Covid male sterility papers + HPV, herpes

as previously discussed:

https://onlinelibrary.wiley.com/doi/10.1111/andr.12859

A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile.

Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line. As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.24 

However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?

IN ADDITION TO-

https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.26667

The other side of COVID-19 pandemic: Effects on male fertility

RECONCILE ABOVE WITH

The outbreak of novel coronavirus disease 2019 (COVID-19) has become a major pandemic threat worldwide. According to the existing clinical data, this virus not only causes respiratory diseases and affects the lungs but also induces histopathological or functional changes in various organs like the testis and also the male genital tract. The renin-angiotensin system (RAS), also ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2.

Because the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases. As the COVID-19 pandemic has affected the male genital system in direct or indirect ways and showed a negative impact on male reproduction, this paper focuses on the possible mechanisms underlying the damage caused by COVID-19 to the testis and also other components of the male genital tract.

SO THE SPIKE PROTEIN ALONE TARGETS ACE2, FOUND IN THE BALLS, LIKE URINE* (*THAT PART WAS A JOKE)

and they wanna force all young men to get it

college age men too

and all young women

when other papers cite it might act like an STD?

Huh.

Highlight:

  • The male genital system presents high ACE 2 expression therefore, it will be highly important to investigate and clarify the relationship between COVID-19 and the male genital tract.

I’m not even a man but I can feel my lady balls shrink reading that.

If we look at the mechanisms of these changes caused by SARS-CoV-2 in the testis, as mentioned above, this virus uses ACE 2 for entry into the cells through its surface spike (S) proteins. S proteins have two subunits, S1 and S2, which are responsible for receptor recognition and membrane fusion. Studies have shown that SARS-CoV-2 enters into the host cell through the binding of its C-terminal domain of the S1 subunit to ACE 2. Additionally, some studies have reported that the level of autophagy receptor SQSTM1/p62 in SARS-CoV-2 infected cells has increased, suggesting a decrease in autophagy flux.

So, SARS-CoV-2 itself or via ACE 2 can directly induce or inhibit the autophagy pathway to achieve virus survival.

As a result, SARS-CoV-2 may cause male reproductive disorders by regulating the level of autophagy in male germ cells.4 On the contrary, another hypothesis is that testis degeneration in the COVID-19 cases is attributed to an increase in testicular temperature as an indirect effect of the inflammation.5

or :-

Do the jabs cause inflammation?

Can spike proteins microwave your balls? Do they nuke your little swimmers?

BUT WAIT. THERE’S MORE.

Another molecule effective at entering the cell of the SARS-CoV-2 is host proteases like transmembrane serine protease 2 (TMPRSS2), which cleaves the viral S protein to induce a conformational change that allows to a fusion of the virus and host cell membranes.34 TMPRSS2 is the key molecule for the successful infection process.35 

This protease is more expressed in human tissues than ACE 2; co-expression of ACE 2 and TMPRSS2 has been shown in the testis, endometrium, and placenta. Researchers investigated the coexpression of these two molecules in the testis and accordingly, they found that ACE 2 is predominantly expressed in myoid cells, spermatogonia, Leydig, and Sertoli cells, while TMPRSS2 is expressed in spermatogonia and (elongated) spermatids of the testicular tissue34 (Figure 3).

I warned you about endometriosis-like function. Maybe naturally having endo is protection?

It’s lifelong inflammation. Kinda like cancer. You literally have to cut the tissues out.

Like Fight Club, they’d have to take your balls.

Shocked men aren’t more protective of their bollocks and demanding ONE safety study.

ModRNA has owners. Repossession is plausible, legally.

STD angle:

“Recent studies have reported that SARS-CoV-2 is easily found in human bodily fluids.35 The presence of a virus in a semen sample is still a topic of discussion and research due to the small number of studies. For example, two different studies have analyzed SARS-CoV-2 presence in semen samples and according to these studies, SARS-CoV-2 (+) semen samples were found in two patients from 23 cured patients and four patients from 15 patients in the acute phase. Another study reported that SARS-CoV-2 was not detected in the semen samples of 34 COVID-19 patients.31

“It is also known that the prostate gland secretes prostate fluid, one of the main seminal components, and muscles of the gland help in pushing the seminal fluid through the urethra during ejaculation.31 The critical point is that, as we mentioned above, a small percentage of the prostate hillock and club cells express ACE 220 and also TMPRSS2 is highly expressed by the epithelium of the human prostate;37 so it is more likely to get SARS-CoV-2 infection, which may affect its secretions.31 

These mechanisms could explain  the SARS-CoV-2 (+) semen samples of the studies.23

“If the presence of the virus in semen is definitively proved by studies, assisted reproduction techniques will also be affected. For instance, testing all male patients like HIV or Hepatitis B/C cases, and using appropriate sperm washing techniques, or paying extra attention to sperm freezing for COVID-19 positive patients.35

“Like SARS-CoV-2, most viruses enter the human body through nasal and oral routes, and viral particles may break the blood-brain barrier.” but don’t worry about shedding?

“It has been reported that the brain cells (glial cells and neurons) also express ACE 2 receptors, making them a possible target to induce neuronal death for SARS-CoV-2. Importantly, the central nervous system plays a critical role in endocrine control and spermatogenesis.31 

The Hypothalamic-Pituitary-Gonadal Axis (HPGa) exerts a vital role in reproduction; in other words, HPGa can inhibit the body’s reproductive functions via hormones.3138

We have our mechanism for sterility, people.

Gonadotropin-releasing hormone (GnRH) expressing neurons from the hypothalamus secretes GnRH and it activates the release of the follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland. A low level of GnRH causes a decrease in FSH and LH, resulting in impaired function of the Sertoli and Leydig cells.31 Ma et al.39 showed that COVID-19 patients had significantly higher serum LH levels but decreased testosterone/LH and FSH levels than healthy men, suggesting potential hypogonadism. Taken together, patients with COVID-19 have been found to present a reduced testosterone/LH ratio, indicating possible subclinical damage to male gonadal function.5 Additionally, activation of the HPGa and subsequent alterations in hormone concentrations play a critical role in poor sperm quality.38

Therefore, besides its direct effects on testis, SARS-CoV-2 may affect fertility indirectly via the central nervous system.31

Like a remote control, for your balls.

In conclusion, all preliminary findings mentioned above suggest that the COVID-19 pandemic affects the male genital system in direct or indirect ways and shows a negative impact on male reproductive health, inducing spermatogenic failure. Additional studies are necessary to answer all the questions and further investigations are warranted, but ACE 2 and TMPRSS2 play an important role in the cellular entry for SARS-CoV-2. As the male genital system presents high ACE 2 expression, the importance of this pathway increases in COVID-19 cases.

SPERMATOGENIC FAILURE

and onward

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13654

Could COVID-19 have an impact on male fertility?

duh

The pandemic caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to several hypotheses of functional alteration of different organs. The direct influence of this virus on the male urogenital organs is still to be evaluated. However some hypotheses can already be made, especially in the andrological field, for the biological similarity of the SARS-CoV and SARS-CoV2. As well as SARS-CoV, SARS CoV-2 uses the ‘Angiotensin Converting Enzyme-2’ (ACE2) as a receptor to enter human cells. It was found that ACE2, Angiotensin (1-7) and its MAS receptors are present, over in the lung, also in the testicles, in particular in Leydig and Sertoli cells. A first hypothesis is that the virus could enter the testicle and lead to alterations in testicular functionality. A second hypothesis is that the binding of the virus to the ACE2 receptor, could cause an excess of ACE2 and give rise to a typical inflammatory response. The inflammatory cells could interfere with the function of Leydig and Sertoli cells. Both hypotheses should be evaluated and confirmed, in order to possibly monitor fertility in patients COVID-19+.

Specific genes relating to male fertility have already been found e.g.

https://onlinelibrary.wiley.com/doi/full/10.1002/mrd.23314

oddly recommended with covid papers?

Male infertility is a rising problem around the world. Often the cause of male infertility is unclear, and this hampers diagnosis and treatment. Spermatogenesis is a complex process under sophisticated regulation by many testis-specific genes. Here, we report the testis-specific gene 1700102P08Rik is conserved in both the human and mouse and highly expressed in spermatocytes. To investigate the role of 1700102P08Rik in male fertility, knockout mice were generated by CRISPR-Cas9. 1700102P08Rik knockout male mice were infertile with smaller testis and epididymis, but female knockout mice retained normal fertility. Spermatogenesis in the 1700102P08Rik knockout male mouse was arrested at the spermatocyte stage, and no sperm were found in the epididymis. The deletion of 1700102P08Rik causes apoptosis in the testis but did not affect the serum concentration of testosterone, luteinizing hormone, and follicle-stimulating hormone or the synapsis and recombination of homologous chromosomes. We also found that 1700102P08Rik is downregulated in spermatocyte arrest in men.

Together, these results indicate that the 1700102P08Rik gene is essential for spermatogenesis and its dysfunction leads to male infertility.

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13712

As the incidence and severity of SARS-CoV-2 are reported to be higher in males than females, Shastri et al. performed a study to determine the time to viral clearance after infection in a total of 68 individuals (48 males and 20 females) with median age of 37 years (Shastri et al., 2020).

They observed that females were able to achieve viral clearance significantly earlier than males.

Furthermore, a serial follow-up evaluation of three families with both male and female patients demonstrated that female members of the same household cleared the SARS-CoV-2 infection earlier in each family (Shastri et al., 2020). In order to determine the reason for delayed clearance in males, they also checked the expression of ACE2 in tissue-specific repositories.

It was found that testicular tissues were one of the tissues showing ACE2 expression in 3 independent RNA expression databases (Human Protein Atlas, FAMTOM5 and GETx). Interestingly, the ovarian tissue showed very low expression of ACE2 (Shastri et al., 2020).

so women may be the red herring here

ACE2 and fat study, so expect fatty side effects

https://onlinelibrary.wiley.com/doi/full/10.1111/dth.13989

https://onlinelibrary.wiley.com/doi/full/10.1111/and.13791

Impact of COVID-19 and other viruses on reproductive health

They admit the male HPV link I posted about previously.

Male infertility is linked to some viral infections including human papillomavirus (HPV), herpes simplex viruses (HSV) and human immunodeficiency viruses (HIVs). Almost nothing is known about severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) effect on fertility. The possible risk factors of coronavirus disease 2019 (COVID-19) infection on fertility comes from the abundance of angiotensin-Converting Enzyme-2 (ACE2), receptor entry of the virus, on testes, a reduction in important sex hormone ratios and COVID-19-associated fever. Recent studies have shown a gender difference for COVID-19 rates and comorbidity. In this review, we will discuss the potential effect of COVID-19 on male fertility and talk about what needs to be done by the scientific community to tackle our limited understanding of the disease. On the other side, we will focus on what is known so far about the risk of COVID-19 on pregnancy, neonatal health and the vertical transfer of the virus between mothers and their neonates. Finally, because reproduction is a human right and infertility is considered a health disease, we will discuss how assisted reproductive clinics can cope with the pandemic and what guidelines they should follow to minimise the risk of viral transmission.

Remember, viral entry via SPs cause inflammation that might cause sterility? WELL-

Virus entry begins when the virus surface enzyme called Spike (S) glycoprotein binds to the angiotensin-converting enzyme 2 (ACE2) located on the host cell membrane (Hoffmann et al., 2020; Wang et al., 2020). S protein contains two different domain regions: S1 and S2, each one has its own role in virus entry. S1 domain is the part that binds directly to the host ACE2 receptor while the S2 domain helps the virus to fuse with the target cell membrane using its functional elements (Glowacka et al., 2011; Hoffmann et al., 2020). This process is also mediated by a Transmembrane Serine Protease 2 (TMPRSS2) located on the surface of the target cell membrane used for the priming of the S protein causing the virus entry (Hoffmann et al., 2020; Shen, Mao, Wu, Tanaka, & Zhang, 2017; Wang et al., 2020).

When the fusion of the virus with the target cell membrane occurs, the virus releases its genome and using the host cell organelles to replicates its RNA and releases new mature virion to target other cells (Boopathi, Poma, & Kolandaivel, 2020; Jiang, Hillyer, & Du, 2020) Figure 1.

wait wait wait the wild virus replicates its RNA too?

minor flex –

3.1 Human papillomavirus (HPV) and its impact on male fertility

Human papillomavirus (HPV) is a non-enveloped DNA virus and sexually transmitted worldwide. In some cases, it causes either warts or precancerous lesions (Ljubojevic & Skerlev, 2014). More than 170 HPV types have been identified and completely sequenced (Chouhy, Bolatti, Pérez, & Giri, 2013). Recent studies suggest that HPV infection affects male fertility. In cases of idiopathic asthenozoospermia, HPV DNA was observed in the sperm cells of infertile patients (Foresta et al., 2010; Lee, Huang, King, & Chan, 2002) confirming its role of infertility. Strong association between HPV infection and impairment of sperm parameters, especially a reduction in sperm motility and concentration, was observed in HPV-infected men (Garolla et al., 2012; Jeršovienė, Gudlevičienė, Rimienė, & Butkauskas, 2019). Garolla and coworkers (Garolla et al., 2012) reported that HPV can bind to the head of a spermatozoon and impair sperm motility in men. Certain sperm DNA exons undergo apoptotic fragmentation on HPV-infected men suggesting that HPV types degrade different exons of important genes (Lee et al., 2002). Collectively, these evidences suggest that HPV plays a role in male factor infertility.

3.2 Herpes simplex viruses (HSVs) and their impact on male fertility

Herpes simplex viruses (HSVs) are enveloped DNA viruses of the family Herpesviridae. HSVs include two distinct viruses HSV-1 and HSV-2 (Whitley & Roizman, 2017). HSVs are sexually transmitted and targets reproductive system. HSV-1 causes oral and, occasionally, genital sores while HSV-2 is common cause of genital herpes which may lead to infertility problems in both males and females. HSV DNA was detected in semen from about 50% asymptomatic infertile males (Amirjannati et al., 2014; Bezold et al., 2007; Monavari et al., 2013; Neofytou, Sourvinos, Asmarianaki, Spandidos, & Makrigiannakis, 2009). A strong association of HSV infection and low sperm count, poor motility, and increased apoptotic cells were reported (Monavari et al., 2013). Haematospermia and a lower seminal volume and abnormal viscosity were found in HSV-2-infected males which indicate prostate dysfunction (Kurscheidt et al., 2018). Bezold et al. (2007) reported significantly reduced sperm concentration and motility as well as reduced citrate concentrations and neutral α-glucosidase in HSV-infected males, suggested impaired epididymal and prostate function.

The manwhore diseases are listed alongside HIV, lol.
The wages of sin is death, in men as well as women.
How will PUAs recover? They won’t. God Willing.

The concern show that SARS-CoV-2 may affect male reproductive organ and thus results in male infertility stems from several observations. Early studies both in China and Italy showed that males are more susceptible to COVID-19 compared to females (Guan et al., 2020; Livingston & Bucher, 2020).

A recent large cohort observational study from United Kingdom featuring around 20 thousands COVID-19 patients reported that males represented 60% of cases and considered the male sex as one of the risk factors for COVID-19 (Docherty et al., 2020).

DS: MRAs: crickets

More alarming is the result of a new systematic review—included 48 recently published articles and 16 databases—where it found that men are more likely to suffer or to die from the complications of COVID-19 compared to women (Serge, Vandromme, & Charlotte, 2020).

DS: suffer or die? Binary?

Large proportion of these vulnerable males is in their childbearing age, and thus their reproductive ability can be affected.

Finally, like influenza, COVID-19 patients suffer from fever, which may affect sperm production. It was reported that febrile illnesses had an impact on semen parameters (Sergerie, Mieusset, Croute, Daudin, & Bujan, 2007). Total sperm count and motility percentage were reduced significantly at days 15, 37 after fever episode before going back to normal after several weeks (Sergerie et al., 2007). Increase of sperm DNA fragmentation index and alteration in the nuclear protein composition of ejaculated spermatozoon were reported after fever episode (Evenson, Jost, Corzett, & Balhorn, 2000).

Different viruses use different routes to enter into the host cells. SARS-CoV-2 uses the same ACE2 receptor used by its cousin, the SARS-CoV virus, with the help of TMPRSS2 (see Figure 1). Single cell expression analysis has detected the expression of ACE2 RNA not only in the lung epithelial cells, but also in several other organs, among them are the kidneys and the bladder (Fan et al., 2020; Lin et al., 2020; Tipnis et al., 2000). Protein expression analysis also confirmed the presence of ACE2 protein in multiple tissues (Hamming et al., 2004).

Interestingly, the highest expression of ACE2 was found in the testes (Fan et al., 2020). The high expression of the ACE2 receptor in the testes raises a concern that the SARS-CoV-2 has the route to enter some if not all testicular cells and thus could cause damage.

To further analyse the types of testicular cells vulnerable for SARS-CoV viruses, Wang et al. studied single-celled ACE2 expression in the human testes (Wang & Xu, 2020). They found that ACE2 is mainly expressed in spermatogonia, leyding and Sertoli cell, while spermatocytes and spermatids had very low expression (Wang & Xu, 2020). Interestingly, TMPRSS2 expression is similar to ACE2, where TMPRSS2 was also enriched in spermatogonia and spermatids. It has been also shown that ACE2 positive spermatogonia cells express genes that are important for virus reproduction and transmission, while ACE2 positive leyding and Sertoli cells express genes that are required for cell–cell junctions and immunity.

Collectively, these results highlight the risk of COVID-19 on testicular cells and on the spermatogenesis process.

The only direct evidence for the effect of COVID-19 on male reproductive function comes from a study where sex hormones namely testosterone (T), luteinising hormone (LH) and follicle-stimulating hormone (FSH) among others were compared between COVID-19 patients and healthy controls. While the T level was not different between the two groups, the ratio of T to LH and the ratio of FSH to LH were significantly decreased in COVID-19 patients (Ma et al., 2020).

This might be the first direct evidence for the influence of COVID-19 on testicles’ ability to produce sex hormones; however, the results of this study should be followed by a more direct analysis of the seminal fluid of COVID-19 patients to evaluate the effect—if any—on sperm count, volume, morphology or motility. It has been reported that SARS-CoV causes orchitis in addition to other complications (Xu et al., 2006), so it is also possible that SARS-CoV-2 may cause the same complication in males.

Y NO DO THIS ON JABBEES?

And it may kill pregnant women only:

Pregnant women have been shown to be at high risk of comorbidity and mortality related to influenza infections (Rasmussen, Jamieson, & Bresee, 2008; Rasmussen, Jamieson, & Uyeki, 2012). The previous SARS infection showed that pregnant women had higher fatality rate (25%) compared to the general population (10%; Wong et al., 2004). With the rise of numbers of pregnant women and children affected by COVID-19, it is worth to know if pregnant women are a high-risk group for COVID-19 death or increased hospitalisation and also to evaluate the risk of vertical transfer either from the mother to the foetus or from the neonates to the mother.

Neonatal health is another important concern in the COVID-19-infected mothers. In a study from Wuhan, 33 neonates were born to mothers with COVID-19, and no health complications were reported except for shortness in breath in four cases (Zeng et al., 2020). Other studies, including less number of cases, did not report any neonatal health issues except for low birthweight (<2,500 g) and premature delivery (Cao et al., 2020; Chen & Lou, 2020). Two other studies from China and Iran reported two neonatal deaths out of 19 cases studied (Hantoushzadeh et al., 2020; Zhu, Wang, et al., 2020). No cases of miscarriages have been reported in the first trimester of COVID-19 pregnancies. Overall, it seems that neonates delivered by COVID-19 pregnant mothers have no increased risk of clinical complications compared to normal pregnancies and some of the reported neonatal complications could be related to mothers’ overall health status rather than a consequence of COVID-19 infection.

Then why jab them?

The risk of vertical transfer of SARS-CoV-2 between the mother and the foetus is possible knowing that the ACE2 receptor is expressed in the placenta and uterus (Levy et al., 2008); however, most published data do not support this predication as most neonates born for mothers affected by COVID-19 tested negative (Chen et al., 2020; Liu et al., 2020; Yu et al., 2020). A few studies have reported a vertical transfer of SARS-CoV-2 from the mother to the neonates (Hantoushzadeh et al., 2020; Yu et al., 2020), but these studies should be carefully interpreted as they occur less frequently and possibly resulted because of the neonatal exposure to SARS-CoV-2 after delivery.

One way to get you on the hook financially is reproductive tech.

Risk of ovarian hyperstimulation syndrome should be taken very seriously during COVID-19 pandemic crisis and all guidelines clearly stated that reproductive endocrinologists should adopt gonadotropin-releasing hormone (GnRH) antagonist as a default protocol for ovarian stimulation with GnRH-agonist trigger to minimise the risk of ovarian hyperstimulation syndrome (OHSS), hospital admissions and intensive care unit (ICU) occupancy (ASRM; Carugno et al., 2020ESHREJSF).

Isn’t that an endometriosis fertility treatment? Odd. So you’re saying it works?

Many health issues related to COVID-19 have been addressed in this review. Pregnancy and maternal health have been discussed. Many reports have evidences against a direct link between COVID-19 and maternal death. Neonates born to a COVID-19 mothers are not at increased risk of adverse health consequence compared to the ones born for COVID-19-unaffected mothers, and the possibility of viral vertical transfer has not been confirmed. Large cohort studies should be followed to confirm these results; additionally, first-trimester COVID-19 cases should be included and be evaluated for the risk of miscarriages.

The gender difference in COVID-19 incidence, comorbidity and death rates—males are at higher risk—requires prompt actions to understand the source of difference biologically and behaviourally. Viral infection by HPV, HSV, HIVs, HBV, HCV and MuV challenges reproductive health and can be considered as a risk factor for male infertility. These viruses have been detected in semen and can impair testicular function. Some viruses such as HIV, MuV and SARS-CoV are associated with orchitis resulting in male infertility, so it would be interesting to study if SARS-CoV-2 can cause the same problem. Because many males at childbearing age are affected by COVID-19, the high expression of ACE2 receptor in the testes and the association of COVID-19 with fever; a multidimensional andrological translational research project was suggested (Salonia et al., 2020). This project aims to develop international collaboration for data registry, hormonal studies and genomic studies to better understand the sex difference for COVID-19 health-related consequences.

re the endo treatment


GnRH agonists are a group of drugs that have been used to treat women with endometriosis for over 20 years [1]. They are modified versions of a naturally occurring hormone known as gonadotropin releasing hormone, which helps to control the menstrual cycle.

At present, the usual length of treatment with a GnRH agonist is 3–6 months. However, in Germany, 12 months treatment with add-back therapy (5 mg of norethisterone per day) has been approved, and other countries may do the same in the future.

COVID, sperm infertility and STD potential

https://onlinelibrary.wiley.com/doi/10.1111/andr.12859
COVID-19 and human spermatozoa—Potential risks for infertility and sexual transmission?

TLDR: scroll to end

As COVID-19 infections wreak havoc across the globe, attention has rightly been focused on the vital organ systems (lung, kidney and heart) that are vulnerable to viral attack and contribute to the acute pathology associated with this disease.

However, we should not lose sight of the fact that COVID-19 will attack any cell type in the body expressing ACE2 – including human spermatozoa.

These cells possess the entire repertoire of receptors (AT1R, AT2R, MAS) and ligand processing enzymes (ACE1 and ACE2) needed to support the angiotensin signalling cascade.

The latter not only provides COVID-19 with a foothold on the sperm surface but may also promote integration, given the additional presence of a range of proteases (TMPRSS2, TMPRSS11B, TMPRSS12, furin) capable of promoting viral fusion.

This article reviews the roles played by these various cellular constituents in maintaining the vitality of human spermatozoa and their competence for fertilization. The reproductive consequences of a viral attack on these systems, in terms of fertility and the risk of sexual transmission, are currently unknown.

However, we should be alive to the possibility that there may be reproductive consequences of COVID-19 infection in young males that go beyond their capacity to survive a viral attack.

If only someone warned you.

A recent report published in JAMA Network Open revealed that in an analysis 38 semen samples from COVID-19 patients, 6 (four at the acute stage of infection and, alarmingly, two who were recovering) tested positive for the virus by RT-PCR.1 Importantly, at this point, we have no idea whether the actual virus was viable and infectious. Nevertheless, the possibility that this coronavirus could have a pathophysiological impact on the testes was suggested by additional data indicating that active COVID-19 infection dramatically reduced the testosterone-to-LH ratio, suggesting a significant impact on the responsiveness of Leydig cells to LH stimulation.2 

In many ways, we should not be surprised by these observations because the blood-testes barrier is known to offer little defense against viral invasion, given the wide range of pathogenic viruses (HIV, hepatitis, mumps, papilloma) that are known to be capable of damaging the testes and rendering the host infertile. Furthermore, the spike protein that gives the COVID-19 virus its corona is known to target ACE2 (angiotensin-converting enzyme 2), which is highly expressed by several cell types in the testes including Leydig cells, Sertoli cells, and the germ line.

As a result of these factors, several opinion pieces have been published already, raising the possibility of testicular damage and infertility consequent to COVID-19 infection.24 However, it is also possible that the virus could gain access to male germ cells once they leave the testes, either in the epididymis or following ejaculation. In this Opinion Article, I shall be focusing on this post-testicular route of infection pointing out, for the first time, that the mature spermatozoon has all of the machinery needed to bind this virus, fuse with it, and even achieve reverse transcription of the viral RNA into proviral DNA. Such considerations raise the possibility that spermatozoa could act as potential vectors of this highly infectious disease. This happens in insects5—why not us?

“Furthermore, the spike protein that gives COVID-19 virus its corona is known to target ACE2…”

“However, it is also possible that the virus could gain access to male germ cells once they leave the testes… following ejaculation.”

to put it in terms you degenerates can understand

It has been known for many years that the human sperm surface expresses ACE.

Indeed, an examination of existing proteomic databases68 as well as surveys of the sperm surface with monoclonal antibodies,9 demonstrates that these cells, quite literally, hold all of the ACEs.

now I am fucking with you yes indeedy do

They have been known for some time to express a testicular variant of ACE1, which converts the inactive decapeptide hormone, angiotensin I, to the active octapeptide, angiotensin II (Figure 1). Testicular ACE corresponds to the ancestral non-duplicated form of the ACE gene; it lacks multiple 5′ exons and has a distinct N-terminus: biochemically however, it performs exactly the same function as somatic ACE1.10 Spermatozoa also express ACE2, which converts angiotensin II to angiotensin (1-7). Reference to the human sperm proteome also indicates that these cells possess the two known receptors for angiotensin II: angiotensin II type-1 receptor (AT1R) and (angiotensin II type-2 receptor) (AT2R). Furthermore, a recent publication has revealed that human spermatozoa also express the angiotensin (1-7) MAS receptor.9 These cells therefore possess the complete repertoire of ligand-processing enzymes and receptors needed to support angiotensin signaling pathways, raising questions about the physiological roles these pathways play and how they might intersect with COVID-19 (Figure 1).

Germ cells are unipotent stem cells that divide to produce gametes in sexually reproducing organisms. A germ cell undergoes meiotic cell division to produce genetically unique, haploid sex cells, which then fuse during fertilization to form a diploid zygote. In female organisms, germ cells give rise to egg cells and, in males, they produce sperm cells.

Germ cells are the cells that give rise to gametes in all sexually reproducing organisms. In vertebrates, they are the precursors of male sperm cells and female egg cells. Collectively, all the germ cells in an organism are known as the germline.

Germ cells are the type of stem cell that gives rise to gametes. They are, therefore, the origin cells of all sexually reproducing organisms, and allow individual members of a species to pass on genetic information to their offspring. The inheritance of DNA is the driving force behind natural selection and evolution, and the fact that germ cells divide by meiosis ensures maximal genetic variation among gametes.

From top paper:

“The spike protein on COVID-19 specifically targets ACE2 and in so doing removes an important stimulus for PI3K/AKT, thereby compromising sperm viability.”

“Alternatively proteases from the TMPRSS-family, either as intrinsic components of the sperm plasma membrane or delivered by seminal prostasomes, can facilitate fusion between the virus and the sperm surface by cleaving ACE2 and the viral spike proteins (S1 and S2) at the sites indicated by dashed lines, thereby completing the transformation of this cell from procreating gamete to viral vector

Big Pharma Balls? Mutant metaplasia.

“Actual fusion between the virus and human spermatozoa requires the presence of the above-mentioned protease, TMPRSS2, to cleave the viral spike proteins (S) at the S1/S2 boundary or within S2 subunit, thereby removing the structural constraint of S1 on S2 and releasing the internal membrane fusion peptide (Figure 1). This protease is known to be present in prostasomes that are released into seminal fluid from the prostate gland at ejaculation.29 As one of the major functions of these exosome-like structures is to transfer their contents, including proteins, to the spermatozoa following ejaculation, the incorporation of TMPRSS2 from this source seems probable.30 “

How many times must I try to save your nuts?

The presence of these activating proteases as well as ACE2 in the sperm plasma membrane would be expected to allow the COVID-19 virus to bind to the cell surface and ultimately fuse, either in the testes or during the prolonged sojourn of these cells in the epididymis. In contrast, oocytes appear to be completely devoid of TMPRSS2,33 making infection of the female germ line highly unlikelyunless, of course, they are fertilized by a COVID-19 carrying spermatozoon. In this context, it should be emphasized spermatozoa have a demonstrable capacity to carry viral infections from the male to the female reproductive tract, as happens during the sexual transmission of the Zika virus, for example.34 They also have a proven capacity to fuse with enveloped viruses35 and possess reverse transcriptase activity capable of generating proviral DNA,36 as is apparently the case for human immunodeficiency virus 1.37

making infection of the female germ line highly unlikely unless, of course, they are fertilized by a COVID-19 carrying spermatozoon

Why did you think they wanted to inject college kids?

also see https://pubmed.ncbi.nlm.nih.gov/32578263/

We performed this systematic review to evaluate the possibility of an impact of SARS-CoV-2 infection on male fertility. SARS-CoV-2 enters the cells with the help of ACE2; therefore, testicular expression of ACE2 was analysed from transcriptome sequencing studies and our unpublished data. Literature suggested that SARS-CoV-1 (2002-2004 SARS) had a significant adverse impact on testicular architecture, suggesting a high possibility of the impact of SARS-CoV-2 as well. Out of two studies on semen samples from COVID-19 affected patients, one reported the presence of SARS-CoV-2 in the semen samples while the other denied it, raising conflict about its presence in the semen samples and the possibility of sexual transmission. Our transcriptome sequencing studies on rat testicular germ cells showed ACE expression in rat testicular germ cells. We also found ACE2 expression in transcriptome sequencing data for human spermatozoa, corroborating its presence in the testicular germ cells. Transcriptome sequencing data from literature search revealed ACE2 expression in the germ, Sertoli and Leydig cells. The presence of ACE2 on almost all testicular cells and the report of a significant impact of previous SARS coronavirus on testes suggest that SARS-CoV-2 is highly likely to affect testicular tissue, semen parameters and male fertility.

https://link.springer.com/article/10.1007/s10508-020-01757-0

Several studies have demonstrated the presence of viral RNA in the feces of patients affected by COVID-19, suggesting the possibility of viral transmission through the oralfecal route (Nouri‐Vaskeh & Alizadeh, 2020; Zhang et al., 2020). Furthermore, there is evidence proving that fecal tests continue to be positive even after the respiratory specimens become negative (Tian, Rong, Nian, & He, 2020).

Studies aimed at investigating the potential mechanisms underlying SARS-CoV-2 transmission and infection at the level of the oral cavity have shown that ACE2 is expressed by the mucosal epithelial cells. The expression of this molecule is higher at the tongue level than in gingival and buccal tissues, indicating it as a possible route of infection (Xu et al., 2020). Moreover, live viruses were detected in the saliva of infected individuals (To et al., 2020).

In order to explore the possibility of sexual transmission, the presence of SARS-CoV-2 was tested in vaginal fluid and semen of SARS-CoV-2-positive patients. In one study (Pan et al., 2020), Sars-CoV-2 was detected in semen samples of 34 Chinese men recovering from COVID-19 with milder symptoms. In two other studies, one in which 35 female COVID-19 patients were recruited and who came from different geographical areas of Wuhan (Cui et al., 2020) and another in which were 10 postmenopausal woman with severe COVID-19 were recruited (Qiu et al., 2020), Sars-CoV-2 was detected in vaginal fluids. In these studies, SARS-CoV-2 was not found either in semen or in vaginal fluids of positive cases.

This does not exclude the possibility of viral transmission through sexual behavior (e.g., oral/anal contacts). Indeed, viral particles may be transmitted through oral sex and use of saliva as a lubricant. This is supported, as previously described, by the shedding of viral particles through the saliva and the feces and the presence of ACE2 receptors on the epithelium lining the oral cavity and the rectum.

…Shut down Tinder.

Physicians should inform their patients about these risk behaviors in order to avoid further spreading of the virus. The importance of increasing awareness on less common transmission routes stems from the high number of contagious persons, including asymptomatic individuals and patients with doublenegative oro/nasopharyngeal swab, but still potentially contagious (persistent fecal elimination of the virus).

The wages of sin – HPV in men and sperm infertility

https://pubmed.ncbi.nlm.nih.gov/32386620/

TLDR – NOT HARMLESS

Evaluation of human papilloma virus in semen as a risk factor for low sperm quality and poor in vitro fertilization outcomes: a systematic review and meta-analysis

A review of the literature regarding ART outcomes showed an association between HPV infection and decreased PR, and an even stronger association between HPV infection and increased MR.

-increased miscarriage rate, lower odds of conceiving

Conclusion: Our meta-analysis shows a negative effect of HPV on sperm concentration, motility, and morphology. Further subgroup and categorical analysis confirmed the clinical significance of impaired sperm motility in HPV-infected sperm, although the sperm count and morphology must be carefully analyzed. The studies reviewed reported lower PR and increased MR in couples with HPV-infected sperm. As most studies had a moderate risk of bias, these observations warrant further large, well-designed studies before introducing clinical management recommendations.

https://pubmed.ncbi.nlm.nih.gov/32279923/

Yes, this is a dealbreaker to sane women.

Human papilloma virus: to what degree does this sexually transmitted infection affect male fertility?

No abstract available

irony

MRAs: crickets

https://pubmed.ncbi.nlm.nih.gov/25992782/

Human papillomavirus infection and fertility alteration: a systematic review

Results: HPV infections are shown to be significantly associated to many adverse effects in the reproductive function. These adverse effects were reported in different levels from cells production to pregnancy and may be related to the infecting genotype.

Conclusions: It appears from this study that HPV detection and genotyping could be of great value in infertility diagnosis at least in idiopathic infertility cases. Like for the risk of carcinogenesis, another classification of HPV regarding the risk of fertility alteration may be considered after deep investigations.

https://pubmed.ncbi.nlm.nih.gov/30344281/

Human Papilloma Virus (HPV) and Fertilization: A Mini Review

Sorry but if something makes you less virile, you’re less of a man.

Human papilloma virus (HPV) is one of the most prevalent viral sexually transmitted diseases. The ability of HPV to induce malignancy in the anogenital tract and stomato-pharyngeal cavity is well documented. Moreover, HPV infection may also affect reproductive health and fertility. Although, the impact of HPV on female fertility has not been thoroughly studied it has been found also to have an impact on semen parameters. Relative information can be obtained from studies investigating the relationship between HPV and pregnancy success. Furthermore, there is an ongoing debate whether HPV alters the efficacy of assisted reproductive technologies. An association between HPV and assisted reproductive technologies (ART) programs has been reported. Nevertheless, due to conflicting data and the small number of existing studies further research is required. It remains to be clarified whether HPV detection and genotyping could be included in the diagnostic procedures in couples undergoing in vitro fertilization (IVF)/intrauterine insemination (IUI) treatments. Vaccination of both genders against HPV can reduce the prevalence of HPV infection and eliminate its implications on human fertility. The aim of the present mini-review is to reiterate the association between HPV and human fertility through a systematic literature review.

https://pubmed.ncbi.nlm.nih.gov/21666465/

The role of human papillomavirus on sperm function

I love how many yanks pull a Henry 8th and blame women for their own infertility, in this century.

Recent findings: HPVs are agents of the most common sexually transmitted disease and can lead to warts and cancers both in men and women. A high incidence of HPV infection has been demonstrated in sperm from sexually active men with and without risk factors for HPV and from infertile patients.

Semen infection is associated to an impairment of sperm parameters suggesting a possible role in male infertility. – really???

Interestingly, it has been demonstrated that when HPV is present in semen only a percentage of total cells are infected

-only? a? 100% is a percentage too…

and the virus can be localized in sperm or in exfoliated cells with different impact on sperm motility. Moreover, infected sperm are able to penetrate the oocyte, to deliver HPV genome in the oocyte and HPV genes can be actively transcribed by the fertilized oocyte.

-wouldn’t it be ironic if it made the kids or grandkids infertile instead? because they were conceived with it, a polluted germline

Recently an increased risk of pregnancy loss has been demonstrated in couples undergoing in-vitro fertilization and particularly when HPV DNA was present in semen samples of male partners.

– no blaming women this time, unless women haz sperm?

Summary: To date, no effective treatment, control strategy and prevention is provided for men despite the reported high incidence of HPV semen infection.

– no hurt their feefees? NAW

Because this infection in men is also a problem for partners, and because growing evidence suggests that semen infection may cause infertility and early miscarriage, more attention should be paid to male HPV infection. This study reviews the more recent literature about the role of HPV infection on sperm function and human reproduction.

– Manosphere fears this topic and all male degenerate accountability.

semen infection may cause infertility and early miscarriage

it’s the sins of the FATHER, you see…

https://pubmed.ncbi.nlm.nih.gov/30517657/

High-risk human papillomavirus in semen is associated with poor sperm progressive motility and a high sperm DNA fragmentation index in infertile men

Does the presence of human papillomavirus (HPV) in semen impact seminal parameters and sperm DNA quality in white European men seeking medical help for primary couple’s infertility?

>STD
>DNA quality
>in the germline of
>white men

Never talk about it, I’m sure it’ll be fine.

 HPV seminal infections involving high-risk (HR) genotypes are associated with impaired sperm progressive motility and sperm DNA fragmentation (SDF) values.

TLDR: yes.

HPV is commonly present in semen samples. 

No? F no it’s not. Stop sparing slutty blushes.

The overall rate of HPV positivity was 15.5%

so 1 in 7, uncommon at best. No normalizing pathology please.

And it varies majorly by race and sexuality. Not sex because it’s sexual, obviously.

 Sperm progressive motility was significantly lower (P = 0.01) while SDF values were higher (P = 0.005) in HPV+ men compared to those with no HPV. In particular, HR HPV+ men had lower sperm progressive motility (P = 0.007) and higher SDF values (P = 0.003) than those with a negative HPV test. Univariable analysis showed that HR HPV+ was associated with impaired sperm progressive motility (P = 0.002) and SDF values (P = 0.003). In the multivariable analysis, age, FSH levels and testicular volume were significantly associated with impaired sperm progressive motility (all P ≤ 0.04). Conversely BMI, CCI, smoking habits and HPV status were not. Only age (P = 0.02) and FSH (P = 0.01) were significantly associated with SDF, after accounting for BMI, CCI, testicular volume, smoking habits and HPV status.

It’s worse for the older men.

https://pubmed.ncbi.nlm.nih.gov/32381092/

Impact of human papillomavirus infection in semen on sperm progressive motility in infertile men: a systematic review and meta-analysis

Background: Human papillomavirus (HPV) has been considered as one of the most common sexually transmitted viruses that may be linked to unexplained infertility in men. The possible mechanisms underlying correlation between HPV infection and infertility could be related to the altered sperm parameters. Current studies have investigated the effect of HPV seminal infection on sperm quality in infertile men, but have shown inconsistent results.

Methods: We systematically searched PubMed, Embase, Web of Science and CNKI for studies that examined the association between HPV seminal infection and sperm progressive motility. Data were pooled using a random-effects model. Outcomes were the sperm progressive motility rate. Results are expressed as standardised mean difference (SMD) with 95% confidence interval (CI). Heterogeneity was evaluated by the I-square (I2) statistic.

Results: Ten studies were identified, including 616 infertile patients with HPV seminal infection and 2029 infertile controls without HPV seminal infection. Our meta-analysis results indicated that sperm progressive motility was significantly reduced in HPV-infected semen samples compared with non-infected groups [SMD:-0.88, 95% CI:-1.17 ~ – 0.59]. There existed statistical heterogeneity (I2 value: 86%) and the subgroup analysis suggested that study region might be the causes of heterogeneity.

Conclusions: HPV semen infection could significantly reduce sperm progressive motility in infertile individuals. There were some limitations in the study such as the differences in age, sample sizes and the number of HPV genotypes detected. Further evidences are needed to better elucidate the relationship between HPV seminal infection and sperm quality.

https://pubmed.ncbi.nlm.nih.gov/25659295/

Antisperm antibodies in infertile men and their effect on semen parameters: a systematic review and meta-analysis

what a mystery

The mechanism of ASA cause male infertility is not clear

does it look like HPV?

The present study illustrates that there was a significant negative effect of ASA on sperm concentration, sperm motility (a+b) and sperm liquefaction.

yes

https://pubmed.ncbi.nlm.nih.gov/26793663/

The prevalence of Human Papilloma Virus (HPV) infection in the oligospermic and azoospermic men

The current study shows that HPV infection can affect on sperm count and motility and decrease count of sperm cell and decrease motility capability of these cells.

duh?

Among 50 confirmed oligospermic male, 15 were HPV DNA positive (30%).

In azoospemic group we had 8 HPV DNA positive (40%) and in normal group just 3 of 20(15%) samples were positive.

-what r the odds?

we found statistical significant relationship for sperm count (p<0.05) and sperm motility (slow) (p<0.05) in oligospermic group positive samples compared with negative. In the present study, 13 HPV genotypes were detected among positive samples. HPV genotypes 16, 45 in the high risk group and 6,11,42 in the low risk group were more frequent than the others.

Medicine can’t spare you.

https://pubmed.ncbi.nlm.nih.gov/21536283/

Semen washing procedures do not eliminate human papilloma virus sperm infection in infertile patients

 Fifteen samples

-aka HALF

had HPV DNA on sperm and exfoliated cells. Sperm washing centrifugation showed no changes in the number of infected samples and in the percentage of infected cells. Ficoll and swim-up protocols induced a slight reduction in the number of infected samples (30 and 26, respectively).

no muh scientism and IVF cope

This study demonstrated that conventional sperm selection rarely eliminates HPV sperm infection. More attention should be paid to the reproductive health of infected patients because, not only can HPV be transmitted, but it may also have a negative effect on development of the fetus.

-may, LOL

a negative effect on development of the fetus

so even if they all married a virgin waifu, they’d infect her and have defective babies
comedy GOLD, 24K.

https://pubmed.ncbi.nlm.nih.gov/33763033/

Is HPV the Novel Target in Male Idiopathic Infertility? A Systematic Review of the Literature

Infertility is an important health problem that affects up to 16% of couples worldwide.

1 in 7, where have I heard THAT before….? [scroll up]

Male infertility is responsible for about 50% of the cases,

NAY, men are never responsible for their own in/fertility, have you been online recently?

and the various causes of male infertility may be classified in pre-testicular (for example hypothalamic diseases), testicular, and post-testicular (for example obstructive pathologies of seminal ducts) causes. Sexually transmitted infections (STI) are increasingly widely accepted by researchers and clinicians as etiological factors of male infertility. In particular, several recent reports have documented the presence of HPV in seminal fluid and observed that sperm infection can also be present in sexually active asymptomatic male and infertile patients.

In this review, we aimed to perform a systematic review of the whole body of literature exploring the impact of HPV infection in natural and assisted fertility outcomes, from both an experimental and a clinical point of view. Starting from in-vitro studies in animals up to in-vivo studies in humans, we aimed to study and evaluate the weight of this infection as a possible cause of idiopathic infertility in males with any known cause of conception failure.

https://pubmed.ncbi.nlm.nih.gov/30291691/

Significant Correlation between High-Risk HPV DNA in Semen and Impairment of Sperm Quality in Infertile Men

brace yourselves

guess the result

c’mon

go on
think

just guess

….

ready?

A total of 140 subjects participated in the current study. Among 70 confirmed infertile males, only 8 (11.43%) cases tested positive for high-risk HPV and all fertile men were HPV-negative. This data revealed a significant association between high-risk HPV and male infertility (P=0.03). The percentage of normal sperm morphology and sperm motility rate significantly declined in men infected with HPV (P<0.001).

and all fertile men were HPV-negative

oof and the sluts of both sexes are dying out, I am distraught.
The genetics of the future are fairing brighter than you’d think.

Conclusion: There was a significantly higher prevalence of high-risk HPV in infertile men than fertile men. HPV infection seemed to be a risk factor for male infertility. Additional, larger studies should be conducted to confirm the impact of HPV on male infertility.

Player burnout shall henceforth be dubbed HPV-driven infertility?

https://pubmed.ncbi.nlm.nih.gov/33666259/

2021

Association between human papillomavirus infection and sperm quality: A systematic review and a meta-analysis

Human papillomavirus (HPV) has a high incidence rate in both males and females.

-maybe where you live

HPV infection in women has been shown to affect fertility and lead to foetal death and pregnancy loss. However, research on HPV infection in men is limited.

-well the husbands are freshly infecting the wives so

-Ashley Madison wasn’t full of women stepping out, was it?

The aim of this study was to study the effect of HPV infection in semen on sperm quality and present the findings of previous studies through a meta-analysis. Databases including PubMed, MEDLINE, EMBASE, Web of Science, Cochrane Library, WanFang data and China National Knowledge Infrastructure were searched for relevant studies. A systematic review and meta-analysis were performed, and 17 studies were included for analyses based on a set criterion. Meta-analyses indicated that HPV infection in semen significantly reduced sperm concentration (SMD = -0.12, 95% CI: -0.21 to -0.03, p = .009), sperm motility (SMD = -0.55, 95% CI: -0.780 to -0.33, p = .000), sperm viability (SMD = -0.55, 95% CI: -0.780 to -0.33, p = .000) and sperm morphology (SMD = -0.34, 95% CI: -0.61 to -0.07, p = .015). The high-risk HPV (HrHPV) infection could significantly reduce sperm count (SMD = -0.65, 95% CI: -1.11 to -0.18, p = .007) compared with high-risk HPV (LrHPV) infection.

In conclusion, HPV infection in semen significantly reduced sperm quality, and the HrHPV infection could significantly reduce sperm count compared with LrHPV.

b-b-but what does that matter? – bluepills

https://pubmed.ncbi.nlm.nih.gov/33725837/

tick tock goes your biological clock, nobody can wait as long as they want
NOBODY

Male sperm quality and risk of recurrent spontaneous abortion in Chinese couples: A systematic review and meta-analysis

Conclusions: The results of this analysis support an association of sperm density, sperm viability, sperm progressive motility rate, normal sperm morphology rate, sperm deformity rate, as well as sperm DFI with RSA. 

IF you conceived, magically, it would kill your baby. REPEATEDLY.

https://pubmed.ncbi.nlm.nih.gov/8671172/

Semen parameters and sperm morphology in men in unexplained recurrent spontaneous abortion, before and during a 3 year follow-up period

Baby death aborts the defective DNA, HPV fucks with your sperm’s DNA. Water is wet.

HPV makes you biologically unfit. According to the ultimate test, the womb.

To investigate the role of the ‘male factor’ in the pathogenesis of recurrent spontaneous abortion (RSA), especially sperm morphology abnormalities, 120 previously selected couples with unexplained RSA were studied for sperm parameters retrospectively and prospectively. The patients were subdivided into three subgroups, depending on their reproductive outcome during the 3 years of follow-up study: (i) 48 RSA couples who achieved a successful pregnancy; (ii) 39 RSA couples who experienced further abortions, and (iii) 33 RSA couples who experienced infertility during the follow-up period. A semen analysis was performed twice at the time of inclusion in this study, and twice again during the 3 year follow-up period. No significant differences in semen parameters were observed between RSA males and fertile controls. Instead, significant differences were observed between the group of RSA couples who experienced infertility during the follow-up and the other two groups (RSA couples who achieved successful pregnancy and RSA couples who experienced miscarriages and no live birth during the follow-up) for sperm concentration (P < 0.01 and P < 0.01 respectively), sperm motility (P < 0.01 and P < 0.01 respectively) and sperm morphology abnormalities (P < 0.01 and P < 0.01 respectively).

dat p-value

MORE STUDIES

https://pubmed.ncbi.nlm.nih.gov/23278374

Sperm DNA fragmentation in couples with unexplained recurrent spontaneous abortions

(((((“”unexplained“”)))))

The aim of the present study was to evaluate the degree of sperm DNA fragmentation in couples with idiopathic recurrent spontaneous abortion (RSA) and in those with no history of infertility or abortion. In this cohort study, 30 couples with RSA and 30 fertile couples as control group completed the demographic data questionnaires, and their semen samples were analysed according to World Health Organization (WHO) standards (September 2009-March 2010) for evaluation of sperm DNA fragmentation, using sperm chromatin dispersion (SCD) technique. The percentage of morphologically normal sperm was significantly lower in RSA patients compared with control group (51.50 ± 11.60 versus 58.00 ± 9.05, P = 0.019), but not in other parameters. Additionally, the level of abnormal DNA fragmentation in the RSA group was significantly higher than in the control group (43.3% versus 16.7%, P = 0.024). Our results indicated a negative correlation between the number of sperm with progressive motility and DNA fragmentation (r = -0.613; P < 0.001). The sperm from men with a history of RSA had a higher incidence of DNA fragmentation and poor motility than those of the control group, indicating a possible relationship between idiopathic RSA and DNA fragmentation.

– idiopathic? Are you shitting me?

(((idiopathic)))

sure it is

sure

https://pubmed.ncbi.nlm.nih.gov/23042403/

Correlation of recurrent pregnancy loss with sperm parameters and sperm DNA fragmentation

This study has indicated that sperm from men with a history of RPL have a higher incidence of DNA damage and poor motility compared with fertile males.

Water is wet. Miscarriage is meant to happen to dodgy DNA.

https://pubmed.ncbi.nlm.nih.gov/22519675/

Sperm chromatin integrity may predict future fertility for unexplained recurrent spontaneous abortion patients

“unexplained” – just assume the echo for comedic effect by now

The RSA group was further separated into three subgroups, depending on their reproductive outcome during the 12 months after they were enrolled in the study: the pregnancy subgroup consisted of 43 men whose partners achieved a successful pregnancy up to at least the 24th week of gestation; the abortion subgroup included 31 men whose partners experienced further abortions; and the infertile subgroup had 37 men whose partners did not have any positive pregnancy test after regular, unprotected intercourse. Significantly lower proportion of sperm with normal morphology was found in the abortion subgroup (14.7 ± 4.3%) than in the control group (17.5 ± 5.0%). Sperm concentrations were significantly lower in the infertile subgroup (55.7 ± 24.1%) than in the controls (68.6 ± 27.8%). The rates of abnormal sperm chromatin integrity were significantly higher in the abortion (16.7 ± 7.7%) and infertile (16.3 ± 6.6%) subgroups, compared to the control group (13.0 ± 4.4%). Logistic regression analysis showed that the subsequent reproductive outcome of the 111 RSA patients was negatively correlated to the rates of abnormal sperm chromatin integrity. In conclusion, sperm chromatin integrity, sperm morphology, and sperm concentration were associated with future reproductive outcome of RSA patients. The sperm chromatin integrity was a significant predictor for future abortion and infertility.

But men are never responsible for miscarriage, perish the THOUGHT.

I mean – where are the STUDIES?!

https://pubmed.ncbi.nlm.nih.gov/21806662/

Cytochemical evaluation of sperm chromatin and DNA integrity in couples with unexplained recurrent spontaneous abortions

unexplained….. sigh, ok.

Our study showed that in the cases of RSA, slow motility had a significant reduction in comparison with controls and also spermatozoa of men from RSA group had less chromatin condensation and poorer DNA integrity than spermatozoa that obtained from fertile men with no history of RSA.

https://www.sciencedirect.com/science/article/abs/pii/S000293780133898X

Known for 20 years.

Human sperm deoxyribonucleic acid fragmentation by specific types of papillomavirus

Conclusion: Human papillomavirus type 16 and 31 deoxyribonucleic acid caused deoxyribonucleic acid breakages characteristic of apoptotic but not necrotic sperm.

CAUSED

The data suggest that these human papillomavirus types may adversely affect subsequent embryonic development after fertilization. Sperm deoxyribonucleic acid appears to resist human papillomavirus types 18, 33, and 6/11 or repairing mechanisms occurred. Although enhanced motility was found in human papillomavirus–exposed sperm, important velocity parameters were decreased, suggesting impaired sperm function.

-swimming in circles isn’t motility, really

damages your baby DNA, kills babies =/= harmless!

it’s a viral abortion, really

https://www.mdpi.com/2077-0383/10/4/717

Negative Impact of Elevated DNA Fragmentation and Human Papillomavirus (HPV) Presence in Sperm on the Outcome of Intra-Uterine Insemination (IUI)

i.e. no, you won’t just get IVF

We wanted to determine the sperm DNA fragmentation index (DFI) cutoff for clinical pregnancies in women receiving intra-uterine insemination (IUI) with this sperm and to assess the contribution of Human Papillomavirus (HPV) infection on sperm DNA damage and its impact on clinical pregnancies. Prospective non-interventional multi-center study with 161 infertile couples going through 209 cycles of IUI in hospital fertility centers in Flanders, Belgium. Measurement of DFI and HPV DNA with type specific quantitative PCRs (HPV 6, 11, 16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66 and 68) in sperm before its use in IUI. Clinical pregnancy (CP) rate was used as the outcome to analyze the impact on fertility outcome and to calculated the clinical cutoff value for DFI. A DFI criterion value of 26% was obtained by receiver operating characteristic (ROC) curve analysis. Couples with a male DFI > 26% had significantly less CPs than couples with DFI below 26% (OR 0.0326; 95% CI 0.0019 to 0.5400; p = 0.017). In sperm, HPV prevalence was 14.8%/IUI cycle. Sperm samples containing HPV had a significantly higher DFI compared to HPV negative sperm samples (29.8% vs. 20.9%; p = 0.011). When HPV-virions were present in sperm, no clinical pregnancies were observed. More than 1 in 5 of samples with normal semen parameters (17/78; 21.8%) had an elevated DFI or was HPV positive. Sperm DFI is a robust predictor of clinical pregnancies in women receiving IUI with this sperm. When DFI exceeds 26%, clinical pregnancies are less likely and in vitro fertilization techniques should be considered

When HPV-virions were present in sperm, no clinical pregnancies were observed.

but CLEARLY this is just my OPINION – misogynists reee-ing

https://www.sciencedirect.com/science/article/abs/pii/S0165037813000508

Sperm viral infection and male infertility: focus on HBV, HCV, HIV, HPV, HSV, HCMV, and AAV

Chronic viral infections can infect sperm and are considered a risk factor in male infertility. Recent studies have shown that the presence of HIV, HBV or HCV in semen impairs sperm parameters, DNA integrity, and in particular reduces forward motility. In contrast, very little is known about semen infection with human papillomaviruses (HPV), herpesviruses (HSV), cytomegalovirus (HCMV), and adeno-associated virus (AAV). At present, EU directives for the viral screening of couples undergoing assisted reproduction techniques require only the evaluation of HIV, HBV, and HCV.

-all trust the EU guys

However, growing evidence suggests that HPV, HSV, and HCMV might play a major role in male infertility and it has been demonstrated that HPV semen infection has a negative influence on sperm parameters, fertilization, and the abortion rate.

-somebody else look up herpes, I’m lazy

Besides the risk of horizontal or vertical transmission, the negative impact of any viral sperm infection on male reproductive function seems to be dramatic.

-Really, f-ing fascinating!

In addition, treatment with antiviral and antiretroviral therapies may further affect sperm parameters. In this review we attempted to focus on the interactions between defined sperm viral infections and their association with male fertility disorders. All viruses considered in this article have a potentially negative effect on male reproductive function and dangerous infections can be transmitted to partners and newborns. In light of this evidence, we suggest performing targeted sperm washing procedures for each sperm infection and to strongly consider screening male patients seeking fertility for HPV, HSV, and HCMV, both to avoid viral transmission and to improve assisted or even spontaneous fertility outcome

>male fertility disorders

k.

Oh, I’m not done yet.

https://www.cambridge.org/core/journals/epidemiology-and-infection/article/hpv-infection-in-semen-results-from-a-new-molecular-approach/B0B63D2A2760A03FCFF243F1DD5E9A7F

HPV infection in semen: results from a new molecular approach

Let’s get molecular.

Human papillomavirus (HPV) is the agent of the most common sexually transmitted diseases causing a variety of clinical manifestations ranging from warts to cancer. Oncogenic HPV infection is the major cause of cervical cancer and less frequently of penile cancers. Its presence in semen is widely known, but the effects on fertility are still controversial. – how? allergic to facts?

We developed a new approach to evaluate virus localisation in the different semen components. We analysed also the specific genotype localisation and viral DNA quantity by qPCR. Results show that HPV DNA can be identified in every fraction of semen: spermatozoa, somatic cells and seminal plasma. Different samples can contain the HPV DNA in different fractions and several HPV genotypes can be found in the same fraction. Additionally, different fractions may contain multiple HPV genotypes in different relative quantity. We analysed the wholeness of HPV DNA in sperm cells by qPCR. In one sample more than half of viral genomes were defective, suggesting a possible recombination event. The new method allows to easily distinguish different sperm infections and to observe the possible effects on semen. The data support the proposed role of HPV in decreased fertility and prompt new possible consequences of the infection in semen.

>HPV DNA can be identified in every fraction of semen: spermatozoa, somatic cells and seminal plasma

If you’re wondering why your nation is infertile, look in the mirror. Mutant sperm.

Your superpower is probably autism.

Sexual studies dump

This should keep you all busy for a while.

https://pubmed.ncbi.nlm.nih.gov/26332467/

Women’s Preferences for Penis Size: A New Research Method Using Selection among 3D Models

Women’s preferences for penis size may affect men’s comfort with their own bodies and may have implications for sexual health. Studies of women’s penis size preferences typically have relied on their abstract ratings or selecting amongst 2D, flaccid images. This study used haptic stimuli to allow assessment of women’s size recall accuracy for the first time, as well as examine their preferences for erect penis sizes in different relationship contexts. Women (N = 75) selected amongst 33, 3D models. Women recalled model size accurately using this method, although they made more errors with respect to penis length than circumference. Women preferred a penis of slightly larger circumference and length for one-time (length = 6.4 inches/16.3 cm, circumference = 5.0 inches/12.7 cm) versus long-term (length = 6.3 inches/16.0 cm, circumference = 4.8 inches/12.2 cm) sexual partners. These first estimates of erect penis size preferences using 3D models suggest women accurately recall size and prefer penises only slightly larger than average.

but different races have sexually selected different averages, even by nation? So the mean IS the ideal.

https://pubmed.ncbi.nlm.nih.gov/19139986/

The association between penis size and sexual health among men who have sex with men

Larger penis size has been equated with a symbol of power, stamina, masculinity, and social status. Yet, there has been little research among men who have sex with men assessing the association between penis size and social-sexual health. Survey data from a diverse sample of 1,065 men who have sex with men were used to explore the association between perceived penis size and a variety of psychosocial outcomes. Seven percent of men felt their penis was “below average,” 53.9% “average,” and 35.5% “above average.” Penis size was positively related to satisfaction with size and inversely related to lying about penis size (all ps < .01). Size was unrelated to condom use, frequency of sex partners, HIV status, or recent diagnoses of HBV, HCV, gonorrhea/Chlamydia/urinary tract infections, and syphilis. Men with above average penises were more likely to report HPV and HSV-2 (Fisher’s exact p <or= .05). Men with below average penises were significantly more likely to identify as “bottoms” (anal receptive) and men with above average penises were significantly more likely to identify as “tops” (anal insertive). Finally, men with below average penises fared significantly worse than other men on three measures of psychosocial adjustment. Though most men felt their penis size was average, many fell outside this “norm.” The disproportionate number of viral skin-to-skin STIs (HSV-2 and HPV) suggest size may play a role in condom slippage/breakage. Further, size played a significant role in sexual positioning and psychosocial adjustment. These data highlight the need to better understand the real individual-level consequences of living in a penis-centered society.

so men with big wangs, at least the ‘gay’ ones, are rendering themselves infertile or birth defect risks by sharing it around. Y NO str8 studies?

https://pubmed.ncbi.nlm.nih.gov/32201145/

Female Orgasm and Overall Sexual Function and Habits: A Descriptive Study of a Cohort of U.S. Women

Results: FSFI scores, which were calculated for the 230 women who reported having had a steady male sex partner in the preceding 6 months, showed that 41% of the 230 women were at risk for female sexual dysfunction (a cutoff less than 26.55) and 21% were dissatisfied with their overall sexual life. Almost 90% of the overall cohort reported good emotional contact with their partner, that their partner was willing to have sex, satisfaction with the partner’s penis size (wherever applicable), and good erectile function and ejaculatory control of their partner (wherever applicable). 81% of the overall cohort claimed to be sexually active. Around 70% (70-72) did reach orgasm frequently, but around 10% never did so. Vaginal intercourse was reported by 62% of the overall cohort as the best trigger of orgasm, followed by external stimulation from the partner (48%) or themselves (37%). External stimulation was reported to be the fastest trigger to orgasm.

Clinical implications: The knowledge on how women reach orgasm and how it is related to the partners’ willingness to have sex and other factors can be incorporated in the clinical work.

Strengths & limitations: The use of a validated questionnaire and the relative large number of participants are strengths of the study. Limitations are the cross-sectional design, the lack of a sexual distress measure, and a possible selection bias.

Conclusion: Most women in the overall cohort were satisfied overall with their sexual life and partner-related factors, even though 41% (of those who cited a steady sex male partner) were at risk for female sexual dysfunction. Most women did reach orgasm through different kinds of stimulation. Correlation was good between preferred and performed sexual activities and positions. Shaeer O, Skakke D, Giraldi A, et al. Female Orgasm and Overall Sexual Function and Habits: A Descriptive Study of a Cohort of U.S. Women. J Sex Med 2020;17:1133-1143.

I bet the inorgasmic had ‘cut’ men, who produce fewer orgasms in all women in studies.

https://pubmed.ncbi.nlm.nih.gov/22729523/

Impact of penile size on male sexual function and role of penile augmentation surgery

Penile augmentation is an ongoing debate. Emerging evidence proves a relationship between dissatisfaction with penile size and sexual dysfunction. Despite a widespread belief of the value of penile size, and the prevalent complaint of a “small penis,” penile augmentation still stands short of addressing the demand. This report highlights the studies added to medical literature on penile augmentation in 2011-2012, including data on normal penile dimensions and the expected dimensions for a normal person, determination of the prevalence of the dissatisfaction with penile size, its effect on erectile function, female partner’s opinion of the value of penile size, as well as further experience with augmentation techniques.

It’s mental, they need therapy. Also, I see the joke.

https://pubmed.ncbi.nlm.nih.gov/26639576/

Why Are Men Satisfied or Dissatisfied with Penile Implants? A Mixed Method Study on Satisfaction with Penile Prosthesis Implantation

The issue is mental?

Content analysis revealed four main themes for men’s satisfaction with the PPI: (i) psychological factors were reported 54 times (n = 54) and included positive emotions, self-esteem, confidence, enhancement of male identity, major live change, and self-image;

– mental

(ii) improvement of sexual function was reported 54 times (n = 54) and referred to achievement of vaginal penetration, increase of sexual desire, sexual satisfaction, penis size, and improvement of erectile function;

– satisfaction is a female metric? ED is mental?

(iii) relationship factors were reported 11 times (n = 11) and referred to relationship improvement and the possibility of giving pleasure to the partner; and (iv) improvement in urinary function (n = 3).

– not possible with implants, all surgeries produce numbness and see above study

https://pubmed.ncbi.nlm.nih.gov/18649002/

Association between human papillomavirus in men and their sexual partners and uterine cervical intraepithelial neoplasia

“The sample size employed was not large enough to be able to determine any differences between both study groups.” aka useless study

Stop linking to bullshit. Slutty men are just as bad for society as the women. Blame shifting is blue pill.

https://pubmed.ncbi.nlm.nih.gov/33793040/

A preliminary investigation of a novel method to manipulate penis length to measure female sexual satisfaction: a single case experimental design

Results: On average reducing the depth of penetration made a statistically significant 18% reduction of overall sexual pleasure with an average 15% reduction in length of the penis. The longer the erect penis, the less likely the rings had an impact on sexual pleasure. There was however a range of individual responses with a minority of women reporting that reducing the depth of penetration was more pleasurable on some occasions.

– the G spot?

Conclusions: Size may matter in women in a healthy stable relationship when there is penile shortening. Because of the small number of couples and men with an apparently long penises, our results are preliminary, and we welcome replication in a larger sample with a more diverse range of penile lengths. Our results should not be misinterpreted as meaning that increasing penile length will increase sexual pleasure in women.

shortening with age, and no, supplements don’t help

unless you want earlier mortality (T-levels)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715194/

Non-pharmacological and non-surgical strategies to promote sexual recovery for men with erectile dysfunction

-quit the porn? sigh

the tobacco-lung cancer connection of this generation
history will know you as a bunch of wankers

Erectile dysfunction (ED), the most commonly reported sexual problem for men,

in dick-mutilated, porn-addled America? also Israel?

reduces the quality of life for both patients and their partners. Even when physiologically effective, long-term adherence to ED treatments is poor.

– it’s behavioral…

We review here the implication of having patients’ partners involved in ED treatment, starting with treatment selection. We suggest that having partners engaged from the outset may promote an erotic association of the treatment with the partner, i.e., conceptually linking the aid to the sexual pleasure that the partner provides.

– quit ‘supernormal stimuli’ aka lechery, your dopamine is fried?

We hypothesize that this erotic association should enhance the sexual aid’s effectiveness and might potentially help improve long-term adherence. The primary focus of this review, though, is non-pharmacological and non-surgical options for maintaining sexual activity for men with ED. Though not ED treatments per se, anecdotal data suggest that these options may be effective for some patients and their partners in regaining a satisfying sex life. The aids discussed include external penile prostheses, penile sleeves, and penile support devices.

-easier just to give up the sexual visual crack, surely?

These devices can allow men to participate in penetrative sexual intercourse despite moderate to severe ED.

-aging happens, it’s natural selection

External penile prostheses can be personalized so they match in size and shape a man’s normal full erection.

– that is sad

Penile sleeves can similarly be customized with a lumen that fits best a patient’s penis for optimal tactile stimulation.

– so they’re fucking a toy? …. not the man…..

We review how multi-sensory integration can enhance sexual arousal for men who use such devices, allowing them to achieve orgasm despite intractable ED.

-it’s a silicon sock

Patients are not always advised within ED clinics about these options nor why and how they can facilitate non-erection dependent sexual recovery. Clinicians need to be aware of these devices and their positive attributes, so they can objectively counsel and encourage couples to explore their use as an alternative to more invasive treatments. The most commonly promoted non-medical ED aid offered to patients is the vacuum erection device. We discuss how erections achieved with the vacuum erection device have a “hinge effect”, that is an underappreciated barrier to the effectiveness of the erection. With a hinged erection, the penis points downward rather than upward. We show how the normal kinematics of the penis during coitus is not strictly linear (i.e., not uniaxial; not just in-and-out), and is impeded by hinging. Positional adjustment, such as the receptive partner being on top, may help overcome this problem for some couples. Lastly, we suggest that, in the case where ED can be anticipated from a pending medical treatment, such as a prostatectomy, pre-habilitative approaches may potentially improve adherence to sexual aid use in the long-term. In conclusion, non-pharmacological and non-surgical options for sexual recovery are available. Scientific studies on the effectiveness of these interventions in restoring satisfying sex are warranted.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5039517/

Is Internet Pornography Causing Sexual Dysfunctions? A Review with Clinical Reports

Traditional factors that once explained men’s sexual difficulties appear insufficient to account for the sharp rise in erectile dysfunction, delayed ejaculation, decreased sexual satisfaction, and diminished libido during partnered sex in men under 40.

-no shit

This review (1) considers data from multiple domains, e.g., clinical, biological (addiction/urology), psychological (sexual conditioning), sociological; and (2) presents a series of clinical reports, all with the aim of proposing a possible direction for future research of this phenomenon. Alterations to the brain’s motivational system are explored as a possible etiology underlying pornography-related sexual dysfunctions. This review also considers evidence that Internet pornography’s unique properties (limitless novelty, potential for easy escalation to more extreme material, video format, etc.) may be potent enough to condition sexual arousal to aspects of Internet pornography use that do not readily transition to real-life partners, such that sex with desired partners may not register as meeting expectations and arousal declines. Clinical reports suggest that terminating Internet pornography use is sometimes sufficient to reverse negative effects, underscoring the need for extensive investigation using methodologies that have subjects remove the variable of Internet pornography use. In the interim, a simple diagnostic protocol for assessing patients with porn-induced sexual dysfunction is put forth.

– it’s a supernormal stimulus designed to make you impotent, it’s a delusion that alters the brain

Based on the findings of historical studies cited earlier, older men would be expected to have far higher ED rates than the negligible rates of younger men [2,7]. However, in just a decade, things changed radically. The 2001–2002 rates for older men 40–80 were about 13% in Europe [5]. By 2011, ED rates in young Europeans, 18–40, ranged from 14%–28% [6].

duh, porn addicts also look older, do that study

Finally, another 2015 study on men (mean age approximately 36), reported that ED accompanied by a low desire for partnered sex is now a common observation in clinical practice among men seeking help for their excessive sexual behavior, who frequently “use pornography and masturbate” [15].

aimed at Europeans, squarely

make them hypersexual, extreme r, and re-productively useless

The sole qualification for being a masculine man is having a functioning dick but they cuck for the industry ruining their lives.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679165/

The Potential Associations of Pornography Use with Sexual Dysfunctions: An Integrative Literature Review of Observational Studies

This paper reviews the associations between pornography use and sexual dysfunction based on evidence from observational studies. The existing data in this regard mostly derive from cross-sectional investigations and case reports. There is little if no evidence that pornography use may induce delayed ejaculation and erectile dysfunction, although longitudinal studies that control for confounding variables are required for a full assessment.

– decades later, we’ll be dead demographically…

The associations between pornography use and sexual desire may differ between women and men although the existing data is contradictory and causal relationships cannot be established. The strongest evidence is available for the relation of pornography use with decreased sexual satisfaction, although the results of prospective studies are inconsistent. The paper outlines future research prospects beneficial in understanding the nature of associations between pornography use and sexual dysfunctions in men and women.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6352245/

Online Porn Addiction: What We Know and What We Don’t—A Systematic Review

In the last few years, there has been a wave of articles related to behavioral addictions; some of them have a focus on online pornography addiction. However, despite all efforts, we are still unable to profile when engaging in this behavior becomes pathological.

– publishing bias

Common problems include: sample bias, the search for diagnostic instrumentals, opposing approximations to the matter, and the fact that this entity may be encompassed inside a greater pathology (i.e., sex addiction) that may present itself with very diverse symptomatology.

= excuses so you don’t get later sued

Behavioral addictions form a largely unexplored field of study, and usually exhibit a problematic consumption model: loss of control, impairment, and risky use. Hypersexual disorder fits this model and may be composed of several sexual behaviors, like problematic use of online pornography (POPU). Online pornography use is on the rise, with a potential for addiction considering the “triple A” influence (accessibility, affordability, anonymity). This problematic use might have adverse effects in sexual development and sexual functioning, especially among the young population. We aim to gather existing knowledge on problematic online pornography use as a pathological entity. Here we try to summarize what we know about this entity and outline some areas worthy of further research.

dupe

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874247/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4994844/

brain differences in the slutty

Risky sexual behaviors typically occur when a person is sexually motivated by potent, sexual reward cues. Yet, individual differences in sensitivity to sexual cues have not been examined with respect to sexual risk behaviors. A greater responsiveness to sexual cues might provide greater motivation for a person to act sexually; a lower responsiveness to sexual cues might lead a person to seek more intense, novel, possibly risky, sexual acts. In this study, event-related potentials were recorded in 64 men and women while they viewed a series of emotional, including explicit sexual, photographs. The motivational salience of the sexual cues was varied by including more and less explicit sexual images. Indeed, the more explicit sexual stimuli resulted in enhanced late positive potentials (LPP) relative to the less explicit sexual images. Participants with fewer sexual intercourse partners in the last year had reduced LPP amplitude to the less explicit sexual images than the more explicit sexual images, whereas participants with more partners responded similarly to the more and less explicit sexual images. This pattern of results is consistent with a greater responsivity model. Those who engage in more sexual behaviors consistent with risk are also more responsive to less explicit sexual cues.

– it’s r/K

trans. r-types seem to have dulled sexual perception (abnormal) so over-estimate opportunity in compensation

Reminder:

Mother Nature WILL have her pound of flesh.

The buried risk factor in colon cancer

I hate the need for gross posts, the syphilis rates in Asia one was bad enough.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917541/
“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?

HOW?

“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) [11], 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.

11 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729501/

There’s a known colon cancer connection to Type 2 diabetes.
https://www.nature.com/articles/s41598-020-71456-2
So it’s probably also preservatives. Just throwing that in.

Like nitrates used on cheap meats, not the actual meat. Ban nitrates. Really.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856114/
“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.”

K.

“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″

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4745930/

https://www.hindawi.com/journals/grp/2016/7896716/
Ban Tinder.
“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.

https://clincancerres.aacrjournals.org/content/11/8/2862
“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.

Dat p-value.

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.

May?

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.”

https://www.ncbi.nlm.nih.gov/pubmed/20528894

HPV 6 and 11 Finland
https://pubmed.ncbi.nlm.nih.gov/19408160/
“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.”

https://pubmed.ncbi.nlm.nih.gov/19939209/
16, 18 Finland

https://www.webmd.com/sexual-conditions/hpv-genital-warts/news/20191120/hpv-blamed-for-rising-rates-of-anal-cancer
Is that new?

Young people at higher risk, why?
https://www.cancer.org/latest-news/study-finds-sharp-rise-in-colon-cancer-and-rectal-cancer-rates-among-young-adults.html
“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?

https://onlinelibrary.wiley.com/doi/abs/10.1111/codi.12257
“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).

Conclusion
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

Explaining Adultery, parts of the Bible, disease etc.

No one has typed out an explanation of this, to my knowledge. Sure there are linguistic essays but… still.

Here’s the logical explanation of certain things. Ending with collaborating science.

Adultery is a sin because it’s a pollution of bloodlines, that’s why it’s called that but the sexual action or compulsion is already covered under the coveting commandment. Fornication between two singles, while a sin, is not polluting the bloodlines of the marital couple. It doesn’t defile the marital bed, as the Bible puts it (Hebrews 13:4). It’s “and” adulterers, they’re discrete categories. The adultery involving one married party may produce a child with defects (especially with the effect of STDs from sleeping around, which they’d bring back to the marital bed, onto their own children – and might kill them), or the child maritally or the one “extra-maritally” may eventually marry their own part-sibling and then produce defect. All the sexual prohibitions are henceforth founded in an avoidance of bloodline corruption.

They’re not being ‘lame’ and killing your ‘buzz’ man, it’s babymaking. Don’t make broken babies!

The sterile view of reproduction is like a Marxist’s view of labour – delusional.

re Deut 23:2 and the mistranslation in later editions:
Legitimacy is based on bloodlines more than marital status but under the parent-approved marriage model the former suitability led to the latter ceremony. They’d have veto power on funding the wedding and allowance of inheriting anything should the child try to brattishly insist on an adulterous match. Banishment (disowning) is the parental right should the child “dishonour” (commandment) their parent’s standards. A bastard didn’t refer to unmarried parents back then but moreso what we’d call politely a hybrid, Darwin a mongrel. Later editions mistranslated the concept of ‘bastard’ for ((reasons)). Logically, unmarried parents could feasibly marry at any point in the next 18 years and 9 months, the insult cannot be based on something so easily remedied. Instead it’s “in the blood”, it’s about the “seed”, it’s genetic. It’s the existence of the kid itself which is the affront, the offense to the holy, and that’s why ‘bastard’ is levied at the child – not the parents! They brought shame on their pre-existing family (bloodline) by virtue of their dishonourable existence, of a blemish. The OT often condemns men who mate with ‘foreign women’, the archetype of demonic seductress. That’s why usually understanding God (who forgives individuals) forbade the child to enter the church, holy ground, sacred temples, unto the 10th generation, because it was a perversion of his creation and divine, famous plan for separation of peoples; its existence was Satanic, a testament to playing God. Its existence was an insult to God, directly, it was an ABOMINATION.
Now we have the medical stats to back this up from the individualist perspective, from mental problems to organ death from child cancer, nobody mentions it…?
Why? Why not? Who’s behind that cultural ignorance?
https://www.kingjamesbibleonline.org/Bible-Verses-About-Race-Mixing/
The sins of the father onto the child i.e. you produce an unnatural thing, it suffers unnaturally.

Period blood isn’t the only unclean thing: https://bible.knowing-jesus.com/topics/Semen

So bad marital discernment (selection) relates to the reprobate mind. Selection is the ONE job of men looking for a wife. The Bible gives plenty of advice on men seeking a wife, what to look for.

Cast not ye pearls among swine, neither spill your seed, it’s very simple conceptually. Don’t waste a breeding opportunity with a bad match or selfishness. You want societal shame back? Start with masculine self-control (Lev 22:4) because you’ll be healthier for it. This isn’t just spiritually good but physically too. Like don’t stick your dick in crazy. At least a woman’s period isn’t alive for all the stigma, there’s nothing to kill. God designed women to self-clean the baby oven, there’s no shame in it. Poor analogy to the modern Onans. You have a specific story about sexual continence, sexual hygiene, call it whatever, it’s being a man.
https://www.openbible.info/topics/spilling_your_seed
https://biblereasons.com/evil-women-and-bad-wives/

If you marry badly, that doesn’t absolve you of responsibility for her sins. You’re the man, you’re responsible, be she some Polish whore (they’re mostly marrying Arabs and Japs) or an ABG/LBFM thot (mostly autists).

Prov 22:14  The mouth of an adulterous woman is a deep pit; a man who is under the LORD’s wrath falls into it.

I’m picturing the conceited weebs who start lecturing the rest of us (projection in ego defense of their error) on how white people in the West should become more Asian. You eat the bugs first, bug boy. Such cucking is, as you can see, Biblically predicted as God’s wrath upon the reprobate mind. Insecurity breeds insecurity, misery loves company, fuck-ups want you to copy them.

If everyone fails, the sexual Marxists reason, then nobody fails!

They want no holy (wholesome, pure) group to be able to compare poorly to.

deceit, malice, envy….

https://biblehub.com/romans/1-28.htm

why be envious of people you claim to be doing better than? Why talk about the West at all after you left? Why are you obsessing over it, if it’s inferior culturally? Racial deserters should STFU and stay in their jungle. We don’t want to hear from you, stay gone. There’s a rise in snarky gammas online giving weeb “commentary” that sounds like CCP propaganda. It’s anti-white, sod off. Why should we care what you think? You ran away from the problems, drop them. It’s like a Boomer who retired to France complaining about UK immigration. No Susan. You don’t get to.

Stats show up their forum anecdotes as fantasies. They wanted mixed bloodlines, right, they’ll be happy with the black grandkids I presume (since mixed dates other mixed, statistically).

In Deut 7:3 even the unequal yoking between the races is forbidden, before the prospect of children is mentioned.
https://www.biblegateway.com/passage/?search=Deuteronomy%207&version=KJV
Cultures are intended to be sovereign. Interconnection is weakness.
7:4 says how mixed marriages are insults because of cultural cucking i.e. your child will adopt foreign ways.
Learn to tell your kids no, Boomer. JUST SAY NO.

Otherwise, unchecked, they “invent new forms of evil” like the conceited weebs that are becoming the new Fedora Boy.

insolent, arrogant, boastful….

It’s like the Gap Year story that never ends.

NEVER.

And we’re all expected to listen to it.

One word: why?

Do evil, fine, don’t be boastful though. I shouldn’t be socially expected to listen to some woman’s sob story about how she married a Muslim either. Tough tits, bitch. You knew they was a snake. You signed up for shit. It’s like the thots joining Islamic State, I no longer feel loyal to you either. I owe you nothing.

Stop coddling them. They’re grown men rationalizing objectively, scientifically shit marriages.

And encouraging the same multicultural evil to other men, that’s gender treason. You shouldn’t enable it.

There were 10 basic rules. Multicultural tradlarpers moved, so please stop talking to us like you’re a Westerner. You’re an outsider now, ree.

https://biblehub.com/romans/1-32.htm

Although they know God’s righteous decree that those who do such things are worthy of death,they not only continue to do these things,but also approve of those who practice them.

Worthy of death, how would God manifest that in case of adulterous children?

Suicidal temperament, perhaps?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1448064/

Cancer risks?

https://pubmed.ncbi.nlm.nih.gov/25792752/

Our results confirm that there are ethnic and racial differences in the incidence of childhood leukaemia. These differences indicate that some genetic and/or environmental/cultural factors are involved in aetiology of childhood leukaemia.

American diet means you should compare to European whites for accuracy. Twinkies are thots, not food groups.

The highest risk of ALL was observed for children with a combination of Hispanic ethnicity and White race compared with non-Hispanic whites (OR=1.27, 95% CI 1.12 to 1.44).

They actually leave out mixed of most studies e.g. https://pubmed.ncbi.nlm.nih.gov/14559954/

unless they can rig the numbers from the small group because it’s so bad in outcome. It’s impossible to find prevalence data, why?

It’s true in other species scientifically, outbreeding depression is unholy, it defiles the wholesome in God’s eye. That invites wrath.

https://pubmed.ncbi.nlm.nih.gov/10762398/

https://academic.oup.com/jhered/article/96/2/114/2187513

https://pubmed.ncbi.nlm.nih.gov/12144669/

Mixing stunts growth, even in plants. Sure, you might have kids but great-grandkids won’t happen.

So what was the point?

https://pubmed.ncbi.nlm.nih.gov/15487997/

https://pubmed.ncbi.nlm.nih.gov/14983018/

https://pubmed.ncbi.nlm.nih.gov/15807418/

https://pubmed.ncbi.nlm.nih.gov/9375532/

https://pubmed.ncbi.nlm.nih.gov/4066391/

Deny the lies of the spiteful mutants, anti-natalists aren’t so toxic to the zero sum of Darwinian competition. To actively encourage our genocide is evil.

Funny that the cuckservatives slagging off the Boomers want a free pass to act just like them despite decades of data now. That didn’t exist for them. You’re living in the experiment.
And yes, the Boomers should’ve been disowned by their parents for marrying wrong or too often.

They’ll deport, sorry “return” tortoises for their own good – but not humans.

https://www.newscientist.com/article/mg19426071.300-galapagos-tortoises-untangling-the-evolutionary-threads.html

The spiteful mutants of the Boomer gen became worse in the spiteful mutants of Gen Y and Z – but nobody is condemning them.

Science and Bible agree, how much do you need?

I heard a theory the trash segment of Boomers should’ve been picked off by war like Vietnam and the draft dodging is the main cause of our dysgenics. Possible and funny.

So how to know the weeb boys abroad are lying?

Weeb offspring and mental problems:

https://www.eurekalert.org/pub_releases/2008-08/uoc–baa081108.php

A new study of Chinese-Caucasian, Filipino-Caucasian, Japanese-Caucasian and Vietnamese-Caucasian individuals concludes that biracial Asian Americans are twice as likely as monoracial Asian Americans to be diagnosed with a psychological disorder.

A+ parenting.

Zane and his co-investigator, UC Davis psychology graduate student Lauren Berger, found that 34 percent of biracial individuals in a national survey had been diagnosed with a psychological disorder, such as anxiety, depression or substance abuse, versus 17 percent of monoracial individuals. The higher rate held up even after the researchers controlled for differences between the groups in age, gender and life stress, among other factors.

1/3. Over a THIRD of them are literally mentally diseased at the intensity to diagnose.

The study included information from 125 biracial Asian Americans from across the U.S., including 55 Filipino-Caucasians, 33 Chinese-Caucasians, 23 Japanese-Caucasians and 14 Vietnamese-Caucasians.

Stop listening to spiteful mutants.

Nobody’s jealous, they’re clinically evil. Shun the reprobate mind.

High diversity, low trust society: https://web.archive.org/web/20061013041712/http://www.ft.com/cms/s/c4ac4a74-570f-11db-9110-0000779e2340.html

deport the whores

nb. The edgy anti-natal rhetoric worked on the Boomers first, ask the dead half of Gen X. However, there’s more than one way to skin a cat and clearly more than one way to commit genetic suicide.

The womb is a very sophisticated form of printer. It prints people. That’s why women hate being conflated for one, it’s an appliance. Don’t defile the womb of your people, that’s treason. Do not corrupt the seed.

Plato’s natural slaves, do not follow. Degenerates are compulsive liars e.g.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3203037/

https://sti.bmj.com/content/87/Suppl_2/ii14

Syphilis infection in sex workers ranges from 8.8–9.5% in the Yunnan province to 8% in Guangdong to 3.5% in Beijing (Chen XS, personal communication, 2010).

https://academic.oup.com/femspd/article/24/4/431/503360

High levels of infection in these groups are found in most sub-Saharan African and South-East Asian countries. There is a high rate of concurrent infection for HIV and other well known STDs in patients. Rates as high as 70% of HIV infection are found in African patients with STD, whereas the rates are reaching 15–20% in patients with STD in Thailand [9,10].

Ting Tong has HIV. 1 in 5, roll the die to die. Is it really cheaper to live there with pozz med bills?

If you wanna larp as a gay guy, at least do fun things with your prostate.

If you get her a green card?

https://hyphenmagazine.com/blog/2010/05/study-finds-disturbing-std-rates-among-asian-americans

Over the course the study, Hahm unmasked some myths common about Asian Americans. She said, “There’s a perception that Asian Americans in particular aren’t practicing sexually risky behaviors.  But we found that Asian American young women are at risk of high STDs.  For instance, Asian American women had a higher prevalence of STDs than White women in both 1995 (10.4% vs. 7.7) and 2001 (13.5% vs. 8.3%).  The incidence of STDs (not diagnosed with STDs in 1995, but developed STIs in 2001) among Asian American women was also higher than that of White women.” Moreover, the power dynamic between genders became immediately clear.   Asian American women were four times more likely to have a STD than their male counterparts. “This was shocking,” said Hahm, “It was so much higher than the males.” Accounting for the gender disparity, Hahm suggested that…“Asian and Pacific Islander women also have broader interracial dating patterns than Asian American men. This might explain why these women are exposed to higher rates of STDs.”

when you mix, expect an itch

I think these findings definitely go against some prior conceptions about Asian Americans and sexually transmitted diseases. The 4:1 ratio of STDs among Asian American women to men is astounding. To see what this means, I looked up some global data of STD rates around the world, broken down by gender. In East Asia, and on every other continent, women have slightly higher STD rates than men, however nothing comes remotely close to the 4:1 ratio among Asian Americans.

It’s unclear what the study means by “power dynamic,” whether it means sexual power/demand, or power within the culture. One can speculate on a wide variety of reasons for why the STD rates are the way they are. I’ll refrain from doing so, but nevertheless I thought it was noteworthy to bring up, as a point of discussion. How does this strike you?

it means they culturally celebrate and enable whores – like the childbearing geisha

Trust no thot nor weeb.

Video: UK disease vectors and plague

Reminder: applies to all infections, not just sexually exclusive ones.

The prohibition on sodomy also applied to sodomy with women for the same reasons. It’s the same exact act, normalised in Jewish entertainment.

Sexually, it’s always men who are the main vectors of any disease (for many reasons, including going out more, washing hands less). Until literally a few years ago, biologists assumed the male urethra was always clean (immunoprivileged, like the eyes) – until they actually checked it... Turns out no vital pipe is clean, if you’re being a slut (sorry, “sexually active”). Men are the main vectors of any condition, and with HIV, ebola, this obvious “corona” (really pneumonic plague*) virus going round, knowing who’d be the likeliest carrier socially could save your life.

R-types are known for being happy Typhoid Marys, it isn’t just bug chasing “gift givers”, they can consciously pass on lesser conditions from spite (usually homoerotic, so other men are largely at risk). Even with a simple stomach bug or a norovirus, they’ll have an impulse to “meet up with old friends” so delay those ‘invitations’ past the incubation window and they’ll suddenly lose interest.

(Borderline and sociopathic women also do this, but usually it’s men).

Making people sick gives them a thrill of power over your body. And it’s mostly legal (with certain STD exceptions, that are ABH here up to GBH dependent).

*The Chinese gov keeps writing COD as ‘pneumonia’ because it isn’t corona. It’s plague.

The Black Death came from Asia too. Do your research. This is why they refuse to share DNA with Australia – it isn’t corona. Just a theory, but it’s the only thing that fits their paranoia. COD docs are legally binding.

They never did find a cure for plague, it’s almost Biblical.

B-b-b-but muh appeal to authority?! – some moron

K.

https://www.nature.com/articles/s41541-020-0156-y

A few days ago:

Yersinia pestis, the cause of plague, could be weaponized.

Unfortunately, development of new vaccines is limited by lack of correlates of protection.

aka unlike other diseases, they can’t pump out a plague vaccine on the pipeline

We used pre- and post-vaccination sera and peripheral blood mononuclear cells from a flagellin adjuvanted F1/V vaccine trial to evaluate for protective markers. Here, we report for the first time in humans that inverse caspase-3 levels, which are measures of protective antibody, significantly increased by 29% and 75% on days 14 and 28 post-second vaccination, respectively. In addition, there were significant increases in T-cell responses on day 28 post-second vaccination. The strongest positive and negative correlations between protective antibody levels and gene expression signatures were identified for IFNG and ENSG00000225107 genes, respectively. Flagellin/F1/V subunit vaccine induced macrophage-protective antibody and significant CD4+ T-cell responses. Several genes associated with these responses were identified that could serve as potential correlates of protection.

Paper for compulsory vaccination… just like Spanish Flu.
Fun fact: Most of those who died were vaccinated.

But wait, why would you need a vaccine for a bacterial infection?

Don’t ask questions citizen, just take the injection.

nytimes.com/2019/11/13/world/asia/plague-china-pneumonic.html

Pneumonic Plague Is Diagnosed in China

Memoryhole absolut.

EARLY NOVEMBER, 2019.

It turns out, I have been researching this stuff for my health.

The Twenties are gonna be funny.

What would happen to their economy if we knew the truth?

Even if it were coronavirus:

https://www.nejm.org/doi/10.1056/NEJMc2001468

The novel coronavirus (2019-nCoV) from Wuhan is currently causing concern in the medical community as the virus is spreading around the world.1 Since its identification in late December 2019, the number of cases from China that have been imported into other countries is on the rise, and the epidemiologic picture is changing on a daily basis. We are reporting a case of 2019-nCoV infection acquired outside of Asia in which transmission appears to have occurred during the incubation period in the index patient.

Asymptomatic, Typhoid Mary types.

Late December 2019.

You know what spreads great during the invisible stage? Plague. Just sayin’.

What’s more likely? A disease magically changes on an almost daily basis* – or the Chicoms are lying?

*According to the NEW ENGLAND JOURNAL OF MEDICINE, redditfags! They’re throwing shade in academese.

I hate being smarter than everyone but I waited for them to release the truth, sportingly, and they didn’t so screw you, China.

 

[#~*intermission*~#]

 

If AA wants a wild ride, check homosexual studies of paraphilia if you can find them – inc. sadism (especially rape, interest in actual rape), cross-dressing, pedophilia (attraction to minors) and bestiality. When surveyed, interest in death and necrophilia is also reported but it’s hard to find that stuff online. Most serial killers are homosexual. (and also circumcised)

HPV contaminating gyms, doctor’s tables and virgins

Figured I’d linked this. Not clickbait.

What happens when you let the sluts run rampant.

https://theluxuryspot.com/new-hpv-warnings-you-can-get-it-at-the-gym/
https://www.thehealthsciencejournal.com/germs-in-the-gym/
https://www.womenshealthmag.com/health/a19929167/hpv-without-having-sex/

School gyms too, health hazard. It can even be on the floor.

Study link from women’s health:

http://www.publish.csiro.au/nid/164.htm

“Researchers analyzed 51 studies on HPV transmission, and they noticed that the virus was found in the genital tracts of 51 percent of female virgins. This left them asking: If not through sex, how are people contracting it?”

VIRUS.

Plus the speculums they can’t actually clean?

“The second possibility makes us even more squeamish. You might be able pick up HPV by coming into contact with an infected surface at the doctor’s office or in public places like the gym. If the examining table or bike seat you sit down on in your booty shorts hasn’t been properly cleaned, you could be at risk.”

Why did people wear so many layers of clothing in public?

History was so weird. And gloves! How absurd!

Who wears gloves, the Queen? She isn’t long-lived, is she?

I’m just picturing the HPV strains of Hollywood and its forced kissing, on and off screen.

Men who visit hookers are a huge disease risk

https://www.pinknews.co.uk/2019/01/06/anti-gay-pastor-fired-prostitutes/
But they think THEIR degeneracy is normal.

I love especially how he criticizes homosexuals when you know he’s probably the anal guy.

Literally the same behaviour, same disease risk.

If you practice sodomy, you are a sodomite.

This is not hard to understand.

The sodomy problem is only half gay.

It’s also half straight.

Why scapegoat? It won’t lower your disease risk.

You’re not morally superior to sodomites if you ARE ONE.

These guys don’t realize nobody is impressed, they’re actually disgusted. That’s what you do if you’re desperate in prison, not popular. Porn stars almost always get HIV eventually from it, what a role model.
Plus they’re functionally gay, if not identifying with it.

The delusion is STRONG.

“I can act like one but don’t judge me like one” er no?

Nobody wants to hear about how you love coating your penis in fecal microbes.
Many men don’t wash their hands. We have every right to be disgusted.

Keep that shit to yourself.

Little known fact, mutilated men prefer anal because the circumcision ripped out many of their nerves. No, the sensation isn’t better – that’s how intact men feel normally. Men circumcised as adults are horrified in studies at what it does to their sexual pleasure, that’s why they don’t wait to perform the surgery – no sane man would want it!
Update: I posted about this fact here since the data wasn’t posted here before:
https://disenchantedscholar.wordpress.com/2019/01/07/circumcision-risky-behaviours-studies/

Porn is trying to kill you. The saliva thing makes it worse.
http://www.publichealth.pitt.edu/Portals/0/IDM/MPH%20JC%20Articles/Saliva%20and%20Gonorrhea.pdf?ver=2016-04-11-084337-140
http://www.catie.ca/en/pif/fall-2014/getting-bottom-it-anal-sex-rectal-fluid-and-hiv-transmission
Trannies are a health risk because of anal. Nothing else.
https://bmcpublichealth.biomedcentral.com/articles/10.1186/1471-2458-13-1108
Women are now catching HIV like men – thanks to anal propaganda in porn.

Click to access EF08L44.pdf

Act like a gay guy, catch the same diseases.

Because bisexuals exist – guess which orifice they prefer?

Protective disgust

https://phys.org/news/2018-06-filthy-firstthe-common-disgust-disease.html
Shaming someone for being evolved is really counter-intuitive.

“By analysing participants’ responses, researchers were able to identify the six common categories of disgust, which each relate to regularly occurring types of infectious disease threat in our ancestral past. Historically for example, eating rotting food could have led to diseases like cholera, close contact with unhygienic people could have transmitted leprosy, promiscuous sexual practices could have put an individual at risk of syphilis and contact with open wounds could have led to the plague or smallpox infection.”

Syphilis was germ warfare from American Indians, actually. Modern.
And basically all infectious diseases qualify as STDs. Depending how they’re caught.

“The results confirm the ‘parasite avoidance theory‘, in which disgust evolved in animals, encouraging them to adopt behaviours to reduce the risk of infection. This behaviour is replicated in humans where disgust signals us to act in specific ways, which minimise the risk of catching diseases.”

Slut shaming is just civilized. It’s the reason the disgust-numb largely died out. Dead amygdala, dead host. e.g.
https://academic.oup.com/brain/article/130/7/1715/327525
“However, very much unexpected was the disproportionate deficit in recognizing disgust, which was significantly larger than the deficit observed for recognition of fear.”

Disgust is a survival instinct, not to have it is biologically wrong. It’s as wrong as a psychopath with no conscience (they also feel no disgust at violent or diseased stimuli, this is why they’re promiscuous). Something is missing.

A grid-down would be funny because all the rich sluts on anti-virals would look like something from a zombie movie. STDs mutilate the appearance and without modern meds suppressing it, it would ruin the face.

Hell, a weakened immunity from a minor blackout would cause a vulnerability in the immune system to allow any former diseases to seize control (old age also does this). Sluts never survive dangerous turns of history for that reason, picked off by the wages of sin. People have forgotten, not really informed by ‘educators’. Brummel died in an asylum, a disgrace.

“Interestingly, the survey results showed that there were gender differences in reactions to the disgusting scenarios that were presented, with women rating every category more disgusting than men. This is consistent with the fact that men are known to indulge in riskier behaviour than women, on average. The categories women in the study found most disgusting were risky sexual behaviour and animals carrying disease.”

Science confirms what all women knew – male sluts are more disgusting than female sluts.

Women need to be discerning as a sex, this isn’t surprising. Birth defects, miscarriage and infertility aren’t fun.

This corresponds to an evolutionary view of the emotions which are for action; emotions make us do things that put us in a better state with respect to our survival and reproduction.”

We spot them.

And we shun them.

K-select women especially.

“Researchers say the findings could be used to develop instruments for measuring disgust, to investigate how disgust might vary across cultures and to understand how moral disgust, for example, relates to disease disgust.”

It’s been done.

Relevant, sexual disgust at stupidity.

https://bigthink.com/philip-perry/men-who-have-tattoos-think-it-impresses-women-study-says-it-doesnt/

Low IQ markers are repulsive, really?

Women answer politely to conform about attractiveness, hook them up to lie detectors and they’d say they hate tattoos.

I’ll post it separately.