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Five years ago, when actor Michael Douglas candidly revealed that his throat cancer was linked to having oral sex, two things happened.

He made headlines that mortified his family. And he helped publicize the fact that a pervasive, sexually transmitted virus called HPV was unleashing an epidemic of oral cancer among men.

Since then, scientists have made headway in figuring out why HPV, the human papillomavirus, has this glaring gender bias. Men are four times more likely than women to be diagnosed with oral cancer, a hard-to-detect, hard-to-treat disease that has overtaken cervical cancer as the most common HPV-related malignancy in the United States.

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To be sure, changes in sexual norms over the last few generations have played a role in this alarming trend. But research increasingly shows the real problem is something men have practically no control over: their immune response.

Compared with women, men are more likely to get infected with HPV – including “high-risk” cancer-causing strains. They also are less able to wipe out infection on their own, and more likely to get reinfected. The reasons are unclear.

“There is good evidence that men acquire oral infections more readily than women, even if they have similar sex practices,” said Ashish A. Deshmukh, a University of Florida HPV researcher. “And more than the acquisition, it’s the persistence of the virus. The clearance rate is not that fast in men.”

HPV is a family of more than 100 virus types that can live in the flat, thin cells on the surface of the skin, cervix, vagina, anus, vulva, penis, mouth and throat.

The virus is spread through contact with infected skin, mucous membranes, and bodily fluids. Some types can be passed during intercourse or – as Douglas pointed out – oral sex.

While virtually all sexually active people will get infected at some point, the virus is usually wiped out by the immune system without so much as a symptom.

But not always.

In the cervix, persistent infection with high-risk HPV types can lead to precancerous changes that, left alone, slowly turn malignant. Fortunately, the Pap smear enables the detection and removal of abnormal cells before cancer develops. What’s more, age-related changes in cervical cells reduce the risk that HPV will take hold there as women get older.

No such screening test exists for oropharyngeal sites – the tongue, soft palate, tonsils, the throat behind the nasal cavity – and symptoms usually don’t appear until cancer is advanced. Becker, for example, had metastatic disease by the time he noticed a lump under his jaw line in late 2015.

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HPV-related tumors have increased more than 300 percent over the last 20 years. The virus is now found in 70 percent of all new oral cancers.

About 13,200 new HPV oral cancers are diagnosed in U.S. men each year, compared with 3,200 in women, according to federal data. Treatment – surgery, chemotherapy, radiation – can have disfiguring, disabling side effects. About half of late-stage patients die within five years.

Oral HPV infection rates are skewed by gender, just like the resulting cancers. The latest national estimates of this disparity, published in October, come from Deshmukh and his University of Florida colleagues. They used a federal health survey that collected DNA specimens to estimate that 7.3 percent of men and 1.4 percent of women have oral infections with high-risk HPV types. That translates to 7 million men and 1.4 million women.

In men, something goes awry. The HIM study – for HPV in Men – documented this by collecting genital, anal, and oral samples from 4,100 unvaccinated men in Florida, Mexico and Brazil between 2005 and 2009. The samples were tested for the presence of two high-risk HPV types and two that cause genital warts.

Among 384 men who developed infections during a 24-month period, only 8 percent produced antibodies. But this response rate varied depending on the site of infection; none of the small number of orally infected men produced antibodies.

Rather than putting the immune system on guard and protecting men from the virus, infection sharply increased the chance of getting infected again with the exact same HPV type. And many men who got reinfected were celibate at the time.

How could this be?

Anna R. Giuliano, the researcher at the Moffitt Cancer Center in Tampa, Fla., who led the HIM study, said recurring infections may be due to reactivation of dormant virus, or to auto-inoculation – the man spreads infection from one part of his body to another. Or to something else entirely.

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Mr Americana, Overpasses News Desk
March 8th, 2018