Covid male sterility papers + HPV, herpes

as previously discussed:

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?


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


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.


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?



  • 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?


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.


and onward

Could COVID-19 have an impact on male fertility?


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.

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.

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

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.


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.

Nanolipids gather in ovaries, adrenals and liver

Imagine my shock.

“We have documented the pharmacokinetics and biodistribution of lipidots, synthetic 55-nm-diameter lipid nanoemulsions with potential applications for diagnostics and drug delivery. After intravenous injection in healthy mice, lipidots are stable in blood and taken up preferentially in liver, adrenals, and ovaries, where they release their lipidic cargo. Lipidots depict an original biodistribution, not previously reported for other inorganic or organic nanoparticles, toward organs involved in steroid hormone synthesis and storage (adrenals and ovaries) and localize to precise sites in these organs, suggesting potential applications for imaging and drug delivery.”

The nanolipids are the modRNA carrier. So where lipids go… I think we have our organ sequester, gentlemen.
NLs are in at least the moderna and Pfizer ‘vaccines’.

A friend suggested the Pfizer one may be ‘safe’ because rich areas are buying it. That was Boomers avoiding the heart effects reported from AZ, possibly to push them to the others, none of them are safe.
Potassium is also used in lethal injections, to stop the heart. It’s in Pfizer. Talk about red herring. Watch deaths from heart disease in, say, the next three years.

In this country, they don’t give you even the illusion of choice, it’s largely based on age and supposed availability. There is no safe one.

The lipids preferentially allow the modRNA to ‘slip into the cell’ of those organs, as the enclosed PDF plainly states.

nb The effects described in Malice or Mistake? in the brain are prionlike, they needn’t be actual prions.

COVID, sperm infertility and STD potential
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

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.

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).

They want to sterilise you (hCGβ)

It isn’t just Mark of the Beast, the Satanists want to sacrifice all your children, including potential. All count to Moloch.

The Mark is also a marker of infertility. Mark(er) of the Beast (whose sacrifice is what).

You know, owned infertility, like a pet. The Bible says never to get tattoos, and your duty on this earth is to be fruitful and make godly children. Scroll for just studies but context is important, I feel.

HCG-beta sterilises women (and children), what’s the bet it’ll be in one dose of one mandatory thingey, eventually?  As you’ll see, all it needs is one. It mimics fatal cancer, encouraging the body to shut down reproduction to struggle to fight it off. Maybe not the first dose officially to force you all, better space it out to avoid suspicion.
I wonder where they’ll put this, along with other sterilising agents? Mistakes were made, woops! You can’t sue!
Am I crazy now? I’m only covering HCG-beta today, 101 style. Do your own damn research and share share share the studies, 4chan, 8kun, the works.

Sterilization programme imminent like Bill and others did in Nigeria (and other places). Then again with HPV (which reduces fecundity, when checked with age-peers) as previously covered by me.

“The fear of vaccines: Fear that a vaccine used by the WHO to combat polio can cause sterility in both men and women, has spurred some Northern Nigerian states to block a crucial vaccination campaign that is aimed at eradicating the disease from West Africa. “

And you call Africa dumb? They’re not.
Herd immunity is a myth, also covered by me, even at 100% “coverage” (impossible) doesn’t work (unfalsifiable, fake science).
Remember, most spanish flu dead were vaccinated soldiers (and nurses), that’s why it got so many young people.
A pawpaw tested positive for this, FFS. A fruit and a goat!
They never say in ‘outbreaks’ of measles etc, how many who got sick ALREADY HAD the vaccine (most), they’ll deflect or try to hide that topic.

“Efforts to produce a contraceptive vaccine targeting human chorionic gonadotropin (hCG) face several important challenges.”

A ‘vaccine’ to stop you from reproducing. Don’t believe me?

Journal of Reproductive Immunology:
“Gonadotropin-releasing hormone/human chorionic gonadotropin β based recombinant antibodies and vaccines”

Vaccines have been developed against both GnRH and hCG and these have undergone Phase I/II clinical trials documenting their safety, reversibility and efficacy. The heterospecies dimer hCG vaccine prevented pregnancy in women of proven fertility without impairment of ovulation or derangement of menstrual regularity and bleeding profiles.”

Jump through their evil hoops and they might let you be a free human again. Keep reproduction free! Also, end medical segregation. Slaves weren’t allowed to breed until their master said so.

Anti-fertility vaccines, you only naturally express it when you have ‘advanced’ cancer.

“Ectopic expression of hCG/hCGβ is observed in many advanced stage cancers of various origins.”

Mandatory? Medical Marxism argument: I can violate your body with bio-rape implants because it may possibly help me, theoretically – or some hypothetical person.


“These reduce serum testosterone to castration levels causing atrophy of the prostate.”


The prize is disappointment. No lollipop.
“Castration levels” you couldn’t make it up. Evil has a PhD.

Guessing atrophy is permanent? Sounds kinda permanent.
Linked to ‘adverse prognosis’ (death).

Expression of the free β-subunit of human chorionic gonadotropin (hCGβ) in malignant tumors is frequently associated with aggressive disease. The pretreatment serum concentration of hCGβ is an independent prognostic variable in renal cell carcinoma (RCC). The three so-called type II genes (hCGβ 3/9, 5, and 8) have been shown to be up-regulated in relation to type I genes (hCGβ 6/7) in some malignant tumors.”

“This vaccine consists of a synthetic peptide representing, the carboxy-terminal 37 amino acids of hCG beta subunit coupled to diphtheria toxoid. The immunogen is pre- pared by linking the peptide to the carrier using a bifunctional reagent (6-maleimido caproic acyl N- hydroxy saccinimide ester)is in a manner to achieve predictable…”

Search engine (DDG) description:

“The second candidate vaccine is oLH.hCG-TT/CHB: a-subunit of ovine LH associated with hCG, linked to carriers such as TT or cholera toxin chain B (CHB). The third vaccine preparation is a physical mixture of hCG and oLH, each linked to carriers. These vaccines have completed phase I clinical trials in five centres in India.”

1989 publication date.


When you click:

Vaccines are under development for the control of fertility in males and females. This review discusses developments in anti-fertility vaccines at the National Institute of Immunology, New Delhi, India. A single injection procedure for the sterilization or castration of male animals depending on the site at which the injection is given, has passed through field testing and is expected to be on the market in the near future. Vaccines inducing antibodies against the human chorionic gonadotropin have gone through phase I trials with satisfactory results. A vaccine producing a consistently bioeffective antibody response against gonadotropin-releasing hormone is ready for phase I/II clinical trials in patients of carcinoma of prostate after due experimenation in animals and toxicology studies. Research to identify sperm antigens for incorporation into second generation vaccines is in progress.

This, in 1989. I didn’t exist then. Imagine what they have now.

Calling white people (or any) ‘females’ and ‘males’ is dehumanizing, especially intended to destroy you/r genetic lineage. Your God-given right. It just so happens black men recently popularised this use in rap, which isn’t controlled by a certain group with certain investments, is it? Phew.

They want you allergic to your own body. Autoimmune infertility, sterilization by antibody, it’s right there. CASTRATION, CHEMICAL CASTRATION.

A single injection procedure for the sterilization or castration of male animals”

It relates to cancer vaccines

Anti-fertility vaccine again

“Peptides representing the amino acid sequence of the carboxy‐terminal of the human chorionic gonadotropin (HCG) beta subunit were used in studies to determine whether an immunogen could be prepared that would be suitable for an HCG antifertility vaccine. Peptides of varying length were conjugated to several macro‐molecular carriers, in varying peptide‐carrier ratios…”

Chemical human neuter sounds so cruel.

They think they own you.

Target for cancer therapy, apparently? Nice excuse. Sounds so comfy, philanthropy.

WHO knows?

“The World Health Organisation (WHO) Task Force on Birth Control Vaccines has selected the pregnancy hormone human chorionic gonadotropin (hCG) as a target molecule for a contraceptive vaccine.”

You didn’t wanna breed, right?
How much would you pay for an anti-anti-fertility vaccine?
Task Force on Birth Control Vaccines….. selected…. target… fucking Nazi ‘eugenics’ again.

Christians are up first.

They later changed the name for being too obvious on a scale of really fucking obvious to taking le piss. Henceforth, it has become really fucking obvious.

“Over the past 18 years, the WHO Task Force on Vaccines for Fertility Regulation has been supporting basic and clinical research on the development of birth control vaccines directed against the gametes or the preimplantation embryo.”

So including chemical abortion, like the Pill.

18,years, as of writing, totally off the cuff.


NO SHIT, THAT’S THE TITLE. They think they own you.

During 1986-1988, the WHO Special Programme of Research, Development and Research Training in Human Reproduction used the diphtheria toxoid as a carrier for a fragment of the human chorionic gonadotropin (hCG) molecule (a conjugate immunogen) and an immunostimulant in a phase I clinical trial of this prototype antifertility vaccine in sterilized women. Between 1990 and 1991, it conducted teratology studies in rats and rabbits to determine whether the vaccine causes fetal abnormalities. The vaccine did not adversely affect either the animals or their fetuses. Clinical trials of the vaccine’s effectiveness (phase II trials) are scheduled for 1992. At least 2 injections several weeks apart, are needed to produce an anti-hCG immune response which is only effective for 3-6 months, however. So the same components of the original vaccine were placed in a polymer to deliver the vaccine slowly over a prolonged and predetermined time frame. WHO hoped that this advanced vaccine would raise effective immunity levels long enough to last for at least 1 year after 1 injection. WHO is conducting dose-response and toxicity studies of this prototype vaccine in rabbits and baboons to identify the optimal dose which would elicit an effective immunity level over a desired period of time and would be safe for testing in humans. WHO hopes to begin a phase I clinical trial with this advanced anti-hCG vaccine in late 1992. WHO anticipates that the preclinical and clinical trials will reveal a need for further modifications and improvements. WHO is supported multicenter research on antitrophoblast vaccines which target membrane cells of the preimplantation embryo since 1985. It uses monoclonal antibodies (MABs) and recombinant DNA technology to identify and isolate surface molecules. So far this research has tested 15,000 MABs but is centering on 9 MAbs. A study in baboons showed that 1 MAB reduced fertility, even though researchers could only use minute amounts of the protein in the injection.

Population control = PR for genocide. Go after the guidestones people and their love of carving stone.

PR is rebranded propaganda to the post-war period, rebranded deliberately by the likes of one Bernays. That is historical fact.

“Vaccines based on hCG have been proposed as a means either to prevent metastatic cancr6 or to control fertility’. Approaches to development of such vaccines have been pursued usij either the complete beta sub unit of hCG (hCG-fl) or the 37 amino acid CTP alone”

Most people wouldn’t want an anti-cancer anything if it made them sterile.

“The WHO Task Force on Vaccines for Fertility Regulation. Its formation, objectives and research activities”

“As a result of this inter national, collaborative effort, a prototype anti-HCG vaccine is now undergoing clinical testing, raising the prospect that a totally new family planning method may be available before the end of the current decade.”

Guess the year. Guess. I’ll tell you in a few lines.*
“Immunization to regulate fertility…”
“produced by placental cells”

*It’s 1991 published above re WHO. 
PDF here:

save save save

bookmark, usb, email, any way you can get this all out there

This one is tricksy.

“Even though the idea of a birth control vaccine was gaining traction

… WHO task force trial undertaken on women in Sweden testing the vaccine …”

described in SEO brief

paywalls should be illegal

maybe you can find this paper on the piratebay of academic papers

No excuses. Weird they hide this recent one re Swedish info, because it’s ongoing?

Published 1997.

Contesting claims on the safety and acceptability of anti-fertifity vaccines

spellings are often deliberate to thwart SEO

Contesting claims on the safety and acceptability of anti-fertility vaccines


This paper describes the controversy surrounding anti-fertility vaccines, focusing on the antihCG vaccine. It deals first with the rationale that researchers give for the development of antifertility vaccines, and the specific requirements that they set for the new contraceptive method.
Two distinct prototypes of anti-hCG vaccines are clearly emerging, one of which might be
characterised as maximising safety and the other as maximising efficacy. A vocal group of
women’s health advocates have opposed the development of both prototype vaccines, pointing to
theoretical health risks and the potential for abuse, and call for a stop to further research. This
paper shows how the scientists’ discourse on safety and acceptability of the technology to future
users has changed in response to the critique of women’s health advocates. Finally, it reflects on
the role of women’s health advocates in contraceptive technology development, and the
responses of researchers to their actions.

They took over womens’ groups to avoid discussion of important issues.

TLDR trust the “scientists” what human ‘error’? let alone ‘evil’ trust the ‘experts’

you know, pre-replication crisis

scientists often own stock so….. null appeal


The possibility of a contraceptive vaccine targeting human chorionic gonadotropin has long been recognized, but never fully realized.

weird, previously they’ve claimed success in ‘trials’?

they think you’re stupid

you can’t ban something they claim doesn’t exist (yet)

Here we describe an epitope-specific approach based on immunogenic display of hCG-derived peptides on virus-like particles of RNA bacteriophage. A number of recombinant VLPs were constructed, each displaying a different hCG-derived peptide. Some were taken from the disordered C-terminal tail of the hormone, another came from an internal loop, and yet another was an epitope mimic produced by affinity-selection on an hCG-neutralizing antibody target. Immunization of mice with some VLPs yielded antisera that bound the hormone and neutralized hCG biological activity.”

neutralised, like a threat
neutered you – like a dog

share share share the studies, you don’t have to link to me just SHARE

I haven’t posted this previously to avoid it getting censored prematurely.
Is anyone else keeping a tally of how many times I can piss off the WHO or NWO people without being murdered? Just me?

Female medieval English skeletons study

“However, the period of ‘youth’ in medieval England, before the achievement of full social adulthood, may have extended well past physical adolescence, and the age of 25 years is often used as the cut-off point.14″

Louder for the pedos at the back.

“but for most medieval young women physical adulthood did not equate to social adulthood.16″


“Instead, puberty may have marked the beginning of the phase of ‘maidenhood’ rather than adulthood.17”

We now call it teenagehood but I prefer that name for women.

“Lifestyle changes for the teenager, in particular the onset of formal work, may have marked a further step away from childhood, particularly if this involved a move away from the parental home. That the 14th-century poll tax was levied on all those aged 14 years and above suggests that young women were expected to be earning their own money by this age.18

HA. Yeah, the guys who say women should sit at home all day twiddling their thumbs waiting to marry are 1. wrong and 2. have put too much stock in middle-class novelist Austen.

Like today;
“Although exact numbers are impossible to calculate, it is clear from the documentary evidence that a significant proportion of young women migrated to urban centres such as London and York to obtain employment, most commonly a service position.19″

Exactly like today:
“This move would have been a dramatic, and potentially a traumatic, change in lifestyle for young women. Although it may have brought greater freedom and responsibility, it does not seem to have conferred full adult status; there is evidence that young women in service were always viewed as ‘girls’ regardless of their age, just as young men were not viewed as full adults before the completion of an apprenticeship contract.20″

So they didn’t marry for money, they were already economically independent.

If you actually read history and here, forensics.

“in reality, marriage at such a young age was largely restricted to the nobility, with the average age at marriage in the general population estimated at 20–25 years,22
and perhaps even later following the Black Death.23
This would provide a very late age of achievement of ‘adulthood’ by modern standards. However, although marriage was very much the expected path a significant minority of women — perhaps around 15% — never married.24″

Who is dumb enough to have never looked this up?

I keep seeing Americans who make sweeping fictional statements about what ‘we’ Europeans did and it’s like… no. That’s never happened. Citation? Statistics? They are liars. Even in their revenge fantasies of ‘oppressing’ women from work (oh joy, welfare on the backs of random men? can’t win, can we?) then they assume all women would marry off (literally never happened in human history), all women are fertile and their children all magically survive (LOL) and that all men want to marry and got to choose who (LOL no). The economy also needs young workers, part of the immigrant problem is caused by not allowing teens to work.

They’re in bloody La La Land.

Extended maturation is K-selected, the men and women were tougher as a result.

Just realised my grandmothers might be in here.

Almost certainly. Yeah, don’t lie about my nana/s.

“Alongside these dramatic but infrequent events, most young medieval females would have experienced everyday hardships and hazards.”

” The average femoral diaphysis length recorded for the medieval 14-year-old females (354 mm) is closest to that recorded by Maresh for 20th-century 10-year-olds (348 mm). The average figures for medieval 15- and 16-year-old females (365 mm and 366 mm respectively) are still lower than for 20th-century 11-year-olds (367 mm). These data suggest that growth in medieval England fell well below modern standards, perhaps reflecting the lower standard of living medieval children would have experienced.”

If it was that hard on the girls, you don’t wanna go back to that, guys.

“It does not necessarily follow that medieval women were considerably shorter than their modern counterparts. When compared to dental formation, epiphyseal fusion in the female adolescent skeletons from our sample was delayed by two to three years in comparison to modern standards, allowing them to ‘catch-up’ their growth during the pubertal growth spurt.27 This pattern of extended growth appears to have been common in the medieval period;”

The English are tough.

” Only very slight differences in stature were noted between the women of Lincolnshire, London and Gloucester, although the London females had greater diversity in adult height.”

“This may suggest that girls who experienced poorer conditions for childhood and adolescent growth were more likely to die around or before the age of 25 years.”

K-selection. Stunted or shorter women likelier to die. Same with men.

“It has been suggested that female height may have suffered in comparison to male height in medieval Europe due to preferential feeding and care of male children,33causing greater sexual dimorphism in growth and final stature between the sexes. By comparison, the average stature of young men at our sites (156 individuals) was 169.5 cm (5 ft 7 in). This may simply be the result of sexual dimorphism as such comparisons are similar for modern western populations, and therefore does not support the hypothesis that girls experienced poorer nutrition and living standards than boys.”

K-types invest well in all offspring.

“According to these indicators, it appears that all of the individuals studied had entered the pubertal growth spurt by the age of 14 years. In the modern western world girls tend to begin puberty around the age of 10 years,37 and so this result would fit with modern expectations. “

Puberty begins then takes a few years, 14-18/19 matches what I read elsewhere about menarche (posted here).

The ‘modern’ data is skewed by non-whites, especially Asians and Africans, with much lower menarches.

The African is nine, measured in America, as I recall.

“More information can be gained from examining the epiphyseal fusion of the hand phalanges, a process known to occur during the deceleration phase of the pubertal growth spurt, and correlated with first menstruation in modern females. Although the age at which this event occurred varied in our sample just as among modern girls, fusion appears to have occurred most frequently between 15 and 17 years (Fig 2). At 14 years, only 36% of girls display fusing or fused hand phalangeal epiphyses, but by 17 years this figure has risen to 84%.”

Still not 100%, K-types have a later range of menarche.

“A second skeletal event known to be associated with first menstruation, the ossification of the iliac crest of the ilium, was also only found in girls aged at 15 years or over. Interestingly, this is roughly in line with the average age at menarche suggested by the few available documentary sources.38 An average age at menarche of between 15 and 16 years would be much later than the modern British average of just under 13 years.39In addition to their shorter stature, this finding adds weight to the argument that environmental factors such a deficient diet and disease were having a negative impact on medieval female growth and development. Interestingly, however, this average age at menarche is below the age of 17 years recorded for mid-19th century females,40indicating that urban conditions were not as detrimental as those experienced during rapid industrialisation.”

The female body takes YEARS to develop, periods often occur too early to carry a child to term. Hollywood lies, because it’s full of creeps.

Men shouldn’t be discussing a reproductive system they cannot understand.

“The evidence for medieval England, however, shows a delay in the achievement of this milestone, which appears to have fallen between 17 and 18 years for most girls, based on 247 individuals with this bone surviving (Fig 3). Complete fusion of the iliac crest of the ilium, which signals the end of pelvic growth, was only seen in a minority of women aged below 20 years, based on the 277 individuals “

They’re K-types, it isn’t a delay, it’s NORMAL. Modern people are aberrant.

17-18 periods stabilize (this takes years, I have spoken to doctors about it).

The pelvis keeps growing to carry and support a child though, only when this is done (about 21, spinal plate fusion) is the woman actually sexually mature with a low risk of still birth, miscarriage or death.

Modern medicine is allowing a lot of non-white thots to survive a process Nature is telling them is fatal. Do not confuse that with Nature’s approval.

These data suggest that puberty was extended into the very late teens for young medieval women, pushing back the timing of achievement of full physical adulthood. This extended period of physical adolescence indicates that living standards for young medieval women, at least in the urban and small town environments, were considerably poorer than those of modern British adolescents. Some variation between the sites was noted, with pubertal development most advanced in the small town of Barton-upon-Humber, and most delayed in the urban hospital cemetery of St Mary Spital, London. This presumably reflects the harsher living conditions experienced by the girls living and working in London.”

Nah, hard work and low fat diet. Treating the women like men will delay them more.

“It is believed that the demographic changes caused by the Black Death may have led to increased opportunities for many women to migrate and work.43

Although less documentary evidence is available for women than for men, there is evidence for female servants much younger than 12 years in urban households,44and some migration may have occurred at a very young age. Although legislation was passed to regulate the minimum age for apprentices — 13 years in the early 14th century, rising to 16 years by the 15th century — apprenticeships were rarely available for girls, and no such legal minimum age existed for servants or casual workers. The available evidence suggests that girls started formal work away from home at a younger age than boys.45

This concept of female laziness is really American.

” a degree of personal freedom; the latter is perhaps most clearly indicated by the large number of migrant women recorded as making ‘merchet’ payments for the right to choose their own marriage partner.46 On the other hand, moving away from home, particularly to a town or city, could bring with it new challenges and hazards, such as sexual predation, mistreatment, injury and disease.”

Americans are so wrong it hurts.

” this result indicates that much greater numbers of women living and dying in London were actually suffering from tuberculosis.”

“Again, the numbers are too small for statistical analysis, but this may provide further evidence for girls having a more indoor lifestyle than boys in the medieval period.”

Forcing women to sit at home is literally bad for their health.

We aren’t mole people.

On the whole, the women actually had it harder than men.

“There can be little doubt that this extensive workload was exhausting for many women, but osteological study can provide further direct evidence for the impact that this had on young women’s bodies.

A wide range of trauma has been recorded on the skeletons of young medieval women, including fractures of the upper limb and finger bones, cranium and ribs, lower limbs and feet.57 However, the prevalence of fractures of each type is lower than among males, suggesting that girls were exposed to (or exposed themselves to) fewer risks of injury than boys.”

We hadn’t evolved for that labour, men did.

“It is notable that, of the 48 cases of trauma reported in the grey and published literature, cranial, rib and jaw injuries, suggestive of interpersonal violence, only started to appear in women aged 17–25 years, comprising 18.6% of the 43 fractures for this age group. This suggests that the risk of violence rose as girls turned into young women, perhaps reflecting domestic violence after marriage.58″

That would explain the death rate. Stress and fractures – no healthy baby.

There is one area of the skeleton where young women seem to have suffered virtually the same frequency of fractures as young men, the vertebral column. By far the highest prevalence rate for vertebral fractures (4.7%, n = 9) was found at St Mary Spital suggesting that female workers in the capital, or at least the poor workers buried in this hospital cemetery, were undertaking the activities most likely to cause spinal injury. The majority of these fractures were compression fractures, often caused by falls from a height, although avulsion and hyperflexion injuries were also present.59

The men sitting at a desk in an apprenticeship had it easy.

“Schmorl’s nodes are common, often asymptomatic, depressions caused by herniation of the nucleus pulposus on the superior and inferior surfaces of the vertebral bodies. Their aetiology is complex, although spinal trauma caused by vigorous activity and flexion and extension of the spine is most commonly associated with their formation.60 The age of their occurrence is not clear, but they generally appear before the age of 18 years.61Plomp et al argued that males are more susceptible to these lesions due to the size and shape of their vertebrae.62 In our study, medieval women had a higher prevalence of the lesions). Analysis of the location of Schmorl’s nodes on the vertebrae revealed that the lumbar vertebrae were affected far more often among women, and the central thoracic vertebrae among men. This mirrors vertebral fractures where in the women all of the fractures occurred in the lower thoracic and lumbar vertebrae, while in young men the central thoracic vertebrae were affected. This may suggest different activities; strain on the lumbar vertebrae, in particular, may be caused by bending and lifting.63″

aka back breaking labour, which could cause…

“Further evidence for stress being placed on the spines of young medieval women is provided by cases of spondylolysis. This describes the partial separation of the inferior facets on the neural arch from the vertebral body, usually between the ages of 10–12 years. The condition results from microtrauma in low grade stress on the lower back due to bending and lifting strains, or a fall from a height,64 but may have an underlying congenital cause. This injury was present in 4.4% of the female skeletons examined. This is higher than the prevalence of this condition found by the authors among young medieval males (2.9%), although the numbers involved were too small for statistical analysis. Again, the area involved is the lumbar region of the vertebral column. In addition, three young women, two aged at around 21 years and one at 22–25 years, display early degenerative joint disease of the vertebral column.”

Forcing women into labour like that kills them, reminder.

What emerges from the osteological evidence is that the workload of many young medieval women appears to have been literally backbreaking, and these early injuries may be expected to have led to significant back problems and pain in later life. It seems likely that these early spinal problems were caused primarily by carrying heavy loads at a time when the spine was still forming and vulnerable. Research from the grey and published literature reveals that rates of spinal injury were higher in urban than rural women65 and suggests that the workload of the young migrant women in service was harder than that of the young women who remained in the country or in small towns with their families. For example, the prevalence of vertebral fractures, spondylolysis and Schmorl’s nodes was lowest at Barton-upon-Humber, a wealthy small town.66″

Marriage, Sexual Activity and Childbirth

There is considerable evidence to suggest that marriage was a defining moment in the medieval female life course, marking the transition into true social adulthood.67 It is notable, however, that there was a significant gap between the legal age at marriage (12 years) and the average age at marriage (20–25 years even before the Black Death) in medieval England.68 The new analysis of pubertal development in medieval England discussed above suggests that the average age at menarche was 15–16 years. Full fertility, in terms of the likelihood of conception, carrying a healthy pregnancy to term and surviving childbirth, would only have followed several years after menarche with the completion of pelvic growth,69 which in our medieval sample appears to have been rare before the age of 19 years.

aka what I already typed, dammit

The fact that many young medieval women would not have been fertile before their 20s may be one reason for the relatively late average age of marriage during this period.70 It also suggests that marriage at the legal minimum age of 12 years would rarely have been fruitful, and any pregnancy that did ensue would have carried significant risks for the mother. We know of several medieval legal cases of the marriage of young girls where the ‘physical readiness for marriage’ of the girl in question was debated.71

This don’t go to college because you get periods thing from America is pig ignorant on female anatomy.

There is evidence to suggest, however, that the majority of cases of marriage before 15 years were confined to the nobility.72Today, girls of higher socio-economic status, with a considerably better standard of life, mature earlier than average. For example, high caste girls in 20th-century India have an average age at menarche over a year younger than low caste girls.73 The average age at menarche for noble girls in medieval England may therefore have been younger than the average age of 15–16 years described above.

more r-selected by men, explains eventual decadence and homosexuality rates, especially in the French

Even so, a pregnancy before the completion of pelvic development would have been dangerous; a famous example of this is provided by Margaret Beaufort, who appears to have been rendered sterile by a difficult first birth (of the future king Henry VII) at the age of just 13 years.74 An understanding of these risks is demonstrated by several contemporary authors,75 and was reflected in the Jewish rule that contraception (banned by Christian teaching) could be used to prevent pregnancy if the bride were too young to safely bear a child.767

The guys trying to force women to reproduce young would ironically render their own wife sterile via their stupidity. Good riddance. The Lord works in mysterious ways.

In theory, marriage coincided with sexual initiation for young women, and if the Church’s remonstrations to remain celibate until marriage were universally followed, it would indicate a relatively late age of sexual initiation. In reality, premarital sex among betrothed couples seems to have been common,77

that links to this study, no, they weren’t slutty



and sex with other partners, in not all cases consensual, was far from rare.

Are you really counting rape?

Evidence for this is provided by the erratic enforcement of ‘legerwite’ or ‘leyrwite’ fines on serf women who engaged in premarital sex.78

What about the men.

Premarital sex is thought to have been particularly common among young girls and women living away from home, for example in service roles, due to the greater freedom and availability of partners as well as the risk of sexual predation or pimping from employers.79 The sexual exploitation of girls in service appears to have been a frequent problem based on the legal record,80 and many young women must have lost their virginity in these circumstances. The extensive focus of many writers on admonishing young women to stay celibate until marriage may be taken as further evidence that premarital sex was seen (at least for women) as a significant societal problem.

Rape isn’t sleeping around, WTF.

Pedophiles raping virgins don’t really count as premarital sex, a choice, does it?

Two aspects of osteological analysis may shed light on sexual activity among young medieval women. The first is a sexually transmitted disease. Venereal syphilis, a treponemal disease, affects the skeleton in its tertiary stage, causing distinctive skeletal lesions.81 From the end of the 15th century, syphilis is believed to have been endemic in urban areas of England, although recent work has suggested that it may have been present at a much earlier date.82

Men spread that, sailors caught that. Your point?

If a virgin woman married a man with it, she’d get it. That can happen after marriage.

These female authors really want to present all women throughout history as sluts. Cui bono?

Among the 14–25 year old female individuals examined, four probable cases of treponemal disease were recorded, based on the presence of characteristic gummatous lesions in the cranium or long bones.83 Three of these were found in the young women from London (Fig 5), and one was found in York, at St Helen-on-the-Walls. One further case is known from Blackfriars, Gloucester;84 no cases were identified in the rural or small town sites consulted in the wider survey. The two youngest women to show signs of treponemal disease were aged at just 16 years. It is difficult to rule out congenital syphilis in these cases, as the presentation of the two conditions can be very similar, although none of these skeletons display the typical dental deformations of congenital syphilis.

So their fathers were sluts, so?

If the disease is the venereal form of treponemal disease, or syphilis, this would suggest the girls were very young when first infected. Syphilis generally takes several years to cause such destruction in the skeleton.85 Although the number of cases recorded is small, given that only 10–20% of individuals with tertiary syphilis experience skeletal involvement, and that skeletal lesions take several years to develop,86 it seems likely that much greater numbers of young women were affected by this disease.

To imply they wanted to be raped by syphilitic men is a bridge too far though.

The spread of sexually transmitted diseases such as syphilis was exacerbated by the problem of prostitution in medieval towns and cities. Karras argues that regulations of the Guilds limited women’s access to the normal labour market, forcing them to turn to prostitution out of necessity.87

Assuming that was a mistake.

There is little direct evidence that apprentices were procured as prostitutes, but one extant record from London City and Ecclesiastical Court (ad 1423) attests that one Alison Boston took apprentices who she hired out for the ‘horrible vice of lechery’.88 There are also accounts of men taking young girls (invenculae) to the London stews and selling them as prostitutes, suggesting the types of danger faced by young unskilled immigrant women. Goldberg89 cites the famous references from medieval York in ad 1482 that place prostitutes within the legal realm of ‘lepers’ and pigs in the hazards they caused for the local population.

Enslaved children.

She does not discuss the age at which women may have turned to prostitution, but suggests widows and daughters of labourers, known as ‘spinsters’ and ‘seamstresses’ (sempsters), needed to work several jobs to make ends meet, including petty theft, illegal ale retailing and prostitution. Goldberg argues that although full-time, ‘professional’ prostitutes were rare, many women were forced into occasional prostitution in hard times.90

Contradiction, Goldberg.

also why we have the welfare state

This would have been a particular risk for a migrant girl away from the safety of her family.91 Although it is impossible to state that any of the young medieval women examined were forced into this profession, this must be considered in the cases where possible syphilis is recorded.

No shit, nobody would choose that. The excuses these women make for rape are appalling.

A second consequence of sexual activity, pregnancy, may also in exceptional circumstances be visible in the archaeological record. In total, eight cases of young women buried with fetuses in utero have been recorded from medieval cemetery contexts. These burials represent ‘obstetric catastrophes’ with the death of both mother and child in late pregnancy or childbirth. Although there was a Christian injunction in place in medieval England for infants to be removed from their mother’s womb before burial,92 this does not appear to have been rigorously obeyed.

Yeah, who wouldn’t choose to die like that? I guess they were all just happy sluts, huh Mizz Feminist?

All of the individuals buried with a fetus in utero in medieval cemeteries have an estimated age at death of around 20 years or over, and thus none represent particularly young ‘teenage’ pregnancies.

Because they rarely got pregnant. Look at the evidence.

This may support the idea that in the medieval period teenage girls were not falling pregnant, as first pregnancies are often seen as the most hazardous.93

May? It’s anatomical.

It also fits with the known late pattern of marriage in this society. However, it is by no means certain that all of these women were married. The two examples from St Mary Spital may have represented extramarital pregnancies as the hospital was known to accept unmarried women in pregnancy or childbirth.94 It may be significant that neither of these women received an individual grave or any grave ornamentation. In contrast, the elaborate nature of one young mother’s burial at Barton-upon-Humber, in a coffin within the church and with a cloth of gold artefact,95 surely indicates that this woman was married and held a position of substantial social standing.

Clearly, their situation was a choice.

Given the high mortality rate of women in childbirth in the medieval period revealed by documentary sources,96s it is clear that these rare burials represent a dramatic under-estimation of the real levels of maternal mortality. In many cases, the churches prohibition on burying fetuses in utero may have been observed. In a large proportion of births, too, the child may have been saved, leaving little clue as to the cause of death of the mother.

But doctors (when sane) will elect to save the mother because she can have countless children later but an orphan baby is already financially a goner. Remember this, America.


The period of social adolescence for young medieval women seems to have been an important life stage, encompassing the growth to full physical adulthood and fertility, the adoption of adult working roles and, for most young women, the move from legal dependence on a father to legal dependence on a husband, with perhaps a few brief years of relative independence in between. The comparative absence of young women from documentary sources means that osteological information plays a vital role in our understanding of this group, and it can reveal a great deal about the way in which medieval girls grew into women, the living conditions they enjoyed or endured, the work they did and the health problems they faced.

Many of the conclusions drawn from osteological analysis of this group articulate with and illuminate the documentary evidence. The average age at which full fertility appears to have been achieved, around 20 years, is substantially later than in modern England, but ties in well with the known average age at marriage in this society. The greater susceptibility of young women to respiratory infections, from the relatively benign maxillary sinusitis to the deadly serious tuberculosis, chimes with the picture drawn from documentary sources of an indoor lifestyle for women, close to the smoky fire, and of the cramped living conditions that helped to spread disease. The backbreaking work clearly undertaken by many young women paints a clearer physical picture of their daily lives than that provided by documentary sources alone, and the development of signs of venereal disease in very young women hints at the problem of girls being driven to prostitution in England’s medieval cities.

Gang rape, we still have it. They are driven to it, slave-driven.

Vice celebrates the self-sterilizing

We should be paying them. One-time lump fee. Just enough for a great holiday.
Weed out the high time preference. £4-5k? Conditional on their signature that they’ll never try to reverse it or otherwise breed, or at least won’t take welfare if/when they do.

If they aren’t responsible enough to make this choice at 18, they aren’t responsible enough to consent to sex. The schools should be blamed, since they were nowhere else.

Please make this the hot new trend.

It’s still eugenics if they do it to themselves.

Congratulations Roosh and the other genetic suicides, you’re in the fine company of these lovely ladies.

“Life isn’t just about reproduction.”

Thank you for not breeding.

cool nothing shocks me scientist indiana jones calm haha amused

I bet the majority were already sterile due to undiagnosed STDs.

As one guy put it “your mutations end with you!”

Essentially they’re recognizing their existence is a mistake of nature.

Tell me Peter Pan Syndrome isn’t a thing.

What would they say to people who think 19, or even 29, is too young to make a decision so final? That this is a narcissistic lifestyle choice designed to hold onto their not-quite adult status? 

Katelin assuredly disagrees.


“I want time alone, time with my partner and time to travel and spend money on luxury. And I don’t think there’s anything wrong with that,” she says.

how is that not-

“My generation live in a broken world. We come from broken homes and have broken minds and bodies. Many of us just don’t want to reproduce. It’s my life, and I’m not hurting anyone.

Still a vector for sexual diseases though, huh?

Never mention that?

They never want other tissues and nerves cut, no, that’s crazy!

superman drinking give up nope

Super-gonorrhea will have a long time to incubate in these people, before spreading to the normal population.

Shocker as low time pref predicts ability to maintain relationships

Proxy studied: credit score.

Commitment = ability to choose the long term over the short term.

What a shock.
Also a proxy for class. (Class similarity predicts longevity too, another surprise considering assortative mating).

“Credit scores are widely used in a variety of contexts as an indicator of reliability and ability to honor and maintain a broad range of commitments, such as rental and employment relationships, not just those involving debt and credit.”

Time preeeeeeeference.

The honor is IN the maintenance. Sure, I guess you married her with the best intentions, but that doesn’t change the fact you slept with the secretary, you know?

We know that impulsivity predicts poor relationship skills, and low credit scores may reflect impulsive spending behavior. In fact, one of the primary characteristics of Dark Triad males is impulsivity. (Jonason & Tost, 2010; Jones & Paulhus, 2011).

What matters here isn’t the brevity of their relationships (which might be agreed upon) as much as the fact they cannot maintain them. It isn’t an ability in their repertoire. They fall short, they fail.

Another study found that “Individuals who have intercourse in the context of hookups are differentiated by high impulsivity, low concern for personal safety, low dependency, their erotic approach to relationships and an avoidant attachment style.” (Paul, McManus and Hayes, 1999)

Anything other than secure attachment style is relationship hell for the other party. They’re afraid of emotional intimacy (and commitment, which is like emotional prison for them because of it).

Clearly, the inability to defer gratification through saving should be a massive red flag.

I love how attention whores brag about their shitty relationship skills. They wouldn’t do that with any other ability, like driving. Maybe maths, since these people aren’t especially bright. Stupid people tend to pair off again. Most couple’s fights are over money (generally, the man’s job, I should point out).

And blogging (public!) about a woman’s sex life without her permission is about as bad as posting a guy’s small penis selfie to his boss and colleagues: These are the same type who’ll go on about a woman’s reputation and how important it is, totally flouting the trust placed in them (they’d make such wonderful husbands, that 4 and 5) to have a sexual connection.

The male will compromise his standards for short-term mating, but not abandon them altogether. He attempts to maximize quality given the tradeoffs required by his overall goals.

Furthermore, the vast majority of men want to marry. They seek a monogamous lifelong partner. Research shows that when asked how many sexual partners a man wants in the next five years, the median answer is 1. (See the research HERE.) Marriage is by far the most successful way for men to pass on their genes.

Actually, the masculinity of what was called ‘sexual congress’ was bound up in the virility of the Pagan Gods. It was said The embrace of a god is never sterile or some such. It had nothing to do with the sex act itself. A man who has sex with 3 women and gets 2 pregnant is batting 66% reproductive recombination average. Hell, a virgin who marries and has children with one woman has a 100% success rate. A man who beds 500 women and bears no heirs (the male incentive, legacy) is a genetic failure. A man who beds every single, fertile woman on the planet with no heirs is judged impotent (not the same as infertility originally, because he could physically have children but the problem was …psychological). It used to be grounds for divorce if a man refused or didn’t want children with his wife, in a time when women didn’t have much going for them under Patriarchy (which always sides with the K-selected legacy producers aka future taxpayers). Everyone has a personal fertility rate, and in their heart of hearts, most of us don’t want to be genetic suicides.

This is why humans are monogamous. It guarantees not only paternity, but male virility (when in the state of nature, the baby or the mother would die or be killed/aborted without his protection). Evolutionary strategies around fitness ONLY APPLY WHERE THE PEOPLE INVOLVED REPRODUCE. It’s like if I applied the archeology of dinosaurs to the Bible, it’s embarrassing, please stop. Evobio comes down to maths, much like game theory. Think of all the sterile sex going on. You think Evolution counts that? It’s a blip in the history of mankind, like men who couldn’t get it up. Nature is culling those people. They are self-selecting OUT of the gene pool. Let them! 

The topic of hypergamy again. ~big sigh~

Oh, now you guys finally give a shit about sociology? Now you think it’s real? Why isn’t it part of the subject called sexology then, genius? What’s the socio- in sociosexual hierarchy all about? They aren’t the same or the topics would be merged. Stop misusing the words again, Christ on a bike, read a book. A textbook. Or make up your own words instead of poaching a thing the means the exact opposite of what you’re trying to prove.

Expecting a woman not to care about social status (read; keeping her safe) is like a fat feminist expecting Ryan Gosling (he’s popular, right?) not to care about physical attraction (read: to get it up). See? It all fits. Quit buying into the undercurrent Narrative that the sexes are meant to be the same. Is/Ought is a guillotine that murders reason. If they were meant to be the same, evolutionally, then sexual dimorphism in our species wouldn’t have happened.

The drop of arranged marriages is actually nixing marriages of social advantage.

…Today most people marry their approximate social equals, and in much of the world hypergamy is…in slow decline.

This is bad for men. The same men who tried to leverage their status (often inherited) into a better quality of wife (works both ways, don’t it?). And patriarchs (fathers) who would only give away their property (daughter) for the best price?
Which sex is more likely to ‘trade up’ (ugly term) after marriage? Clue: which sex had practically all the active profiles on Ashley Madison?

Which one usually has the problem maintaining their end of the relationship (up to marriage vows)?

…Roughly 10-20% of both men and women are promiscuous, though the most promiscuous men are more promiscuous than the most promiscuous women. (Research HERE.)

They believe it doesn’t affect their future prospects (it does with K-women aka wife material).

Futhermore, the opposite of hypergamy is hypogamy, which simply means that men tend to marry down. As hypergamy has declined with assortive mating and the egalitarian marriage, so has hypogamy. The marriage and divorce statistics contradict any notion of hypergamy as guiding female choices today….

I quibble with this when it comes to divorce settlements but the general point is true.

Here are the reproductive strategies [DS: that is not a moral license] Jared Rutledge and Jacob Owens employed to get sex:


Here’s an example from one of their podcasts (H/T: Wj):

Young Jay (Jacob), after describing a woman as manipulative:

It was really fun cuz we had sex in the shower. Hospital sex is weird! And when she is drugged, it’s strange, but it’s really cool.

Papa Jay (Jared): Could she give consent?

Young Jay: Uh-oh! (Laughter)

Papa Jay: You might have violated some California laws.

Young Jay: That is mah bad. That is mah bad.

Papa Jay: Good thing we don’t live in California. (Much laughter.) 

Projection. Scum. I bet he thinks it’s rape when a man is drunk though.

For the record, the mother of the patient, referred to as “A.” is planning to bring charges against her daughter’s rapist.

Physical Abuse

Jared admits to “wailing on a woman with a belt” and “gagging her with my dick.”

Holistic Game also tweeted this dating advice: “Bitches get stitches.”

See it all HERE.

It’s like they’re doing the jury’s job for them.
See, the problem with jokes is that some total retard is going to do it, thinking you were serious. And that could count as incitement if it’s on a somewhat serious platform like a blog, certainly in Europe. These twits don’t bother to check the laws of the countries they travel to as sex tourists and complain when they get done.

No one is faulting the men for promiscuity. With the exception of the hospital patient, the women described appear to have consented to sexual relations with Rutledge and Owens.

It’s freedom of association. They were literally two-faced (the common stereotype I have no doubt they accuse of women). I doubt those women would’ve done if they had known the other side and that’s why the blogs didn’t use their real names (what social proofing, are they doing something to be ashamed of?). At least guys like Roosh have the balls to use their real name (although he lies about it while travelling which would beg legal questions about consent). A future question on the scene might be “are you a fuckboi or PUA”? for legal protection in case he turns out to be (you laugh but it could happen, nobody likes misrepresentation and those cases are pretty cut and dried).

I. Of the 50 women Rutledge had sex with, only 3 qualified as “carousel riders.”

He found that the rest were seeking monogamous relationships, in some cases agreeing to casual sex in order to get that. He exploited that opportunity.

See what I mean?
That right there is a social contract, folks.

oh shit damn fuck hell no give up dean winchester shrug

The rest is quite pathetic.

“…Women want to be swept up in an emotional whirlwind, and the more I tried to keep my “Alpha cool” the more they responded with flakiness or coldness.”

I know teenage boys with more common sense. “If I don’t show I like her – she’ll think I don’t like her!” actual quote, I was very proud of that one.

They assume you’re politely fading them out. They tend to follow. And being honest, did either look Alpha? Come on. SMV-wise. Come on.

On the manosphere;

“There’s a tremendous amount of ego, and a lot of anonymity.

…They didn’t hear the hurt, they didn’t see my mom cry when she learned how many people I’ve had sex with. They don’t see what the judgmentalism they are still engaging in did to myself and other people.

I am not going to be on my deathbed having engaged in these kinds of judgments anymore, this breaking people down into their component parts. [DS: breaking people down and using their broken-ness to manipulate what you want out of them, leaving them broken – those are the actions of a sociopath] It’s unhealthy for me, and it causes irreparable and widespread damage to other people.”

She knows she raised a scumbag. She sounds like a nice woman and he let her down (and by extension, her sex, which she also let down by producing and raising him, yes women think like that, on that scale of complexity). It’s little better than a drug problem, with a similar rate of disease. If you are aware enough to see the societal decay, you have a civilian duty to never contribute to it, maybe try to repair it. Social problems happen in shockwaves. Never be the rock.

Enjoying the decline is about not causing undue pain to yourself – or anyone else.

This article ends badly, the red-pill isn’t twisted, this information used to be considered Common Sense (e.g. women and men are different creatures) and should form a reaction/reminder to unrealistic PC lessons. A balm to the bruise. Twisted people are using it as a shield to hide behind and hide their abuses of the human condition we all share. I’ve written here this has become a ‘disturbing trend’ and one we here blogging might become known for.

Ironically, real sociopaths with low time preference (called ‘successful’) are almost always married, and quite happily. They slot right into the role, overjoyed to fit in for the first time ever and have a safe outlet for their personal doubts. Those men are not sadists and their wives love them. They make good husbands.

Link: Mutation accumulation and sexual pathology

TLDR: man-woman, fecund, is the only true sexuality, the rest is really fetish. Sexuality is productive and you can forge a society with it. There is also a pathology towards sterility in people who would balk at State-imposed for eugenics, as if they can’t be persuaded it was their own freely made choice.
I think of this as Slag Lag = we allow the r=types, naturally culled, to flourish under maladaptive conditions. Their surviving inferior genes drag the rest of us down, including financially and socially (extra taxes to pay for low IQ Timmy) and the novel selection pressures are applied to the quality e.g. higher education, more childcare cost.
mean girls regina george that's really interesting sarcasm