gillison said a new FDA-approved vaccine, known by its tradename Gardasil, can prevent genital HPV infection in girls and young women, but has not yet been shown to prevent infection in boys and men. The vaccine’s ability to prevent oral HPV infection and oral cancers, which are more common in men, also is not known.

  7. Frank Davis says:

    Taiwan 2001
    The Association of Human Papillomavirus 16/18 Infection with Lung Cancer among Nonsmoking Taiwanese Women
    Ya-Wen Cheng, Hui-Ling Chiou, Gwo-Tarng Sheu, Ling-Ling Hsieh, Jung-Ta Chen, Chih-Yi Chen, Jan-Ming Su and Huei Lee2
    Lung cancer is the leading cause of cancer death in Taiwanese women since 1982. High lung cancer mortality ratio of male:female in Taiwan (2:1) was observed, although less than 10% of female lung cancer patients are smokers. Until now, the etiological factor remains unknown. We hypothesize that high-risk human papillomavirus (HPV) 16/18 may be associated with lung cancer development based on high prevalence of p53 negative immunostainings in female lung tumors compared with that of male lung tumors. In this study, 141 lung cancer patients and 60 noncancer control subjects were enrolled to examine whether HPV 16/18 DNA existed in lung tumor and normal tissues by nested PCR and in situ hybridization (ISH), respectively. The concordant detection of HPV 16 and 18 DNA between nested PCR and ISH method was 73 and 85.5%, respectively. Our data showed that 77 (54.6%) of 141 lung tumors had HPV 16/18 DNA compared with 16 (26.7%; P = 0.0005) of 60 noncancer control subjects. In addition, ISH data showed that HPV 16/18 DNA was uniformly located in lung tumor cells, but not in the adjacent nontumor cells. When study subjects were stratified by gender, age, and smoking status, nonsmoking female lung cancer patients who were older than 60 years old had significantly high prevalence of HPV 16/18 infection. The odds ratio of HPV 16/18 infection of nonsmoking female lung cancer patients is much higher at 10.12 (95% confidence interval, 3.88–26.38) compared with 1.98 (95% confidence interval, 0.84–4.76) of nonsmoking male lung cancer patients. This result strongly suggests that HPV infection is associated with lung cancer development of nonsmoking female lung cancer patients. The high prevalence of HPV 16/18 infection may explain to a certain extent why Taiwanese women nonsmokers had a higher lung cancer mortality rate.

  8. junican says:

    The consequences of ‘climategate’ are far reaching. Much further reaching than politicians are prepared to admit. I suppose that that is why Boris Johnson, as a politician, is loath to accept that the fiddling with the facts as regards climate statistics is important – to accept the possibility that that ‘the facts’ may have been fiddled would undermine the whole edifice of justification for political actions. Politicians of all hues are terrified that they actually have to verify for themselves the facts on which they base their decisions.
    For this reason, I no more accept the results of the ‘research’ into HPV than I accept the passive smoking research results – they may or may not be correct.
    For some reason or other, I have in my mind the possibility that a university professor gives his students a task. “Interview 100 people with lung cancer who have never smoked and check for HPV” The professor then collates the student results and publishes them. Crap science but good publicity.
    Climategate is seriously, seriously important. The question of what constitutes ‘peer review’ has to be examined.
    In the 1800s, the Royal Society published the findings of people like Michael Faraday about electricity and magnetism. His papers fully disclosed the details of his experiments and his conclusions. HIS PEERS were ALL the members of the Royal Society, not just people in the field, and definitely not just his mates.
    These people at the University of East Anglia have not just fiddled the facts, they have also corrupted the ideal of ‘peer review’ by hiding their detailed evidence. That is of great importance.
    If the government have any sense at all, they will insist that, in the future, ALL evidence has to be published, and, since the evidence is gained by use of public funds, it has to be published to taxpayers – via the internet is the obvious way.
    As a result of climategate, there must be no more secretivity. There are lots and lots of intelligent people in this country who are quite capable of analysing facts, and they must be given the opportunity to exercise their skills.
    Further, since THE FACTS are so compromised, there is no alternative but to start again.

  9. Frank Davis says:

    Well, of course HPV research could be as corrupt as antismoking research. But if it is corrupt then all medical research is corrupt, and we have learned nothing about medicine in 200 years.
    I don’t think this is the case, however. I think that a great deal of modern medicine is soundly based. I think antibiotics and vaccines do actually work. But they require slow and painstaking work over many decades, as the virus or bacterium responsible for disease is isolated and examined, before treatments and vaccines are tested and then manufactured on a large scale. It’s been done with a lot of diseases.
    It is beginning to look as if HPV may be a virus that causes cancer. It’s still not fully understood. But it’s being found in more and more cancers. And if it does prove to be the cause, cancer will join all the other diseases for which there are vaccines and cures. It will be just another infectious disease like polio (for which there is a vaccine). The headline-grabbing research of Doll and Hill that pinned lung cancer on smoking will prove to have been mistaken, and will be forgotten. Real science will have caught up with speculation. Real science carried out by numerous scientists checking each others results and publishing them.
    Sure, a professor could get his students to do some sort of headline-grabbing bit of research on HPV. But that’s not real, slow, painstaking, accurate science.
    I agree that Climategate is very, very important. I think it may wake people up to the fact that not all scientists are true scientists, but are instead political activists (like the corrupt climate scientists) or moralists (like the antismokers) who have been using science to further non-scientific ends. They have to be cleared out. There are probably a lot more of them than just these two. Hopefully, science is still robust enough to do this. It’ll need something like a scientific Reformation. Which would result, yes, in far greater transparency.
    In the case of climate science, I agree it doesn’t seem that there is even any raw data. Or not enough of it. And they might have to start all over again.

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