Covid male sterility papers + HPV, herpes

as previously discussed:

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

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

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

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

IN ADDITION TO-

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

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

RECONCILE ABOVE WITH

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

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

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

and they wanna force all young men to get it

college age men too

and all young women

when other papers cite it might act like an STD?

Huh.

Highlight:

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

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

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

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

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

or :-

Do the jabs cause inflammation?

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

BUT WAIT. THERE’S MORE.

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

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

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

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

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

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

ModRNA has owners. Repossession is plausible, legally.

STD angle:

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

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

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

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

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

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

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

We have our mechanism for sterility, people.

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

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

Like a remote control, for your balls.

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

SPERMATOGENIC FAILURE

and onward

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

Could COVID-19 have an impact on male fertility?

duh

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

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

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

oddly recommended with covid papers?

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

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

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

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

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

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

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

so women may be the red herring here

ACE2 and fat study, so expect fatty side effects

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

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

Impact of COVID-19 and other viruses on reproductive health

They admit the male HPV link I posted about previously.

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

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

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

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

wait wait wait the wild virus replicates its RNA too?

minor flex –

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

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

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

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

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

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

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

DS: MRAs: crickets

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

DS: suffer or die? Binary?

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

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

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

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

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

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

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

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

Y NO DO THIS ON JABBEES?

And it may kill pregnant women only:

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

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

Then why jab them?

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

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

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

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

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

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

re the endo treatment


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

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

COVID, sperm infertility and STD potential

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

TLDR: scroll to end

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

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

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

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

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

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

If only someone warned you.

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

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

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

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

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

to put it in terms you degenerates can understand

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

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

now I am fucking with you yes indeedy do

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

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

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

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

From top paper:

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

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

Big Pharma Balls? Mutant metaplasia.

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

How many times must I try to save your nuts?

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

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

Why did you think they wanted to inject college kids?

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

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

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

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

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

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

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

…Shut down Tinder.

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

The sperm allergy vaccine and genocide by sterilisation

Missed this nugget.

https://europepmc.org/article/PMC/PMC4345757

Provoking an allergic reaction to…. one’s own sperm?

Why do under-30s “need” anything, let alone a random new ‘vaccine’ with no ingredients list available?
https://pubmed.ncbi.nlm.nih.gov/12346214/

1995 evidence of precedent for deceptive vector of transmission, official contamination reportage and hence, UN contravention of genocide law established in the 1940s, section (d) and (c):

“PIP: A priest, president of Human Life International (HLI) based in Maryland, has asked Congress to investigate reports of women in some developing countries unknowingly receiving a tetanus vaccine laced with the anti-fertility drug human chorionic gonadotropin (hCG). If it is true, he wants Congress to publicly condemn the mass vaccinations and to cut off funding to UN agencies and other involved organizations. The natural hormone hCG is needed to maintain pregnancy. The hormone would produce antibodies against hCG to prevent pregnancy. In the fall of 1994, the Pro Life Committee of Mexico was suspicious of the protocols for the tetanus toxoid campaign because they excluded all males and children and called for multiple injections of the vaccine in only women of reproductive age. Yet, one injection provides protection for at least 10 years. The Committee had vials of the tetanus vaccine analyzed for hCG. It informed HLI about the tetanus toxoid vaccine. HLI then told its World Council members and HLI affiliates in more than 60 countries. Similar tetanus vaccines laced with hCG have been uncovered in the Philippines and in Nicaragua. In addition to the World Health Organization (WHO), other organizations involved in the development of an anti-fertility vaccine using hCG include the UN Population Fund, the UN Development Programme, the World Bank, the Population Council, the Rockefeller Foundation, the US National Institute of Child Health and Human Development, the All India Institute of Medical Sciences, and Uppsala, Helsinki, and Ohio State universities. The priest objects that, if indeed the purpose of the mass vaccinations is to prevent pregnancies, women are uninformed, unsuspecting, and unconsenting victims.”

UNCONSENTING VICTIMS

https://pubmed.ncbi.nlm.nih.gov/2665354/

“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 experimentation in animals and toxicology studies. Research to identify sperm antigens for incorporation into second generation vaccines is in progress.”

Control, like farm animals. Single injection for castration of male animals possible.

Look forward to the “drop of testosterone levels”. At least you got to drink some bitch tits beer with the ‘boys’. Don’t come crying to me. You wanted to be ‘male animals’.

The wages of sin – HPV in men and sperm infertility

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

TLDR – NOT HARMLESS

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

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

-increased miscarriage rate, lower odds of conceiving

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

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

Yes, this is a dealbreaker to sane women.

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

No abstract available

irony

MRAs: crickets

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

Human papillomavirus infection and fertility alteration: a systematic review

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

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

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

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

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

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

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

The role of human papillomavirus on sperm function

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

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

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

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

-only? a? 100% is a percentage too…

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

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

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

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

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

– no hurt their feefees? NAW

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

– Manosphere fears this topic and all male degenerate accountability.

semen infection may cause infertility and early miscarriage

it’s the sins of the FATHER, you see…

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

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

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

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

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

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

TLDR: yes.

HPV is commonly present in semen samples. 

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

The overall rate of HPV positivity was 15.5%

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

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

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

It’s worse for the older men.

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

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

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

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

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

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

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

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

what a mystery

The mechanism of ASA cause male infertility is not clear

does it look like HPV?

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

yes

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

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

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

duh?

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

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

-what r the odds?

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

Medicine can’t spare you.

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

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

 Fifteen samples

-aka HALF

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

no muh scientism and IVF cope

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

-may, LOL

a negative effect on development of the fetus

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

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

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

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

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

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

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

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

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

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

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

brace yourselves

guess the result

c’mon

go on
think

just guess

….

ready?

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

and all fertile men were HPV-negative

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

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

Player burnout shall henceforth be dubbed HPV-driven infertility?

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

2021

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

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

-maybe where you live

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

-well the husbands are freshly infecting the wives so

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

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

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

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

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

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

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

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

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

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

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

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

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

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

dat p-value

MORE STUDIES

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

Sperm DNA fragmentation in couples with unexplained recurrent spontaneous abortions

(((((“”unexplained“”)))))

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

– idiopathic? Are you shitting me?

(((idiopathic)))

sure it is

sure

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

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

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

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

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

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

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

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

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

I mean – where are the STUDIES?!

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

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

unexplained….. sigh, ok.

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

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

Known for 20 years.

Human sperm deoxyribonucleic acid fragmentation by specific types of papillomavirus

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

CAUSED

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

-swimming in circles isn’t motility, really

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

it’s a viral abortion, really

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

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

i.e. no, you won’t just get IVF

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

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

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

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

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

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

-all trust the EU guys

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

-somebody else look up herpes, I’m lazy

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

-Really, f-ing fascinating!

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

>male fertility disorders

k.

Oh, I’m not done yet.

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

HPV infection in semen: results from a new molecular approach

Let’s get molecular.

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

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

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

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

Your superpower is probably autism.

MSM push on male impotence and normalization of mutation

Studies are in their description, duplicated below.

Reminder: ED is the PC term for impotence – and a common side effect of porn addiction.
How about studying penis size between promiscuous men and chaste ones? They’d never publish it. I’d read it. Why are we not funding this?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1280349/

Decrease in Anogenital Distance among Male Infants with Prenatal Phthalate Exposure

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937858/

Prenatal Exposure to Phthalates and Anogenital Distance in Male Infants from a Low-Exposed Danish Cohort (2010–2012)

https://pubmed.ncbi.nlm.nih.gov/26672060/

Prenatal Exposure to Phthalates and Anogenital Distance in Male Infants from a Low-Exposed Danish Cohort (2010-2012) – same?

https://pubmed.ncbi.nlm.nih.gov/25697839/

First trimester phthalate exposure and anogenital distance in newborns

https://pubmed.ncbi.nlm.nih.gov/16466537/

Possible impact of phthalates on infant reproductive health

https://pubmed.ncbi.nlm.nih.gov/25353625/

Prenatal phthalate exposures and anogenital distance in Swedish boys

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7437820/

Endocrine-disrupting chemicals: implications for human health

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7483495/

The Endocrine Disruption of Prenatal Phthalate Exposure in Mother and Offspring

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7652773/

Phthalates in the diet of Mexican children of school age. Risk analysis

https://pubmed.ncbi.nlm.nih.gov/30677661/

The role of exposure to phthalates in variations of anogenital distance: A systematic review and meta-analysis

Environmental chemicals such as phthalate esters may have adverse effects on anogenital distance (AGD), but the evidence in both genders has not been reviewed systematically. The objective of the present study is to conduct a systematic review and meta-analysis of studies that analyzed the relationship between exposure to phthalates and AGD. English papers published up to March 2018 were searched in PubMed, Scopus, Clarivate-Web of Science, and Google scholar. We applied fixed-effects models to calculate pooled beta coefficient [β]. In the case of heterogeneity, random-effects models were used. Using the comprehensive search strategies, 313 papers were identified and after screening, 10 of them were included in this study. In primary analyses, we found that exposure to phthalates was not associated with short AGD (β = -0.11; 95% CI, -0.27, 0.06; I2 = 0%). However, results of subgroup analyses indicated that in boys, the sum of di-2-ethylhexyl phthalate (∑DEHP) metabolites had significant association with the risk of shortened anopenile distance (AGDAP) (β = -0.915, 95% CI: 1.629, -0.2) and anoscrotal distance (AGDAS) (β = -0.857, 95% CI: 1.455, -0.26). In addition, urinary monobutyl phthalate (MBP), monoethyl phthalate (MEP), and monoisobutyl phthalate (MiBP) were associated with short AGDAP. We also observed significant association between monobenzylphthalate (MBzP) and anofourchette distance (AGDAF) in girls. Our study provided findings on significant association of exposure to ∑DEHP metabolites, MBP, MEP, and MiBP with shortened AGDAP in boys. The mechanisms of phthalates effect on AGD may involve receptors and enzymes involved in steroidgenesis, negative influence on Leydig cells, cell proliferation, gonocyte cell numbers, and testosterone production.

CBD oil push is anti-white, anti-natal, harmful

I have to post this now because the product push is in full swing and it could literally save tiny lives.

I can’t wait until October, all the “influencers” are pushing this online NOW. Ethically, I must put my ego aside.

https://www.sciencedaily.com/releases/2007/05/070524145037.htm
A lot of Pill failures are actually in the hippy chicks taking plant “extracts”. That’s why doctors now ask young women about supplements and herbal remedies immediately after the contraception question. It wouldn’t be ethical to study pill failures but they know there’s a link.

so in context:
How Smoking Marijuana Damages The Fetal Brain” is horrifying.
“Earlier studies have already found that children of marijuana-smoking mothers more frequently suffer from permanent cognitive deficits, concentration disorders, hyperactivity, and impaired social interactions than non-exposed children of the same age and social background.”

so you cannot blame poverty, Karen.

Remember, they’re now encouraging wine moms to drink while pregnant.
They used to claim nicotine was a “safe” plant extract because the addictive property was removed, supposedly.
https://medicalxpress.com/news/2019-11-cbd-thc-early-pregnancy-disrupt.html
“CBD, THC use during early pregnancy can disrupt fetal development”
Nicotine was justified as anti-inflammatory too, and it is:
https://pubmed.ncbi.nlm.nih.gov/15500638/
Still addictive!


Weird how all these CBD products were pushed before safety studies like this, and now we have corona-chan distracting.
A new study published in Scientific Reports, a Nature Research journal, shows how a one-time exposure during early pregnancy to cannabinoids (CBs) – both synthetic and natural—can cause growth issues in a developing embryo. This is the first research to show such a connection in mammals.”
One-time. But not a drug, ya see. That makes sense.

It’s the first research to LOOK. Why was this cleared? And who calls CBD safe? Oh…. the WHO.

https://www.forbes.com/sites/janetwburns/2018/03/18/who-report-finds-no-public-health-risks-abuse-potential-for-cbd/

Let’s trust those guys!

“muh no public health risks”

Buckle up, I found a LOT.

“In this study, the brain and facial developmental effects caused by one-time exposure to CBs—CBD and THC (the primary ingredients of marijuana)—are very similar to what is seen in fetal alcohol syndrome (FAS). Parnell and colleagues also found that when CBs and alcohol were used together, the likelihood of these birth defects more than doubled. They went on to show that these drugs may be causing defects by interacting on a basic cellular level and disrupting signaling between molecules and cells that control growth and development.”
“The CBD amounts administered were within what is considered a therapeutic range for humans.”

trans. minimal.

“It is concerning how little we know about the use of marijuana, its CBs, and products like CBD oil during pregnancy,” Parnell said. “We know that there is no safe period to drink alcohol during a pregnancy, and I think this research shows the same is likely true of marijuana use.”

Drinking once doesn’t cause FAS, so this is objectively worse. Don’t expect the tradlarpers to talk about anything important re child IQ and birth rates. Nope! Let’s talk about some twit on Twitter again.
I don’t care if you like your CBD rollerball, Karen! You’re better off aborting it now it’s brain damaged!

If you want to de-stress take a poxy bubble bath like a non-druggy.

I expect it causes more miscarriage too, with that effect.

With the results of these one-time exposures, Parnell and Fish are planning to now test smaller, multiple exposures throughout a pregnancy that better mimics real-life usage in human pregnancy.”

That came out after this:
https://medicalxpress.com/news/2019-10-women-health-assume-cbd-safe.html

“That’s concerning because CBD may interact with commonly used anesthetics that might be needed during labor and delivery.”

That’s because it’s a drug. It is a drug.

https://www.healthline.com/health-news/children-cannabis-impairs-fetal-brain-development-012814#1

https://www.therecoveryvillage.com/cbd-addiction/cbd-while-pregnant/

“Many women report that they use CBD oil during pregnancy in order to reduce pregnancy-related nausea.

In general, using CBD while one is pregnant is thought to be safer than smoking cannabis itself or THC-rich products.” [DS: we now know this is wrong, see above]

The hippy Karens must be stopped.

I bet it damages sperm too. That’s all the soy boys need.

There is a lack of conclusive data to determine the effects of CBD hemp oil on a fetus. However, it is known that a growing fetus is equipped with an endocannabinoid system, even when the fetus is only composed of two cells. This system is in all humans and even some animals. The endocannabinoid system is a system composed of endocannabinoids, which are neurotransmitters that bind to cannabinoid receptors.

In a study conducted on mouse embryos, researchers found that the compound THC inhibited the development of the embryos which contained less than eight cells. Another natural cannabinoid found in the human body, anandamide, also stopped the embryos from developing. CBD can increase levels of anandamide, so there may be negative effects associated with CBD use during pregnancy. It is important to note that this was a study conducted on mice and the results may not be transferable to human subjects.

If you’re gonna be a Western baby birth rate cult, talk about things like this.

The advice to women must account for this.

https://www.linkedin.com/pulse/does-cbd-oil-cause-brain-damage-dr-daniel-amen/
It’s called dope for a reason.

“marijuana causes significant brain changes by slowing activity in the frontal and temporal lobes”

there’s a known connection to schizophrenia in men, especially those who start before 21, earlier in the teens the higher the risk

“Some argue that marijuana is not addictive, but as it demonstrates, it is a drug like any other.”

I knew this so I had to post.

Alcohol is a drug and it is addictive (alcoholism is an addiction to alcohol, not mere consumption, it’s a pattern of chronic consumption with withdrawal during cessation). As soon as they call their poison “not addictive”, you know it is. It’s like hearing “I can quit any time I want”. Cognitive dissonance, a month of cessation would be intolerable for them.

http://www.j-alz.com/content/new-study-shows-marijuana-users-have-low-blood-flow-brain

re above study:

after studying imaging of 1,000 cannabis users’ brains, there were signs of noticeable deficiencies of blood flow. The study, which included 25,168 non-cannabis users, and 100 healthy controls, shows a scary and obvious difference in blood flow levels for those that used cannabis. Additionally, those that used marijuana showed a significant lack of blood flow in the right hippocampus, the area of the brain that helps with memory formation. This part of the brain is severely affected with those that suffer from Alzheimer’s disease.”

“Our research has proven that marijuana users have lower cerebral blood flow than non-users.”

You also see sluggish cerebral flow in the low IQ. That’s why they call it dope. It has a dopifying effect.
https://ashpublications.org/blood/article/108/1/379/133554/Inverse-correlation-between-cerebral-blood-flow
Stupidity is bliss? It’s diagnostic.

We identified a strong inverse relationship between performance IQ and CBF (-1.5 points per 10 mL/100 g/min increase in CBF, P = .013).”

CBF = cerebral blood flow

I’m not making shit up. If a perma-bachelor over the age of 25 (mature brain) wants to be a druggy, I don’t care. But don’t kill and brain damage the babies!

This has a lot of studies linked: https://www.solcbd.com/blogs/news/cbd-oil-and-fertility-have-facts

In a 2010 Italian paper published online by BioMed Central, the authors argue that disrupting the normal activities of these ECS pathways by adding cannabinoids “can significantly alter many vital in utero processes, including angiogenesis, cellular replication, tissue differentiation, and [fetal] neural cognitive development.” [4] ….

While THC exposure increased sexual receptivity in female hamsters and rats, it also inhibited their release of luteinizing hormones. These hormones are responsible for ovulation and the development of the corpus luteum. The latter is a hormone-secreting structure in the ovary that plays a role during very early pregnancy. [3]

3= https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4034092/

They’re pushing CBD products as harmless and trendy onto MINORS.

https://www.teenvogue.com/story/cbd-beauty-products

https://www.teenvogue.com/gallery/a-shopping-guide-to-cbd-beauty-products

https://www.teenvogue.com/story/charlotte-figi-teenage-cbd-reform-icon-fears-covid-19-death

https://www.teenvogue.com/story/marijuana-myths

https://www.vogue.com/article/vertly-lip-balm-best-cannabis-beauty-products-cbd-thc-claudia-mata

https://www.adweek.com/brand-marketing/e-l-f-s-chipotle-collaboration-and-new-cbd-line-fend-off-pandemic-blues/

Aimed at minors.

It inhibits development. Do the math. I couldn’t wait on this. I was going to post this last year but forgot.

In a 2016 paper published by BioMed Central, it is mentioned that in utero exposure to cannabis has been associated with early pregnancy failure, birth defects, and developmental delays in the fetus.

source?

close:

https://www.nature.com/articles/pr201125

“The results of this study show that the use of cannabis in pregnancy is associated with increased risk of adverse birth outcomes. Prevention programs that address cannabis use during pregnancy are needed.”

I think this is the one: https://bmcpharmacoltoxicol.biomedcentral.com/track/pdf/10.1186/s40360-016-0085-6?site=bmcpharmacoltoxicol.biomedcentral.com

“With the increasing publicity of marijuana due to recent legislation, it is pertinent that the effects of fetal exposure
to the drug are assessed. While in utero cannabis exposure has been associated with early pregnancy failure, birth defects and developmental delay, the mechanisms of such outcomes are largely unexplained. Furthermore, the use of cannabinoids in cancer treatment via growth inhibition and apoptosis may indicate how cannabis exposure likely harms a growing fetus. Cannabinoid signaling is required for proper pre-implantation development, embryo transport to the uterus, and uterine receptivity during implantation. In post-implantation development, cannabinoid signaling functions in a multitude of pathways, including, but not limited to, folic acid, VEGF, PCNA, MAPK/ERK, and BDNF. Disrupting the normal activity of these pathways can significantly alter many vital in utero processes, including angiogenesis, cellular replication, tissue differentiation, and neural cognitive development. This paper aims to demonstrate the effects of cannabis exposure on a developing embryo in order to provide a molecular explanation for the adverse outcomes associated with cannabis use during pregnancy.”

The authors also argue that cannabis exposure could very likely harm a fetus due to phytocannabinoids’ effect on cells. This is because CBD and other cannabinoids are associated with cell growth inhibition and cell death, which may be good news for the treatment of cancer, but not for a growing fetus. [4]

4 =

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041313/

These findings were based on petri dish research, but the same trend was observed in most cell cultures, not just in cancer cells. Obviously, this could mean that healthy cell growth can also be affected. [5]

5 =

https://www.sciencedirect.com/science/article/pii/S0002937813008284

This is speculative, however, and not an easy subject to study clinically, but it is clear that much more research is needed before any phytocannabinoid can be declared safe for use by pregnant women.

Men:

There appears to be no traceable data regarding CBD and male fertility. The available research centers mostly on marijuana and fertility in males, and it is mostly negative, except for one finding.

How are these products on the market? HOW?

It feels like a DDT style case study waiting to happen.

This research, conducted by Dr. Hans Hatt of Ruhr University in Bochum, Germany, has discovered a receptor in sperm cells that is part of the ECS.

Called the GPR18 receptor, it plays a big role in conception. Dr. Hatt explains its function very simply: “The endocannabinoid activates the spermatozoa for fertilization.” This means that it helps the sperm to fertilize the egg or the ova.

The doctor also pointed out that this receptor responds to THC and another cannabinoid, anandamide, with involvement in the sperm’s ability to penetrate the ova. This is encouraging news, but much more study is needed before phytocannabinoids can be considered a possible therapy for male infertility. [6]

This is also because other research points in the opposite direction for men.

Birth defects suggest it messes with the sperm’s genetics.

And it does.

https://www.ncbi.nlm.nih.gov/pubmed/26283092

A total of 1,215 young Danish men aged 18-28 years were recruited between 2008 and 2012 when they attended a compulsory medical examination to determine their fitness for military service. The participants delivered a semen sample, had a blood sample drawn, and underwent a physical examination. They responded to questionnaires including information on marijuana and recreational drug use during the past 3 months (no use, use once per week or less, or use more than once per week). A total of 45% had smoked marijuana within the last 3 months. Regular marijuana smoking more than once per week was associated with a 28% (95% confidence interval (CI): -48, -1) lower sperm concentration and a 29% (95% CI: -46, -1) lower total sperm count after adjustment for confounders. The combined use of marijuana more than once per week and other recreational drugs reduced the sperm concentration by 52% (95% CI: -68, -27) and total sperm count by 55% (95% CI: -71, -31). Marijuana smokers had higher levels of testosterone within the same range as cigarette smokers. Our findings are of public interest as marijuana use is common and may be contributing to recent reports of poor semen quality.

I think we found a cause of generational infertility in men, suck up that red pill.

https://www.bbc.com/news/world-europe-45512312

IVF high in Denmark, wonder why?

Peak health by age and it still impairs their sperm….

https://www.theguardian.com/science/2017/jul/29/infertility-crisis-sperm-counts-halved

The cause is STDs and drugs, obviously. Always has been.

Men are lied to and the SJWs love it.

https://www.newscientist.com/article/mg23631522-900-fertile-territory-for-change/

From the sol link:

The inability to conceive affects both men and women equally. Among couples experiencing infertility, roughly 35 percent is due to problems in the male, while another 35 percent is due to issues in the female. Another 20 percent is a combination of issues in both the male and the female, and the remaining 10 percent is unknown.

Apart from CBD oil for fertility, a number of alternative or complementary therapies are on the rise, all with varying degrees of success.

They claim CBD is antidepressant despite cerebral flow connection to causing it. Gotta keep selling those SSRIs.

New Research Shows How Marijuana Drops Blood Flow to the Brain. Should You Be Concerned?

“demonstrates that marijuana can have significant negative effects on brain function. The media has given a general impression that marijuana is a safe recreational drug, this research directly challenges that notion.”

Beware anything the MSM pushes. What do druggies do? Sit around watching TV and consuming other ‘entertainment’ like Netflix.
It’s a known scandal that American farms of it are basically a monopoly.
If the effect is anti-stress, it’s a drug. If that’s the only purpose, drink tea. Put on a nicotine patch.
They never explain fully the biological mechanism that makes it work like a drug, without literally being a drug.
https://en.wikipedia.org/wiki/Sublingual_administration
The dropper form of CBD is literally a drug, drops are used in pediatrics on babies. It’s sublingual absorption. If it’s ‘extracted’ from a drug, works like a drug and is delivered like a drug… it’s a drug.
Should adults be allowed to be druggies? Over 25, maybe. But why must I pay for stressed-out Karen’s “treatments” on the NHS? Must I pay for her alcohol too? Can she pay for my naps and chocolate?
Why not legalise morphine and laudanum and all the other naughties you used to buy over the counter before the nanny state?
Because people would grow their own poppies. That’s why. It’s too easy to extract.

The method was flawless, before AND after.

“Several studies of perfusion imaging in marijuana users have shown similar results compared to ours. A small O15 PET study in a sample of 12 marijuana users used a randomized clinical trial design to examine brain perfusion before and after marijuana use. The study results found frontal, temporal and occipital lobe hypo-perfusion – all findings concordant with our study.

Zoomers aren’t stupid, they’re polluted.

Although it is often portrayed as harmless, and sometimes even therapeutic, there has not been nearly enough studies done to prove this. In fact, marijuana is often prescribed for issues like anxiety, though studies cannot comprehensively show this to be true. Currently, the available information on the impact marijuana has on the neurophysiology of the brain show, predominantly, depressive effects.”

It’s pushed on women to harm their fetus. Skin cream lingers for hours and ends up in the blood.

Darwin Awards global finale

me watching the weebs trapped in Asia and the stock bros during circuit breakers

Nobody’s laughing at the preppers anymore and they’re fast reckoning that it’s an actual skillset taking years to develop instead of buying 500 toilet rolls like a hoarding normie.

Nobody’s calling me racist for righteously hating China and Communism, which is nice.

All in all, I’m pleased as punch. I hope it gets worse so we skip a repeat (pandemics repeat if the first case is mild). It’s the first thing to wake up the middle-class cucks that open borders can and shall hurt them. No holiday to Italy now, Karen!

Pandemics always hit the sluts hardest.

repost link; https://www.medrxiv.org/content/10.1101/2020.02.12.20022418v1.full.pdf

“From the paper: “The protein and mRNA expression of ACE2 in the testes is almost the highest in the body. Moreover, both cells inseminiferous ducts and Leydig cells showed high ACE2 expression level. These results indicate that testicular cells are the potential targets of 2019-nCoV.

The bioweapon’s coming for yar balls.

We believe in you, Corona-Chan! Sterilise the Commies! Sterilise them all!

https://www.ncbi.nlm.nih.gov/pubmed/20449780

Orchitis and male infertility

Infections and inflammations of the genital tract are considered the most frequent causes of reduced male fertility, but conclusive epidemiological data are not available. In view of the exposure of germ cells to pathogenic components as well as the cells and mediators involved in the inflammatory processes, irreversible damage to spermatogenesis and corresponding decline of ejaculate quality are to be expected, particularly in cases of chronic orchitis. While the consequences of orchitis and epididymo-orchitis that exhibit clinical symptoms due to systemic or local infections are well known, including testicular atrophy and complete loss of fertility, those cases of inflammatory reactions of the testicles that manifest an asymptomatic or subclinical course, or are not even due to an infection, have received little attention until now. However, systematic histopathological analyses have shown a high prevalence of asymptomatic inflammatory reactions in testicular biopsies from infertile men. The mostly focal lymphocytic infiltrates correlate with the degree of damage to spermatogenesis and corresponding clinical and endocrinological parameters of testicular function. Noninvasive diagnostic techniques are not yet available so that chronic asymptomatic inflammations of the testicles as the primary cause or cofactor of male fertility disorders are underestimated. Except for administration of pathogen-specific antibiotics, treatment recommendations are to a large extent still lacking.

Slutty men make themselves infertile with repeat infections. Even with antibiotics, it inflames the area and eventually it just… shuts down. The male reproductive set is external because it’s fragile. God hates sluts. ‘Sowing your oats’ is Satan rhetoric, dear. Scientism won’t save you.

Some thots are still going shopping in person in London.

It’s called the internet, bitch!

Spoiled rich pricks are complaining they were corona-cancelled.

I don’t think anyone’s told them no before. GOOD.

BE OFFENDED. Pandemics are marvelously impersonal.

Most of all, I was 100%, totally completely right.

and now I can be a cunt reminding everyone for the next ten years.

I wonder if tranny girls will stop taking T because high T makes viruses worse?

The problem with meditation rituals +IQ

Not meditation as in thought, contemplation but the Indian-seeming ritual.

Not yoga, which is a made-up substitute religion sold to Boomers, I already linked about that (it was in the New Yorker too).

Skip to the end at the IQ bit if you don’t care about genetic load and IQ as a related tangent.

New Age meditation is for rich people to pretend they have problems. If they were spiritual at all, they’d quit their vices. They would see how vice harms them and their soul. They connect with nothing real. It’s a hallucination projected on their bubble.
Meditation as it’s sold in the West is an opiate for idiots, they’re already mindless drones of conformity. As a form of prayer, it’s egocentric (muh Higher Self – do you mean Holy Spirit?). As a biological thing, Muh Scientism, it over-develops the parietal lobe (a bad thing, sloth ensues, fine if you’re a mountain man?) at the expense of the frontal lobe (a VERY bad thing, they’re crippling their critical thinking, humans need that rationality). An IQ study in fully developed adults who start meditation would be interesting, but they’d never be able to find a publisher* for the fact, with a good method, IQ would go down. Imagine all the products they couldn’t sell! The horror!

*Why you never hear the downsides of many antisocial practices, but meditation does reduce in-group loyalty, which “they” actually want (less genophilia, less love of your family where it should be, with your KIN). Phrased like that, the “love” rhetoric falls flat. If you cannot love your kin, you don’t love. Anyone.

Can Meditation Increase IQ?

Though no standardized test was developed as a result, the study interestingly demonstrated head size has almost nothing to do with intelligence.

True.

Also, women can have larger heads than men and the men who don’t get this… are morons.

IQ is simply a good method for representing intelligence in an individual, compared to the general population. IQ testing has its limits, but there is a reason for its sustained and wide acceptance in psychology.

You have to act on your IQ. Bitching on reddit how “misunderstood” you are is worse than being average.

Genuine intelligence does seek out truth though, not just info to show off.

The biggest contributors, such as…

  • Genetics
  • Conditions in utero
  • Experiences at a very young age

…were never much under our control.

Yes, an individual’s IQ score can vary mildly throughout life, and more can almost always be learned, but there is simply very little evidence that intelligence itself can be increased over time.

It can’t. Anyone who says otherwise is selling you something. Most of it’s genetic.

Attention gains are often just using the idiot-phone less and avoiding EMF.

Think about it – where do they meditate? Low EMF areas. What don’t they do? Check their phone every five minutes. It isn’t the ritual. Put down the Apple products.

So wherever you are in the distribution, whether or not you’ve even taken an IQ test, is where you’ve been from a young age and where you will stay.

It’s a big pill to swallow.

That’s the main red pill. Most men in particular refute this and become full-blown sociologists (sociologist fallacy) going on and on about nurture-theories. Noooope.

DNA is destiny, dude.

Plus, logically, if your score were already high… you wouldn’t feel a need to increase it?

Hey, I’m just being rational, pretty sure that’s illegal. As a woman.

A study published by Dan Simons and colleagues looked at these brain training games, and only found:

  • Strong evidence of subjects improving in the trained tasks themselves. Meaning, the more they played the game, the better they got at the game.
  • Less evidence that subjects had improved performance at closely-related tasks.
  • Little evidence that the subjects increased performance on distant-related tasks (anything outside the game, in the real world) or enhanced their everyday cognition in general (meaning, no raise in IQ).

Let them profit off idiots. By going for that IQ boost stuff, you’re admitting you’re low IQ already.

http://journals.sagepub.com/doi/abs/10.1177/1529100616661983

It’s like men who take dating advice from other men, especially bachelors. At least talk to really old, happily married men? But noooooo. Or since the sexes are mentally different, talk to women about how they assess men to become the best competitor (and other men ARE your competition). …And they wonder why they attract angry, manjaw women – because they’re vibing with what another man told them.

Men also tend to give one another terrible advice, consciously or subconsciously to scupper competition. Rarely even trust relatives, same fact sadly holds with women.

Money shot:

Meditation can’t increase intelligence because there is little evidence intelligence can be increased by anything at all.

That’s it, that’s the fact.

ANYTHING. AT ALL.

Stop looking.

However, meditation can help you increase your IQ score by sharpening your mind and maximizing your ability to focus.

No such thing. Marketing gimmick you cannot measure (see study above, no real results, self-report is crap). ADD is also bullshit, it’s the new dyslexia (as Spectator leaked) for describing low IQ offspring to narcissistic parents who also refused to discipline their brain as babies and toddlers (easy to spot, the baby holding an iPad). You cannot have an attention deficit, that would make you a vegetable, in a COMA. It’s an alternative state of consciousness like anesthesia, which literally winds down your attention to a deficit aka below consciousness (it can be measured by EEG). They literally give the kids amphetamines, club drugs, because a key sign of low IQ in kids is low energy, listlessness, ennui (side effect arrogant atheism), later called “failure to thrive” (as spiteful mutants) since the mutation load doesn’t process for energy in the body effectively. Think about it – they’re only slow, compared to the genetically healthy norm of age peers. Again, their genetic inferiority -compared to the norm population of the parents requires them to take SPEED.

What is the Amphetamine Speed?

“The amphetamine speed is actually a “slang” name for the entire class of drugs known as amphetamines. All amphetamines, whether legal or illegal, activate chemical processes throughout the brain and body and so “speed up” most every bodily function.”

They have degenerated that far down. The drug category of speed. Why would energy level drugs “help” unless the root issue is genetic?

esp when the effects inc.

  • Loss of interest in sex
  • Impotence
  • Restlessness
  • Irritability
  • Agitation

Adderall

Impotence and no libido is great for depopulation efforts. But they want the low IQ to be productive workers for the companies.

But isn’t a supposed symptom of ADHD already the last three?

Yeah, don’t expect logic. Low IQ people often self-medicate with drugs anyway. It’s the dirty little secret of drug addicts. They often lack the full frontal lobe function for impulse control. Making it legal makes them worse, it enables them.

How can we tell it’s genetic? Look for a paternal age effect. All fathers biologically contribute is DNA.

https://www.cbsnews.com/news/aging-dads-more-likely-to-have-kids-with-autism-adhd-schizophrenia-and-more/

ding ding ding

Researchers examined all births that happened in Sweden between 1973 and 2001, and found a child born to a 45-year-old dad was 25 times more likely to have bipolar disorder, 13 times more likely to have ADHD, 3.5 times more likely to have autism, 2.5 times more likely to exhibit suicidal behavior or a substance abuse problem, and twice as likely to have a psychotic disorder like schizophrenia when compared to kids born to a 24-year-old father.

13x more likely past middle age

13, men have a right to be told this stuff in Sex Ed, family planning is important

and yes paternal is a bigger risk:

https://www.cbsnews.com/news/older-dads-may-increase-childs-health-risks-more-than-older-moms/

the real QED? missing link:

https://www.webmd.com/baby/news/20090309/older-fathers-lower-iq-in-kids#1

Children born to older fathers don’t perform as well on tests of thinking skills during infancy and early childhood, while those born to older mothers have higher scores on the same tests, a study shows.

Ouch.

It’s like how single parent fathers also have kids with crap outcomes and test scores. The manosphere is in serious, life-ruining denial. Any single parent is a crap-shoot. Men have a right to know this young, to prepare.

The reason for this discrepancy is simple and evolutionary.

In fathers, early breeding (20s) is a sign he can mature faster than peers and lock down a quality woman earlier. He’s just a better man. Sorry.

Society shouldn’t enable dysgenic men to breed at all, especially in the teens. Also, sorry. But social policy matters here.

Women settle earlier, the lazier they are (dysgenic, r-select) from less discernment, the feminine trait. High IQ women complete education first, before assortative mating with a man in their class and general IQ band (eugenic, K). Child IQ maps most onto maternal IQ, as previously linked about if you search. The mother is the one raising it, don’t choose a bimbo. Also, her DNA having a high mutation load in utero will hamper the kid’s IQ regardless of the father. You’ll note in men with more than one wife, the kids with the wife who settled later are smarter, she’s more feminine and discerning. Women prepare for marriage and kids too. You need a woman who isn’t just a breeding sow. A woman who takes kids seriously and wants them, not a meal ticket. Avoid the Meghans.

McGrath’s team analyzed data from a large study called the U.S. Collaborative Perinatal Project, which recruited pregnant women from 12 sites in the U.S. from 1959 to 1965. The data from this ongoing project has been a “treasure trove” for researchers, McGrath says.

His team looked at more than 33,000 children born between 1959 and 1965 and then looked at their results on cognitive tests administered at ages 8 months, 4 years, and 7 years. The tests evaluated the children’s ability to think and reason, measuring such skills as concentration, learning, speaking, reading, arithmetic, memory, and motor skills such as coordination.

Finally, they looked for links with the father’s age, the mother’s age, and in one analysis also adjusted for socioeconomic factors such as family income and parental education.

The average age of the fathers in the study was 28.4 and ranged from 14 to 66. The mother’s average age was 24.8 and ranged from 12 to 48.

same average as the middle ages

In recent years, according to the paper, it has become very common for couples to delay having children until their late 30s.

They’re falsely told it makes the kids smarter, only in the case of good genetics (and so higher natural IQ), solid education before (no Marxism) and only the woman (who can then raise the kid better). Men constantly regenerate gametes so mutate in a compounding way. Their DNA becomes more mutated with age. Eventually it’ll be seen as child abuse to delay on purpose too long (when you already found the right person and have your health). Women are born with most of our eggs for this reason, to maintain the species. What’s eugenic in a woman is dysgenic in a man, the sexes are opposites! This gives men incentives to improve his tribe. Nature doesn’t hate you, it’s a challenge and men are failing by assuming they’re like women.

The older the father, the more likely the child was to score lower on the tests, except for one measure of motor skills.

When they looked at the mother’s age, however, they found that the older the mother, the higher the children scored on the thinking skills tests. (That finding, reported in earlier studies as well, may be due to a more nurturing home environment if the mother is older, but this study suggests children of older fathers don’t reap the same benefit.)

I love how they try to nurture it away. Nope. It’s biological mainly.

However, when the researchers adjusted for such factors as the parents’ socioeconomic status, including income and education, it modified the effect of both parents’ ages on the intelligence tests. For instance, the average score on the Stanford Binet Intelligence Scale was nearly 6 points lower for children born to fathers age 50 compared to those born to fathers age 20. But when the socioeconomic factors were taken into account, the difference dropped to 2.2 points.

Incentives for high IQ men. Only low IQ men complain about fitness tests.

While the study findings may suggest the best combination of parents is an older woman with a younger man, McGrath says it’s too early to make any specific recommendations.

Suuuuure, PC liar. Protect those feels at all costs! Baby-killers.

They don’t mean by much, a few years, but modern men commonly lack any maturity to have a commitment in their twenties. I have noticed a trend of older women (5,10 years) settling with younger men, though. They also seem oddly fertile? The birth rate cult must take serious note of this. Older men regret not freezing their sperm but the egg freezing jokes are misplaced. Gametes degrade vastly faster in men. Sorry, you’re not like women?

If you really care about fixing sub-replacement fertility, look at what the data says is ideal and not your ego.

What’s behind the link between older fathers and lower IQ? “There is a growing body of evidence suggesting that the sperm of older dads develop more mutations, that is, spelling mistakes in the DNA code,” McGrath says. His team is researching this idea further in animal studies comparing young mice with older ones.

ding ding ding genetic load

Their train of thought is the same as mine.

They’re avoiding getting this out in case more men take paternity leave they don’t deserve (since men can’t give birth and have nothing to recover from medically). They’ll tiptoe around old guy’s feels about impotence even if it gives their eventual, panic spawn a low IQ and bipolar disorder. Don’t pin your hopes on having grandkids in that case, what a waste.

They don’t wanna get sued, so they won’t tell men how serious this is. Better have no kids than invest in a sickly one and have no grandkids. But Big Pharma doesn’t like that.

We have known about the paternal age effect for many years,” says Harry Fisch, MD, director of the Male Reproductive Center and director of urologic microsurgery at Columbia University Medical Center of New York Presbyterian Hospital. Yet, he says, “We are just starting to scratch the surface.”

Testosterone levels begin to decline slowly at age 30, Fisch says. Ideally, men should father children “sooner rather than later,” he says.

No, supplements aren’t bio-available the way real T is. Your DNA is still being damaged.

“The 20s and early 30s are ideal, but real life intervenes,” he says, making that time frame not feasible due to lack of a partner, difficulty getting pregnant, financial restraints, or a host of other factors.

Fix the economy so high IQ men can settle in their 20s. Stop forcing them to fund the kids of the feckless men.

That’ll sort sub-replacement fertility AND the spiteful mutants won’t bother anyway. People are not genetically equal. Spiteful mutants actually think they can have kids and avoid being a parent. You can’t just hand the kid to the mother 100% and act like a bachelor. Then the kids won’t give you grandkids out of actual spite, as happens to narcissistic parents. Abandonment is abuse, and that includes Don Draper careerism.

In a perspective on the study, published in the same issue of PLoS Medicine, Mary Cannon, MD, of the Royal College of Surgeons in Dublin, Ireland, says it is important to take socioeconomic factors into account when looking at the effect of a father’s age (as well as a mother’s).

IQ predicts SES so no. Shut up, Mary.

Men reap as they sow. They wanted to shirk patriarchy first. The ‘Sexual Revolution’ killed patriarchy in part by making it kill itself. Yes, waste your best sperm jacking it to porn, you’re free. Your sperm will be super potent for autism by the time you figure it out. Wait until they find out all those clubbing STDs make mutations more damaging.

Is it a coincidence the Boomers are the first generational product of ‘free love’? I think not. I have a pet theory the bad type of Boomer’s father picked up STDs during the war from brothels (men were enticed to attend by YKW) and warped their brain development by passing to the mother. The military won’t do that study.

Back to meditation.

The frontal lobe issues “muh concentration, et al.” are low IQ, from their heavy genetic load; the dumbness, the dense quality of them is a symptom of the IQ range. AKA being thick. Attention is filtered by your brain structure and informed by genetics.

from top:

It’s there at that maximum level of focus where you are the smartest you can possibly be. But unfortunately, neither meditation, or anything else, can increase where that limit is.

Denial of humanity is narcissism, denial of human limits. Pure egocentrism, spiritual bypassing for the ritualists.

It’s funny how both groups (New Agers and ADD/ADHD excuse-makers) are often also IQ denialists, while simultaneously wanting to ‘boost’ the thing they claim doesn’t exist? Deny mutation load, bitches. When we can test for it at birth, welcome to Gattaca. IQ tends to predict certain personality traits e.g. laziness, so people would actually be happier. Telling everyone we’re genetically equal makes the stupid miserable. They assume the system is against them, actually their parents.

Many relaxation symptoms of meditation rituals are just coping with a coffee addiction, mostly Starbucks, which they never drop. They love Starbucks more than any God. The breathing exercise kind isn’t meditation. It’s most commonly fighting a histamine, pesticide, GMO and/or mycotoxin response from a bad diet and sleep pattern. It’s suppressing your immune system from healing the damage. Like mega-dosing antioxidants means those free radicals can’t kill the cancer in you – so the cancer kills you. Stop trying to fix your biology, the train is fine.

They never mention that parietal/frontal issue but cranial space is at a premium, when one part grows, another is damaged and atrophies. When a person is stressed, they must address the causes in their life, rather than hoping for some genie to wing it for them. Opening your mind up invites all sorts of trauma and bad karma in, like opening your front door and leaving it unguarded overnight. Guard your heart, your mind and your soul. Cynically, the New Age people probably know what they’re doing, and they’re injuring the competition. Do not assume their sincerity. Most New Agers are deeply intellectually dishonest and they rip one another off all the time. A person who believes in moral absolutes and karma would never! Avoid the communal narcissists who are basically cult leaders. In another time they’d be leading witch trials for a girl who rejected them. If their object is material, that’s an abuse of the spiritual. Look at the vice in their personal life, where it cannot hide. Drink, drug, debauchery problems? They help no one, they are Will O Wisps guiding you to your own destruction. Siren songs are not a myth. They constantly travel, to hide from themselves? They seem weirdly lonely and depressed when not distracted by travel? Don’t take their life advice, they cannot be happy. The particular reasons for them don’t matter. Don’t let it be your problem. Spiteful mutants are nomads. They cannot settle – in a job, in a country, by marriage. They’ll search until they die.

Meditation amplifies your emotion, the way it’s packaged now to rich people will be interesting as they lose their fortunes. Especially Boomers, with no time to recoup or ability to compete in the Brave New Multicultural World they generally voted to import in. Sorry Boomer, you’re too white and male to be manager this time! Here’s your AA boss.

They haven’t tried it from a state of loss and deprivation, but a bubble of delusion and “I deserve this”. Meditating from any bad place, as a ritual, is like the surest way to become suicidal. New Agers know but never talk about this. If you ask around, people know this commonly but the topic gets banned or taken down. It’s ritualised rumination. Rumination is actively bad for your health (unless your health is already bad and you mistake normal for good).

That’s a cult indicator, forbidden bad experience discussion, it puts off new recruits.

They prefer to shame people for bad results, like that’s the first person it ever happened to.

(There’s drug abuse purging from the body years after the fact, a common cause of sudden health problems and ‘depression’ or ‘anxiety’ in celebrities. It takes years for drugs to fully leave all the organs. Who cares?)

Superstitious minds

Mini post. Kinda. Why is Benedict Cumberbatch so ugly?

No really. If we’re doing red pill observations, humour me.


I mentioned before about old world superstitions forgotten in recent years.
As recently as my parent’s generation, they considered ugly children the product of sin, that God was punishing their parents for their sin. You can still find this info around if you look but they rarely dive into it.

You could say it’s about STDs but back then people rarely travelled and slept around enough to frequently catch them. The modern microbiome of the slut is more taxed. So what?

Back to the school mocking. If a child had always married parents but became ugly in the teens, questions would be asked openly and they would get teased about whether one or both parents had ever cheated. This is where we get the term bastard. It isn’t actually about bastards, it’s about ugliness. The ugliness of parental deceit.

You can pretty much tell when there’s a birth defect in a baby, the eyes look dull if it’s mental. It’s a known indicator of fatal defects.

https://www.sciencedirect.com/science/article/pii/S1875957214001703

2015 Birth Defects in the Newborn Population: Race and Ethnicity

Overall birth defect prevalence was 29.2 per 1000 in a cohort of 1,048,252 live births, of which 51% were Caucasians.

Full white or mongrelised? Let’s assume pureblood despite America (mixed white, mostly). American whites are on average less attractive as white blended than single nation counterparts, even living in America. Models tend to come from homogeneous national areas, (i.e. subrace) a finding that is known to apply to white settlers in Brazil to this day, they send scouts. Specifically.

https://www.thecut.com/2010/06/model_scouts_find_more_than_ha.html

Compared with Caucasians, the risk of overall birth defects was lower in African–Americans (relative risk = 0.9, confidence interval 0.8–0.9) and Hispanics (relative risk = 0.9, confidence interval 0.8–0.9).

Failure to consider abortions for “no” reason or gender as defective. Selection bias. A lot of those already had abortions because they’re high abortion groups!

The risk of overall birth defects was similar in Caucasians and Asians. Relative to the Caucasians, African–Americans had a lower risk of cardiac, genitourinary, and craniofacial malformations but a higher risk of musculoskeletal malformations. Hispanics had a lower risk of genitourinary and gastrointestinal malformation. Asians had a higher risk of craniofacial and musculoskeletal malformations.

Didn’t control for proportion in the population, then non-whites are way ahead.

Craniofacial = ugly. 

Musculoskeletal = ugly. Well, dumpy.

Unless you’re going to argue a big is beautiful for literal birth defects?

And “similar” isn’t same. It isn’t statistical. This is like IVF success studies again (see below).

Why did some old world men witness the birth? All babies look like those reddish potatoes, it can’t be a resemblance. You can tell a resemblance to one parent over another by middle childhood to puberty.
We’re told that it’s about adultery and it might be true if you suspect a man with certain features e.g. skin colour, an extra finger.

Yet, what can you tell at birth? Ugliness.
Whether or not the man in question remembers that reason.

Cinderella effect also applies to genetic but ugly kids (lookism, it’s aka). The parents reject them, even if one genetically caused their fug.

Take Cumberbatch, product of a union involving adultery.
Fugly. Nice voice, but his father is the looker. Mother is a looker too. The issue cannot be genetic.

Some superstitions have a basis in fact.

Why did old ladies peer into a pram to judge the ugliness of the babe?

To see if you’re a SINNER!

[inc Thou shalt not adulterate]

Picking on an ugly white guy wouldn’t be totally kosher. I have other evidence.

We’re looking for spiteful mutants.

Now the post gets huge.

To more data, ever more data, smother the liars in data:

https://www.ons.gov.uk/aboutus/transparencyandgovernance/freedomofinformationfoi/informationregardingmixedraceparentage

“Please may I request the following information, records and documentation under the Freedom of Information Act:

Information in regard to people of mixed race parentage- often called ‘white and black Caribbean’, ‘white and black African’, ‘white and Asian’, ‘other mixed’- being at increased risk of being born with a birth defect, stillborn, or of suffering from fertility problems in their adult lives, which is related to their mixed race parentage

Information regarding NHS policy and practice on the advising of interracial couples, who are prospective parents, about the increased risk of their child being born with a birth defect, stillborn, or infertile in adult life, which would be connected to their, the child’s, mixed race parentage

Please may I also request statistical information and records which display the following:

The percentage of overall cases of babies born with a birth defect, which is attributable to each ethnic group

The percentage of overall cases of babies still born, which is attributable to each ethnic group

The percentage of overall cases of infertility, which is attributable to each ethnic group

The percentage of overall births, which is attributable to each ethnic group”

Reply:

“In Tables 8 and 10, mixed race is included in a single category of Mixed, Chinese and any other ethnic group. This is because the numbers in these groups are sufficiently low to risk being disclosive, and follows agreed statistical guidelines.
a) being born with a birth defect – this information is shown in Table 10.
b) being still born – this information is not published. However, you could request a special extract (further details of how to do this are explained below).
c) we do not hold any information on infertility, and are therefore not able to answer your question about adults suffering from fertility problems, connected to their mixed race parentage.”

Do not hold information my lily-white arse.

https://www.independent.co.uk/voices/infertility-ivf-nhs-race-lgbt-asian-black-women-a9216921.html

Table link: https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/causesofdeath/bulletins/gestationspecificinfantmortality/2014-10-15

“Page does not exist”.

It’s this paper.
https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/causesofdeath/bulletins/pregnancyandethnicfactorsinfluencingbirthsandinfantmortality/2014-10-15

“Some research suggests that Black and Asian women have shorter gestation than White European women, and that this may be due to earlier fetal maturation (Patel et al., 2004). The discrepancies in gestation by ethnicity may also be explained by socio-economic, behavioural and physiological differences among the different ethnic groups (Gray et al., 2009).”

In an ONS report. They know.

“Table 10 (184.5 Kb Excel sheet) shows that for four of the five combined ethnic groups analysed, the most common cause of infant death was immaturity related conditions

(Black, 54%;

Mixed, Chinese and any other group, 44%;

White, 43%;

For a majority, that’s incredibly low.

and those where ethnicity was

not stated, 49%).

For the Asian group, the most common cause was congenital anomalies (41%). A higher incidence of congenital anomalies in Asian populations is well-documented (Gray et al. 2009).”

http://www.ons.gov.uk/ons/rel/child-health/gestation-specific-infant-mortality-in-england-and-wales/2012/rft-table-1.xls

Low birthweight and prematurity are both measures of fetal development. Another measure is the baby’s size in relation to its gestational age. Babies whose birthweight lies below the tenth percentile for their gestational age are known as ‘small for gestational age’ (SGA).

Not all babies who are SGA have a pathological growth restriction; they may just be constitutionally small.

read: racially

This may explain why babies of Bangladeshi, Indian or Pakistani origin are more likely to be SGA than White British babies.”

Smaller brains too. Inbreeding depression but also group average by nation. Look at national IQ.

https://www.photius.com/rankings/national_iq_scores_country_ranks.html
Bangladesh 82
Over one whole standard deviation below. According to the likes of Peterson, useless to a Western economy. The average Bangladeshi.
India 82
Recall regression to the mean. Also, friendliness correlates more to low IQ. Do not be fooled.
Pakistan 84
Thailand 91
Philippines 86
Nigeria 84
Jamaica 71, where we’re picking up new NHS nurses.

Enjoy that decline.

Tables 8 and 10 mentioned in FOI request not listed, have to know it’s there.
Under Downloadable Tables:

“Table 8: Live births, neonatal and infant mortality by ethnic group and gestational age at birth, 2012 birth cohort, England and Wales

Table 10: Infant mortality by ONS cause groups and broad ethnic group, 2012 birth cohort, England and Wales”

For future reference, write your FOI requests as “concern for services provided to BAME women” and “progressive need for up-to-date medical guidance for mixed race couples and the biracial in family planning”.

You have to download the excel, click to tables 8 and 10, then read the footnote of superscript 1 to know to scroll right.

Table 8: All others^1
7.1% under 37wks
9.2% SGA

Black SGA: 9.2 and 12.3%.
Bangladeshi, Indian, Pakistani only SGA: 17%, 16.3%, 14.2%.
White SGA: 7.2%, 6.2%.
Unknown 8.2%.
ALL SGA average: 8.2%.

Something’s off.

Pre-term neonatal deaths
Total: 869
B,I,P: 9, 30, 47
Black: 39, 13
White: 549, 63
Unknown, not stated: 32
All others^1: 87
For such a vanishingly small percentage of the population, how is it 87?
10% of pre-term deaths were “1 Chinese, Other Asian, Other black, Other and all Mixed groups.”

Do you see what I see?

For non-statistically minded people:

Infant death, pre-term
Total: 1232
B 21
I 41
P 66
Black African: 62
Black Caribbean: 20
W native 750
W other 86
Not stated 48
All others^1: 138

See it yet? If you controlled for population ratio, it’d be more dramatic by far.

This is why they hide it and I have to make my own charts.

Term infant deaths
Total: 895
All others^1: 102.
That’s 11.4% from a tiny group of mixed.

Table 10 screen-capped, do your own charts.

Related studies, I do have a point about measurement error.

https://iussp2009.princeton.edu/papers/93139
2009 Fertility by ethnic and religious groups in the UK, trends in a multi-cultural context

Asian tsunami in USA too
https://www.statista.com/statistics/226292/us-fertility-rates-by-race-and-ethnicity/

https://www.statista.com/statistics/281416/birth-rate-in-the-united-kingdom-uk/

From one of the links, can’t find which. Calm down. Either they’re abstaining from having kids once here, infertile, the neonate dies or it’s retarded. Being here is actually a curse since they’re held to the standards and economy of a higher IQ nation. They’re voter birds here for a season or tax chattel and they’ll leave when it’s convenient to.

Ethnicity and IVF

“How a patient’s ethnic background affects her chance of pregnancy, especially with IVF, is a fascinating yet poorly studied area of research. According to a 1995 national survey of family growth, non-Caucasian married women were more likely to experience infertility than Caucasian married women, yet these same non-Caucasian women were less likely to receive any type of infertility treatment—especially treatment with assisted reproductive technologies.

There is very little data in the literature examining ethnicity and its affect upon pregnancy rates with in vitro fertilization (IVF). Ethnic minorities compose a small percentage of patients in the nation’s IVF programs, making it relatively difficult to examine how they respond to various infertility treatments. In the few studies that have examined the affect of ethnicity on IVF pregnancy rates, differing outcomes have been found.

There have been only a few studies specifically comparing IVF success rates between African Americans and Caucasians. The results of two of these studies contradict each other, with one showing that African Americans had decreased pregnancy rates with IVF as compared to Caucasians, and the other finding no difference in pregnancy outcomes with IVF between these two ethnic groups.

Likewise, there are only a few studies directly comparing IVF pregnancy outcomes between Indians and Caucasians. One shows a trend towards decreased pregnancy rates in Indian women and finds that Indian women were significantly more likely to have their cycle cancelled as compared to Caucasian women. In comparison, another study found no significant difference in IVF pregnancy rates between Indians and Caucasians. A more recent study has shown that Asian ethnicity was an independent predictor of poor outcome with IVF. There have been no studies examining IVF pregnancy outcomes in Hispanics in comparison to any other ethnic groups.

We’ll see why.

When I was in training, I published the first study comparing IVF outcomes among multiple ethnic groups. It was a retrospective study utilizing a data set that was the result of the collaboration between three IVF centers in the Boston area: Boston IVF, Brigham and Women’s Hospital IVF Center, and Reproductive Science Center.
We retrospectively reviewed the cycles of 1,135 women undergoing IVF between 1994 and 1998. Only the first IVF cycle for each couple was reviewed. Ethnicity was self-reported. Women who categorized themselves as having a mixed ethnic background were excluded.

Seriously. Measurement bias much?

….In order to better understand how ethnicity affects IVF outcome, it will be necessary to study a larger number of minority patients. In these studies, it is important that all ethnicities be included. If racial differences do exist, IVF treatment protocols could be adjusted to improve the success rates for patients of all ethnic backgrounds. Therefore, further exploration in this area is necessary and very important.”

We did that.

https://www.rcog.org.uk/en/news/bjog-release/

“After adjusting for certain factors including the age of the patient at time of treatment, cause of female or male infertility, and type of treatment (ICSI vs IVF), the study found that White Irish, South Asian Indian, South Asian Bangladeshi, South Asian Pakistani, Black African, and Other Asian women had a significantly lower odds of a live birth than White British women. For example, the live birth rate for White British women was 26.4% compared to 17.2% for White Irish women and 17.4% for Black African women.

The study also found that some groups of women including South Asian Bangladeshi, Black African, Middle Eastern, have a significantly lower number of eggs collected than White British women.

Moreover, South Asian Indian, South Asian Bangladeshi, South Asian Pakistani, Black British, Black African, Black Caribbean and Middle Eastern women were at a higher risk of not reaching the embryo transfer stage.

The paper explores the possible reasons behind the variation and states that while genetic background could be a potential determinant of egg and sperm quality, variation in environmental exposures relating to lifestyle, dietary factors, socio-economic and cultural factors could be influencing egg and sperm quality, accessibility of fertility treatment and behaviour towards seeking medical care and consequently reproductive outcomes.

No, they were living in the same place. Muh Magic Dirt.

Genetics is the ONLY difference now.

You have NOTHING.

DNA causes germline DNA, really? Maybe?

Furthermore, the increased prevalence of polycystic ovary syndrome (PCOS) in South Asian women may have an impact on egg quality and lower implantation rates.

Shit tier WHR tipped us off on that one, see end.

Dr Kanna Jayaprakasan, Consultant subspecialist in Reproductive Medicine, Derby Fertility Unit, Royal Derby Hospital; Honorary Associate Professor in Gynaecology, University of Nottingham and senior author of the paper, said:

“The data suggests that ethnicity is a major independent factor determining the chances of IVF or ICSI treatment success.

“While the reason for this association is difficult to explain, the potential factors could be the observed differences in cause of infertility, ovarian response, fertilisation rates and implantation rates, which are all independent predictors of IVF success.

“The main strengths of the study are the use of the UK HFEA national database which includes a large number of women treated in all UK units. However, the numbers in some of the sub-ethnic minorities, such as Bangladeshi women, were low in the study.”

Professor Adam Balen, spokesperson for the Royal College of Obstetricians and Gynaecologists (RCOG) and Chair of the British Fertility Society (BFS) said:

“Infertility affects 10-15% of the population and more people are seeking fertility treatment.

“This interesting study looking at maternal ethnicity provides useful data based on a large number of women undergoing fertility treatment. The reasons behind the variation need to be looked at in more detail but in the future could potentially help improve success rates amongst all groups of women.”

Nope!

https://www.sciencedirect.com/science/article/abs/pii/S1472648315002564

“Black and South Asian women were found to have lower live birth rates compared with White women”
“Black and South Asian women seem to have the poorest outcome, which is not explained by the commonly known confounders. Future research needs to investigate the possible explanations for this difference and improve IVF outcome for all women.”

Almost like Anglo women evolved to breed in the Anglo climate?

The Ice Age killed the boyish ones.

MORE:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2636517/

“Variation in risk factors and outcomes was found in infants of White mothers by paternal race/ethnicity.”

I wonder which way.
Inbreeding or outbreeding depression?

Guess.

“Status exchange hypothesizes that in a marriage market framework, minority men marry less-desired White women (e.g., of lower education) in exchange for higher social status. The second hypothesis, in-group preference, simply suggests that people prefer members from their own group, and thus, intermarriage is the less desirable scenario.”

Dudebros like “where’s da studies?”

I’m like “Have you even looked?”

“Together they found that mixed-race couples differed significantly with respect to their sociodemographic characteristics from the endogamous couples. After control for those variables, biracial infants were found to have worse birth outcomes than infants with 2 White parents but better than infants with 2 Black parents.6,8–12 (Henceforth, infant’s race/ethnicity will be referred to by the notation “maternal race/ethnicity–paternal race/ethnicity” [e.g., White–Black].)”

DING DING DING DING DING

TIL Wombs iz white supremacist.

“Consistent with Table 1, infants in the White–unreported group had the worst birth outcomes in each category.”

Trans. mixed. Likely Asian since S. America and Black are already covered.

Learn to read, weebs.

“In general, I found substantial variation in birth outcomes within the group of infants with White mothers and fathers of different racial/ethnic groups. This is interesting because it shows that the common practice of using maternal race/ethnicity to refer to the infant’s race/ethnicity, regardless of father’s race/ethnicity, can be problematic.

aka nice way of calling out deception

For example, it is not uncommon for a study to refer to infants of White mothers as “White infants,” even though “White infants” may imply that the fathers are White. In this study, I demonstrated that infants of a White mother and a White father, the real “White infants,” have the better birth outcomes than do those infants of a White mother and a non-White father. Therefore, the practice of using “White mother” to refer to White infants will yield lower estimation of the birth outcomes because there are infants of non-White fathers in the sample.”

They know. It’s a cover-up.

Category errors galore.

“The infants in the White–White group had the most-advantaged birth outcomes, followed by infants in the 3 Hispanic-father groups. Infants in the White–Black group had the second-most-disadvantaged birth outcomes; the differences in birth outcomes between White–Black and White–White infants were statistically significant: White–White infants had a 2% (70 g) higher average birthweight, 26% lower LBW rate (4.64% vs 6.26%), and 39% lower infant mortality rate (0.43% vs 0.71%) than did White–Black infants. Infants in the White–unknown group had the most-disadvantaged outcomes in each category. These heterogeneities within White mothers show that the common practice of using maternal race/ethnicity to refer to the race/ethnicity of the infant is problematic: White–White infants had the best birth outcomes among the groups studied, so any other paternal race/ethnicity pulls down the averages for all White mothers. That is, the birth outcomes of White–White infants are actually underestimated by researchers who use mothers’ race/ethnicity to refer to infants’ race/ethnicity, and thus, the racial/ethnic disparities between White and any other race/ethnicity may be underestimated accordingly as well.”

Relevant!

“…Clearly, the unreported father is a proxy for more-noteworthy factors, because if unreported fathers were merely missing from certificates, their infants’ outcomes should not be so much worse.”

What DO these studies have in common? [Asians]

Could also be child of rape as a confound.

You’ll see.

2012 Biracial couples and adverse birth outcomes: a systematic review and meta-analyses.
https://www.ncbi.nlm.nih.gov/pubmed/22776059

“Biracial status of parents was associated with higher risk for adverse pregnancy outcomes than both White parents but lower than both Black parents, with maternal race having a greater influence than paternal race on pregnancy outcomes.”

Evolution is racist or instincts evolved for reasons? Pick ONE.

Your Third World surrogate plan may need retouching.

If it fails or dies or gets retarded, you still gotta pay up! What are the odds?

Why is it so hard to find studies about the most populous race on the planet?
https://www.ncbi.nlm.nih.gov/pubmed/31238617

https://www.ncbi.nlm.nih.gov/pubmed/30564431
2018
What is associated with IQ and other development issues? Pre-term birth.

“Maternal age, education level, race and ethnicity, smoking during pregnancy, and parity were significant risk factors associated with PTB.”

It’s mentioned along with smoking.

“…The analysis of interactions between maternal characteristics and perinatal health behaviors showed that Asian women have the highest prevalence of PTB in the youngest age group (< 20 years; AOR, 1.40; 95% confidence interval (CI), 1.28-1.54).”

I want more studies about them. I’m not scared of reality.

That suggests a genetic predisposition to be present so young. I’d compare PTB to WHR, personally.

“Pacific Islander, American Indian, and African American women ≥40 years of age had a greater than two-fold increase in the prevalence of PTB compared with women in the 20-24 year age group.”

Their own women.

Pre-term study and IQ:

https://pediatrics.aappublications.org/content/136/3/415
“RESULTS: Across all assessments, VP/VLBW individuals had significantly lower IQ scores than term-born controls, even when individuals with severe cognitive impairment (n = 69) were excluded. IQ scores were found to be more stable over time for VP/VLBW than term-born individuals, yet differences in stability disappeared when individuals with cognitive impairment were excluded. Adult IQ could be predicted with fair certainty (r > 0.50) from age 20 months onward for the whole VP/VLBW sample (n = 260) and from 6 years onward for term-born individuals (n = 229).

CONCLUSIONS: VP/VLBW individuals more often suffer from cognitive problems across childhood into adulthood and these problems are relatively stable from early childhood onward. VP/VLBW children’s risk for cognitive problems can be reliably diagnosed at the age of 20 months. These findings provide strong support for the timing of cognitive follow-up at age 2 years to plan special support services for children with cognitive problems.”

So it doesn’t cause but it is associated. Humans evolved long gestation for the brain.

Clear defect evidence in the genes- study it!
https://www.ncbi.nlm.nih.gov/pubmed/29903290

But surely, you say, genetic issues would be also hormonal (hormones regulate genes as well) and apply to men?
Well…
https://www.ncbi.nlm.nih.gov/pubmed/31348744
Yes. Yes it would.

“A total of 9079 patients were reviewed, of which 3956 patients had complete data. Of these, 839 (21.2%) were azoospermic. After adjusting for age, African-Canadians (odds ratio [OR] 1.70; 95% confidence interval [CI] 1.28-2.25) and Asians (1.34; 95% CI 1.11-1.62) were more likely to be azoospermic compared to Caucasians.”

Some of us form opinions AFTER reading.
White men are literally more fertile and most fertile with white women.

“Similarly, African Canadians (OR 1.75; 95% CI 1.33-2.29) were more likely to be oligospermic and Asians (OR 0.82; 95% CI 0.70-0.97) less likely to be oligospermic. Low volume was found in African-Canadian (OR 1.42; 95% CI 1.05-1.91), Asians (OR 1.23; 95% CI 1.01-1.51), and Indo-Canadians (OR 1.47; 95% CI 1.01-2.13). Furthermore, Asians (OR 0.73; 95% CI 0.57-0.93) and Hispanics (OR 0.58; 95% CI 034-0.99) were less likely to have asthenospermia. Asians (OR 0.73; 95% CI 0.57-0.94) and Indo-Canadians (OR 0.58; 95% CI 0.35-0.99) were less likely to have teratozospermia. No differences were seen for vitality. No differences were seen for FSH levels, however, Asians (p<0.01) and Indo-Canadians (p<0.01) were more likely to have lower testosterone.”

It’s always the damn Asians.
Magic Dirt won’t fix your shitty sperm.

Maybe if we spend more on the NHS! The evolution fairy may visit!

The lower sexual dimorphism of Asians makes them functionally partially infertile. This is why they marry so young (it isn’t traditionalism) and despite this, have a low birth count per person, and are the most populous race on Earth. They’re actually the most r-selected, Mother Nature holds them back from fertilization with mutations. Along with r-selection, more total fertility issues in the male/offspring (azoospermia, infant death), lower volume AND lower testosterone, it all fits!

Is that my fault? No. Stop blaming me for reading. I’m not, in fact, God.

Hey, we have our own group with shitty sperm. Theirs is just bigger and more characteristic of the whole.

from https://www.ncbi.nlm.nih.gov/pubmed/26962784

“AR-CAG repeat length was longer in infertile men in Asian, Caucasian, and mixed races (SMD = 0.25, 95% CI: 0.08-0.43, P <0.01; SMD = 0.13, 95% CI: 0.02-0.25, P <0.05; SMD = 0.39, 95% CI: 0.15-0.63, P <0.01).

Notice p-value difference is so loose for white it doesn’t meet the medical standard? 0.05 is too high. Absurdly.

The overall study shows that increased AR-CAG repeat length was associated with male infertility. The subgroup study on races shows that increased AR-CAG repeat length was associated with male infertility in Asian, Caucasian, and mixed races. Increased AR-CAG repeat length was also associated with azoospermia. This meta-analysis supports that increased androgen receptor CAG length is capable of causing male infertility susceptibility.”

In the interest of intellectual honesty.

WHR

We literally have the studies. e.g. It’s metabolic.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4306982/

“Sixty-four PCOS patients and 40 women served as the control group were studied. The two groups were subdivided according to the body mass index (BMI) into two obese and non-obese groups. Waist:hip ratio (WHR), plasma epinephrine level was estimated, sympathetic skin response (SSR); postural orthostatic tachycardia syndrome, heart rate variability (HRV), and valsalva ratio were measured in both groups.”
“Compared to the control group, obese PCOS patients demonstrated higher BMI and WHR, reduced palmar SSR latency and higher amplitude, altered HRV, higher plasma epinephrine level, and rapid pulse rate. Moreover, non-obese patients show reduced palmar SSR latency and higher amplitude, higher plasma epinephrine level, and higher pulse rate. BMI and WHR of the patients were positively correlated with plasma epinephrine level; while the HRV was negatively correlated WHR.”
“The BMI and WHR were significantly higher in the PCOS patients compared to the control group 36.63±4.23 kg/m2 vs. 34.14±3.39 kg/m2 (p=0.041) and 0.88±0.05 compared to 0.79±0.11 (p=0.001), respectively.”

“We demonstrated high plasma epinephrine level during lying and standing positions in PCOS patients. This could be of obesogenic origin as we noticed a positive correlation between plasma epinephrine level and both of BMI and WHR. PCOS patients of this study exhibited central abdominal obesity and the mechanisms by which central obesity drive an increase in sympathetic activity are not entirely clear. Yet, the fat cells have increased sensitivity to lipolytic agents and/or the factors inducing fat mobilization are turned on (16). This was further supported that adipocytes isolated from the visceral fat depot of women with PCOS had increased catecholamine-stimulated lipolysis (17).”

Nice boy hips. Don’t try for kids. (Goes for all races, Spartans forced girls to be lightly athletic to be ready for childbirth as a woman, that broadens hips beyond racial average).
And when the NHS totally fails, picture the fatal correction to reality when these women expect childbirth interventions. No waist? No taste.

Old expression.

It’s genetic. They’re gonna get fat – or the kids will. We’ve all seen them. I’m just saying, the signs were there. Choosing a woman with a shit tier WHR is like electing for a manlet over the average height. It could rarely work out for health, but rarely. Don’t get angry at me.

Click to access 4755-4761-Metabolic-parameters-in-PCOS-and-abdominal-obesity.pdf

“RESULTS: Women with WHR ≥0.8 had higher concentration of glucose and insulin (both fasting and after 120 min of oral administration of 75 g glucose), as well as HOMA-IR value, than women with WHR value < 0.8. Also, abdominal obesity disorders hormonal parameters. Higher free androgen index and lower concentration of sex hormone binding globulin and dehydroepiandrosterone sulfate were found in female with WHR ≥ 0.8.

There’ll still be guys like “WHR doesn’t matter, medically”.

Muh dudebros going, “at least they’re skinny”. But they’re not?

“Women with WHR ≥0.8 had… abdominal obesity disorders hormonal parameters.”

They’re literally not. Chemically. You can biopsy the tissue and test it.

the fat cells have increased sensitivity to lipolytic agents and/or the factors inducing fat mobilization are turned on”

My feels have zero to do with that, dude. It’s genes?

NOBODY is jealous. You keep your secret fatty.

I implore you to marry the future whale and learn the hard way. They’re a puffer-fish.

Whatever their race. But the shorter they are, the worse it is. Short women should have an even SMALLER waist, since it’s skeletal. My own is far smaller than most Asians, for instance, despite being taller than most of them as white. If you want to piss them off, say (honestly) that men like small waists. Just generally. Gets them every time, although most people wouldn’t say they had a large one (not really looking and they don’t dress for it). They know they’re broad and they hate women who dress to show any different, including lucky exceptions in their own race, since it’s a countersignal. Namely: I can afford to have a smaller midsection, less running and foraging is required.

[If I want to dress to piss off a group of women, bodycon but for the waist only. It’s subtle and you’d imagine as a man they would neither notice nor care. Great way to tell a woman’s natural WHR – do they like bodycon? It needn’t be tight on T&A, actually that’s better, it’s actually about waist fit. Pill women also get larger round the middle, any weight gain is there and ruins WHR so it’s visual slut shaming too. Love it.]

Follicular stimulating hormone, luteinizing hormone, androstenedione, and 17-beta-estradiol, were on similar level in both groups. Elevation in triglycerides, total cholesterol, and low-density lipoprotein levels, as well as decrease in high density lipoprotein level in serum of women with WHR value ≥0.8, were found when compared to women with WHR < 0.8. A statistically significant correlation was found between WHR value and glucose, insulin, sex hormone binding globulin, free androgen index and lipid profile parameters.”

Hips don’t lie because biochemistry.

“CONCLUSIONS: Abdominal obesity causes additional disorders in metabolic and hormonal parameters in PCOS women, which confirmed changes in analyzed parameters between PCOS women with WHR < 0.8 and WHR ≥ 0.8 and statistically significant correlations between WHR value and analyzed parameters.”

Food babies

Insight into vegan menopause.
“Drinking whole fat milk and eating ice cream appears to be better for women trying to become pregnant than a diet consisting of low-fat dairy products such as skim milk and yogurt, according to new research published in Human Reproduction journal. Researchers in the United States have found a link between a low-fat dairy diet and increased risk of anovulatory infertility.”
You don’t have to tell me twice to eat ice cream, mate.
“Further, lactose (the main carbohydrate in milk and dairy products) may not affect fertility within the usual range of intake levels in humans.”
Good to know.
“Consumption of iron supplements and nonheme iron from other sources may decrease the risk of ovulatory infertility.”
Yes, my favourite iron supplement is called steak. Recommend.
Especially with three times “too much” garlic butter.
“Folic acid appeared to explain part of the association between multivitamin supplement use and risk of ovulatory infertility.”
Sorry but I don’t trust Crunchy Nut cornflakes with the fate of my future children’s health.
“Dairy consumption was not significantly correlated with PCOS. However, after adjustment for confounders, there was an direct relationship between milk consumption and risk of PCOS.”

“the results showed that the intake amounts of Ca, Mg, D vitamin, dairy, fruits and nuts and seeds were remarkably low among the women with PCOS.”

What are they living on, Oreos?

“some evidence on the decreased amount of adiponectine, calcium, D vitamin in the patients suffering from PCOS with having a higher thyroglobulin”

Vegans.

“Numerous studies have demonstrated the association between the diet and its components and risk factors developing various diseases.[] However, previous studies did not address the relationship between nutrition choices and type of diet chosen by the patients.[]”
“According to existing data, women trying to achieve pregnancy are encouraged to increase consumption of whole grains, omega-3 fatty acids, fish, and soy and to reduce consumption of trans fats and red meat. In addition, a daily multivitamin that contains folic acid before and during pregnancy may not only prevent birth defects, but also improve the chance of achieving and maintaining a pregnancy. In contrast, there is limited evidence supporting an association betweenvitamin D and human fecundity outcomes despite promising evidence from nonhuman studies.
Yeah because that’s relevant.
Questions for future research included the roles of other types of fat (especially omega-6 and monounsaturated fats) and protein (especially white meat and seafood) on female fertility; particular attention should also be paid to exposure to environmental contaminants in foods. Although much work remains, this review accrued best available evidence to provide practical dietary recommendations for women trying to conceive.”
Bolded valuable parts.
“One approach to minimize the impact of anovulation on fertility is supplementation with progesterone during recruitment, selection and final stages of development of the preovulatory follicle. It is suggested that a minimum of 2.0 ng/mL of progesterone is needed during growth of the preovulatory follicle to achieve P/AI similar to that of cows growing the preovulatory follicle during diestrus.”
But one of the Pills is that….
Does taking that Pill increase odds of pregnancy?
Big if true.
The literature on the relationship between diet and human fertility has greatly expanded over the last decade, resulting in the identification of a few clear patterns. Intake of supplemental folic acid, particularly at doses higher than those recommended for the prevention of neural tube defects, has been consistently related to lower frequency of infertility, lower risk of pregnancy loss, and greater success in infertility treatment. On the other hand and despite promising evidence from animal models, vitamin D does not appear to exert an important role in human fertility in the absence of deficiency.
But most people are deficient….
That’s like saying you can stand outside normally -except when there’s a hurricane.
And there’s currently a hurricane.
Antioxidant supplementation does not appear to offer any benefits to women undergoing infertility treatment, but it appears to be beneficial when it is the male partner who is supplemented.
Duh.
Reduce genetic load.
However, the available evidence does not allow discerning which specific antioxidants, or at which doses, are responsible for this benefit. Long-chain omega-3 fatty acids appear to improve female fertility, although it remains unclear to what extent contamination of shared food sources, such as fish with high levels of environmental toxicants, can dampen this benefit.
Comforting.
Eat this mercury (sushi fad) it’s good for your baby!
Lastly, adherence to healthy diets favoring seafood, poultry, whole grainsfruits, and vegetables are related to better fertility in women and better semen quality in men.
Could you be a little more specific?
You just named, like, most food.
They’re paid with our taxes, daylight robbery.
The cumulative evidence has also piled against popular hypotheses.
I doubt that.
Sounds like someone wants a juicy research grant.
Dairy and soy, once proposed as reproductive toxicants, have not been consistently related to poor fertility.
Because you refuse to test them separately.
If only a group ate one and not t’uther.
CONSISTENTLY.
In fact, soy and soy supplements appear to exert a beneficial effect among women undergoing infertility treatment.
Many have low estrogen, next!
Giving people with scurvy vitamin C helps! Next!
Similarly, because data from large, high-quality studies continue to accumulate, the evidence of a potentially deleterious effect of moderate alcohol and caffeine intake on the ability to become pregnant seems less solid than it once did.
But potentially, if you can’t put down the coffee or wine, Barbara, maybe you shouldn’t be having kids? Same goes for men without the energy. Now. Without kids.
Why do narcs consider children a human right?
Sort your energy level out BEFORE kids, at least?
While a complete picture of the role of nutrition on fertility is far from complete, much progress has been made. The most salient gaps in the current evidence include jointly considering female and male diets and testing the most consistent findings in randomized trials.
Fuck, men influence pregnancy? What witchcraft is this?
Their only biological contribution is determined by things that occurred in the years before conception?
Say it isn’t so.
What term could possibly exist to describe this Darwinian fitness between men?
Hold men responsible for their bad habits affecting their innocent child’s health outcomes and literal lifespan and I might be impressed.
Posting will be patchy because of my feelings.