I hate the need for gross posts, the syphilis rates in Asia one was bad enough.
“Among both men and women, rectal sex was commonly associated with increased colorectal cancer risk. Some Latinos may hold misperceptions about colorectal cancer risks, including an association between rectal sex and colon cancer, that may impact their screening behaviors. Clinicians and public health officials should consider these potential risk misperceptions and explore for other risk misperceptions when counseling and educating patients about colorectal cancer screening.”
How is that a misperception?
“Sexual activity, specifically rectal sex, was also commonly identified as a risk factor for colorectal cancer. While this theme was more prominent in the focus group discussions among men,”
Anal with a woman also counts, guys, sexually they are gay. You should desire the female parts only. The germs can still see you.
It’s funny to see PUAs bitch about muh male cancer rates when they’re endorsing the cause of them.
Is penile cancer da wimminz fault too?
ANY Victorian short of Oscar Wilde would look at those guys and call them homosexual. Sexuality is a preference for body parts in Darwinian classification, not the people owning them. It’s a vital distinction. Even Wilde was averse to anal, he almost exclusively did oral with men. He was icked out by anal. So modern ‘straight’ men are probably more gay than Oscar Wilde. Fact.
btw Boomers are Freudians (pleasure as normal human motive, no deviancy permitted as concept).
Previously living for lust was considered part of savage cultures that people like Burton ‘explored’, mostly with his dick.
“the theme also emerged from female groups. Participants generally referred to increased risk of colorectal cancer among men who have sex with men and some participants made pejorative statements while connecting rectal sex with colorectal cancer risk. However, when questioned further, many participants noted that there is a similar risk among men and women.
No. Not until old age. When the whole body breaks down anyway.
A number of participants provided explanations for their beliefs, including presumed pathophysiologic rationale.”
“Given that anal sex has been linked to anal cancer via human papilloma virus (HPV) , it is possible, but unlikely, that participants erroneously made a connection between rectal sex and colorectal cancer instead of anal cancer. The belief that rectal sex is a risk factor for colorectal cancer is concerning, even if participants did confuse colorectal cancer with anal cancer, given the much lower rates of anal cancer relative to colorectal cancer. By extending the association from anal cancer to colorectal cancer, some may falsely underestimate their risk for colorectal cancer based on their sexual behavior.”
They’re not confused, there’s a link.
The rectum is a name for the end of the colon, this is linguistic hair-splitting.
Colo-rectal – it’s the same thing.
There’s a known colon cancer connection to Type 2 diabetes.
So it’s probably also preservatives. Just throwing that in.
Like nitrates used on cheap meats, not the actual meat. Ban nitrates. Really.
“Inflammatory benign anal lesions are associated with a significantly increased long term risk of anal cancer. In contrast, haemorrhoids appear not to be a risk factor for this malignancy.”
“Anal cancer is an uncommon disease in the heterosexual population, with an incidence of 1 per 100 000. However, the incidence is much higher in men who regularly practice anal receptive intercourse (approximately 35 per 100 000).1 Apart from a strong link to sexual promiscuity and human papillomavirus (HPV) infection, suspected risk factors include genital warts, herpes simplex virus type 2, and smoking.2,3,4,5,6″
35x more likely
We need to ban porn, basically. It normalises it. Perversion is less a judgement and more a description. As covered previously, circumcised men have more sexual difficulties, including porn addiction and are more …oriented toward anal sex to achieve a comparable amount of stimulation as a normal, un-mutilated man. Compare circumcision rates to rape data of that country and also homosexuality. It’s a wild ride.
“In 1863 the first connection between inflammation and cancer was made by Rudolf Virchow.7 Since then several types of cancer have been associated with infection and inflammation,7 and different mechanisms have been hypothesised. Local inflammation may contribute to ovarian cancer8; ulcerative colitis increases the risk of colorectal cancer9,10; infection by Helicobacter pylori increases the risk of distal stomach cancer11; hepatitis B virus and hepatitis B virus infection are well recognised risk factors for hepatocellular carcinoma12; and tumour necrosis factor, a protein mediating inflammation, has been suggested to be involved in the progression and spread of cancer.13
The possible association of benign anal lesions, including fissures, fistulas, perianal abscesses, and haemorrhoids, with anal cancer has long been debated.2,3,14,15 In a case control study, a significantly increased risk of anal cancer was found in patients treated for anal fissures, fistulas, or with more than 12 episodes of haemorrhoids.2 Constant irritation, chronic inflammatory changes, and repeated epithelial regeneration were hypothesised as explanations for the association.2 This was supported by another case control study in which a significantly increased risk of anal cancer was reported in patients with severe haemorrhoids, and a weak association was also observed between anal cancer and other infections and inflammations in the anogenital area.15 A third case control study found an association with haemorrhoids and non‐specific anal irritation among men but not among women.16 Case control studies may be subject to recall bias and thus a cohort study design is favourable although few cohort studies are available due to the rarity of anal cancer. In the only two cohort studies, a null association was reported.14,17″
“HPV-16 genotyping was performed in HPV-positive tissues and the physical status of the HPV-16 genome was determined by E2 detection. HPV was detected in 19 of 45 (42.2%) CRC cases (mean age 61.1 ± 10.7 years, 24 males) and in 1 of 36 (2.8%) controls (mean age 60.9 ± 9.6 years, 24 males) with an OR = 25.58 (95% CI 3.21 to 203.49). HPV-16 was detected in 63.2% of the HPV-positive colorectal tumors; genome integration was observed in all HPV-16 positive cases. This is the first report showing the high prevalence of HPV infections in Caribbean Hispanic colorectal tumors. Despite evidence of HPV integration into the host genome, further mechanistic analysis examining HPV oncoprotein expression and the putative role of these oncoproteins in colorectal carcinogenesis is warranted.”
HPV in 42% of colon cancers, 2.8% in controls.
“genome integration was observed in all HPV-16 positive cases.”
Yup. What it sounds like.
“Results: We found that colorectal tissues from 28 of 55 (51%) patients with colorectal cancer were positive for HPV DNA. Colorectal tissues from all 10 control individuals were negative for HPV DNA (P = 0.0034). Of the 107 usable (GAPDH+) samples collected as paired colorectal tissues (tumor and tumor-adjacent tissues) from the patients, 38 (36%) had HPV16 (n = 31), HPV18 (n = 5), or HPV45 (n = 2), with HPV DNA in both tumor and tumor-adjacent tissues of 10 paired samples, 13 in only the tumor, and 5 in only tumor-adjacent tissues. In situ PCR detection of the tumor tissues confirmed the presence of HPV DNA in tumor cells.
All 10 controls negative.
Conclusion: Our results suggest that colorectal HPV infection is common in patients with colorectal cancer, albeit at a low DNA copy number, with HPV16 being the most prevalent type. HPV infection may play a role in colorectal carcinogenesis.
Smoking may cause lung cancer.
Human papillomavirus (HPV) infection of epidermal or mucosal epithelial cells causes benign and sometimes malignant neoplasms. Certain types of HPVs, such as HPV16, 18, 31, and 45, are detected frequently in anogenital cancers, particularly cancer of the cervix and anus, and are thus considered to be high-risk or oncogenic. Integration of the viral genome into the cancer cell genome is characteristic of infection by these HPVs. Other types of HPV, such as low-risk or nononcogenic HPV6 and HPV11, induce benign anogenital warts and are rarely found in anogenital malignancies (1, 2).
HPV DNA has been detected in tumor tissues of head and neck cancer (3, 4), oral cancer (5), esophageal cancer (6, 7), and some skin cancers (8, 9), as well as lung cancer (10, 11). Detection of HPV DNA in colorectal cancer tissues by in situ hybridization (12) and PCR (13–17) has suggested that HPV infection might be associated with the carcinogenesis of colorectal cancer. However, HPV DNA was not detectable by regular PCR in one earlier study (18) and a survey of HPV16 virus-like particle antibodies in patients with epithelial cancers also failed to provide an association between HPV and colorectal cancer (19), challenging the association of colorectal cancers with HPVs. As a result, we felt that a well-controlled study would be more informative. In the present report, we did a retrospective, controlled study, in which colorectal cancers and tissues adjacent to the cancers were surgically collected from patients with colorectal cancer and subjected to nested PCR and in situ PCR detection of HPV DNAs.”
HPV 6 and 11 Finland
“In addition to cancer of the lower female genital tract, human papillomaviruses (HPV) are associated with a large number of benign, precancer and cancer lesions at different anatomic sites in both genders. Malignant tumours and their precursors are usually attributed to the oncogenic (high-risk, HR) HPV types, whereas benign lesions (papillomas) are associated with the low-risk (LR) HPV types, most notably with HPV6 and HPV11. Until recently, the main interest in HPV research has been focused on HR-HPV types and their associated pathology, and much less attention has been paid to the lesions caused by the LR-HPV types. With the recent licensing of an effective prophylactic vaccine against the 2 most important LR-HPV types (HPV6 and HPV11)”
the ‘low risk’? then why get it?
they said cancer, people assumed high risk
“, it has become timely to make a systematic survey on the annual disease burden due to these 2 HPV genotypes in our country.”
Why not BEFORE?
“These types of data should form the foundation for all calculations of the annual costs needed to treat these diseases by conventional means. Accurate estimates of disease burden are also mandatory for all modelling of the cost-effectiveness of prophylactic HPV6 and HPV11 vaccines. If proven useful for any of these purposes, this document will have fulfilled its purpose. In the first step, published HPV literature was used to create a list of benign, premalignant and malignant lesions associated with this virus at different anatomic sites. GLOBOCAN 2004 (IARC) database was used to derive the global numbers of incident cases for each of these malignancies in 2002, and the Finnish Cancer Registry (FCR) website for obtaining these (y 2005) numbers in Finland. The evidence linking HPV to each individual tumour category was classified as: 1) established, 2) emerging, and 3) controversial. All published evidence was weighted for each individual malignant, premalignant and benign lesion, anatomic region by region, while assessing the attributable fraction of HPV6/11 genotypes in each lesion. Because benign and most of the precancer lesions are not registered by FCR or GLOBOCAN, different approaches had to be used to derive the best estimates for their incidence, based on published literature or other registries (e.g. genital wart registry of the UK and Wales, and mass screening registry of FCR). With a lack of reasonable consensus, a lower and an upper limit was set for the range of estimates. In cases with different age-specific incidence (e.g. genital warts), the population pyramid of Finland was used to calculate the incident cases. Where well established, the different incidence rates among males and females were used to calculate the numbers of incident cases by gender. The malignant neoplasms with established or emerging evidence on the causal role of HPV are listed by their ICD-10 codes in Table I. Included in this list are also 2 controversial malignancies (colorectal cancer and endometrial cancer), of which the contradictory HPV data are critically discussed. The third major cancer in this same category (prostate cancer) was not included in the list, because the data are clearly insufficient to categorize this entity even among the emerging HPV associated malignancies. Estimated disease burden due to HPV6/11 in Finland, calculated as numbers of annual new cases by anatomic region and tumour type is given in Table II, and summarized in Figure 1. The present analysis implicates that a minimum of 12,666 to 13,066 new cases of HPV6- or HPV11-associated clinical lesions would be detected each y in Finland, if all were registered. Notably, these numbers represent the disease burden due to these 2 HPV types. However, these clinical lesions only represent a small minority of the total viral burden due to the infections by these 2 HPV genotypes. This is because the vast majority* of all infections by these ubiquitous viruses are latent, being transient in nature and spontaneously resolving within a few months (up to 1 y*), without ever developing a clinically detectable disease.
*it’s ‘assumed’ but doesn’t always happen, especially with multiple infections of different types
A just-so story for sluts, same with clap.
This spontaneous clearance does not make these latent infections less important, however, because as long as the virus reservoir exists, it serves as the source of viral transmission to susceptible individuals, with a multitude of HPV6/11 associated pathologies as a potential outcome, as described in this document. The implications of these data in the era of effective prophylactic HPV vaccination against HPV6 and HPV11 should be clear.”
16, 18 Finland
Young people at higher risk, why?
“A study led by American Cancer Society researchers finds that new cases of colon cancer and rectal cancer are occurring at an increasing rate among young and middle-aged adults in the US. Once age is taken into account, those born in 1990 have double the risk of colon cancer and quadruple the risk of rectal cancer compared to people born around 1950, when risk was lowest.”
I wonder what ‘young people’ are doing now (define ‘young’) that people in the 50s did NOT?
“The HPV overall prevalence was 31.9% (95% CI: 19.3–47.9). It was lowest in Europe (14.1%, 95% CI: 4.9–34.1) and highest in South America (60.8%, 95% CI: 42.7–76.4).”
Lowest among native white people. No you’re not normal, America. Neither is your herpes.
Is this that magical white privilege I’ve been hearing about?
Thot culture kills. The Bible called it whoredom, you’re not doing anything new. Sodom was famous for….?
Spoiler: sodomy can occur with either sex. It’s the act, not the participants.
“Eight studies presented the results of HPV typing in 302 HPV‐positive colorectal carcinomas. HPV 18 was the virus more frequently found in colorectal cancer cases from Asia (73.34%, 95% CI: 44.9–90.7) and Europe (47.3%, 95% CI: 34.5–60.4). In contrast, HPV 16 was more prevalent in colorectal tumours from South America (58.3%, 95% CI: 45.5–69.9). The analysis of five case–control studies showed an increase in colorectal carcinoma risk with HPV positivity (OR = 10.04; 95% CI: 3.7–27.5).
The results provide quantitative evidence for an association between HPV infection and colorectal cancer risk.”
q u a n t i t a t i v e e v i d e n c e
q u a n t i t a t i v e e v i d e n c e
q u a n t i t a t i v e e v i d e n c e
inspired by this meme