Teen miscarriage in under-developed bodies vs. 20s white women

aka why the r-select pressure to breed as early as possible is directly opposed to the biological science on the subject.

TLDR: K-selection, having kids into the 20s and 30s, is optimal for a woman’s health.

Strap yourself in.

https://www.bmj.com/content/364/bmj.l869

“Conclusions The risk of miscarriage varies greatly with maternal age, shows a strong pattern of recurrence, and is also increased after some adverse pregnancy outcomes. Miscarriage and other pregnancy complications might share underlying causes, which could be biological conditions or unmeasured common risk factors.”

That’s important, write that down.

aka if you go Third World and force women to start breeding too early, they’ll be more likely to miscarry healthy children in future. Mother Nature hates r-types.

“Results There were 421 201 pregnancies during the study period. The risk of miscarriage was lowest in women aged 25-29 (10%), and rose rapidly after age 30, reaching 53% in women aged 45 and over. There was a strong recurrence risk of miscarriage, with age adjusted odds ratios of 1.54 (95% confidence interval 1.48 to 1.60) after one miscarriage, 2.21 (2.03 to 2.41) after two, and 3.97 (3.29 to 4.78) after three consecutive miscarriages. The risk of miscarriage was modestly increased if the previous birth ended in a preterm delivery (adjusted odds ratio 1.22, 95% confidence interval 1.12 to 1.29), stillbirth (1.30, 1.11 to 1.53), caesarean section (1.16, 1.12 to 1.21), or if the woman had gestational diabetes in the previous pregnancy (1.19, 1.05 to 1.36). The risk of miscarriage was slightly higher in women who themselves had been small for gestational age (1.08, 1.04 to 1.13).”

LOWEST of all ranges in the mid-late 20s, which, per The World We Have Lost, happens to be the age our wiser medieval ancestors commonly married and commenced reproduction. Almost like they didn’t want their wife to die?

You can’t expect modern medicine to bail you out of degeneracy.

And forcing a woman to start “too early” (really before the pelvic growth plates fuse at 21) makes it more likely your later heirs will be miscarried too. No blaming the woman for your own impatience.

All those described factors sound r-selected, especially the C-section, which doctors shouldn’t be forcing women into for convenience. These are your future kids they’re risking.

This study isn’t precise enough because they try to dodge the teen death issue but here

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC27416/

scroll to:

“Figure ​3 shows the age related risk of spontaneous abortion stratified by parity status and number of previous spontaneous abortions. The association between spontaneous abortion and age was similar in all strata, although the level increased with increasing number of previous spontaneous abortions.”

Similar. It isn’t a huge difference by age alone like you falsely claim, stop being dumb. However….

if we look at marriage survival against IQ (linked to years ago) and cross-reference the J-curve beneath, delayed motherhood (sufficient time to educate) is healthiest for society in terms of infant survival and marital longevity. Divorce is lower in high IQ women, who tend to marry later, which we can lump into the No Shit category.

Fridge horror: The early marriage of the poor CAUSED a lot of their baby deaths! aka The Oven Ain’t Done Yet!

Pedos reee but nature hates them to breed. They’re extreme r.

“The incidence of spontaneous abortion varied according to a woman’s parity and number of spontaneous abortions in the preceding 10 years; among women aged 25-29 years spontaneous abortion occurred in 8.9% of nulliparous women and 9.3% of parous women without a history of spontaneous abortion, in 12.4% and 11.8% of those with a history of one spontaneous abortion, and in 22.7% and 17.7% of those with a history of two spontaneous abortions. After three or more spontaneous abortions, the proportion of pregnancies ending in spontaneous abortion increased to 44.6% in nulliparous women and 35.4% in parous women.”

Personal history and then family history are more important than age. Men need to get this through their thick skull. This is like the IQ and beauty versus popularity and personality divide. A man who praises his wife’s ‘nice’ personality is admitting her ugliness. She isn’t docile, she doesn’t respect you. If we plan to outlive a man, what does his opinion matter? ‘Nice’ is a quality of puppies, not a viable sexual partner. Your level is the best woman you can get – and keep. Men forget the second part. Cheating on a great wife to lose her is stupid.

Widows were hot commodities because they had proven fertility. Especially great if their husband was stoned to death for adultery, so she’ll be quite young.

Do you want to bet on the horse that has won races or never raced?

If marrying a woman at the proper time, with no personal fertility history, ask about the oldest aunt of theirs who had kids.

Ideally, you’d hear 40s for a firstborn. Those are top-tier genes, especially if the child was perfectly healthy. No genetic load. Miscarriages are common though (about 10% under ideal conditions) and hard to tell early on so it isn’t an exact science. It’s odds, it’s probability. So it isn’t so much age, it’s familial genetic load of mutations compounded by time, it only seems like age. The mutations already in their DNA (and higher in men because sperm constantly need to renew) simply become more of what they already are.

The IVF people do not want normie people to discover the simple ways to ensure better fertility health, they’d go out of business if we had a simple eugenic questionnaire prior to marriage e.g. period frequency. Also, miscarriage is actually good if very early because print error kids get expensive. That’s a sign the body is doing what it should, miscarriages aren’t all created equal, only most are bad.

In future we could probably devise a spiteful mutant test prior to marriage. Very Gattaca. On second thought, that might actually be what the test was. Ks approve.

Obviously with age the mutants (only one parent need be) become more apparent, and this also determines things like aging facial bone structure too, but it isn’t CAUSED by age, it’s their genome!

Age is not the true variable, the confound is mutation burden in your DNA (inc germline). Age can estimate on a population level but I implore you, on an individual one, speak to the family for same-sex history up to cousin level, there’s a reason doctors ask about it! It allows them to adjust their predictions without prejudice.

In general women have less abortions young because 1. it counts the healthiest time to breed, the twenties, which conceals the brief increase in the teens, 2. white women conceal the worse stats for non-white women while still a technical majority and 3. they’d have less time to experience anything, there’s been less time alive. This assumes they’re even having sex. Age is a poor metric. Ask about Aunt Meryl with the four kids after 30. You may strike gold and the woman has twins in the family.

Miscarriage is a J-curve by age, NOT linear.
Younger is not automatically better, learn maths dudebros.

Then we isolate the J-curve with no history:

Gee, why don’t the socialists encouraging teen pregnancies tell you this in Sex Ed class?

For my next trick, because I’m that bitch, compare the teen miscarriage line to other young women? [young being prior to middle-age, for women approx 40s]

Pedos reee.

It’s data from 1,221,546 pregnancy outcomes in a white country.

The mid-30s miscarriage risk is the same for that woman as a teen with the same history.

It’s a deeper 20s scoop if both example women had a miscarriage history of one.

Data doesn’t care about your deviance, pedos.

Mother Nature hates you. So those data-ignorant “dusty egg” jokes of mothers in their 30s should logically be applied to ‘teen whore’ types too. If you were being logical, which we all know you aren’t. Teen mothers (and fathers) also tend to have lower IQ, which suggests spiteful mutant. The data lines up perfectly.

They don’t really ‘believe’ in starting prematurely, it’s their life history strategy talking.

They feel a need to breed immediately because they know they’d likely miscarry if they waited like a K-type. Suck it?

“In women with no history of spontaneous abortions we found a slightly lower overall risk of spontaneous abortion among nulliparous women than parous women (10.0% v 11.6%). This tendency was found in all strata of age except for women aged 40-44 years. “

Again, actual women’s middle age. You’d expect that. The system is shutting up shop.

It’s slightly better to have had NO abortions than ONE. Duh? I think women would agree. So if that one spontaneous abortion would be likelier in the teens, should a fertility-oriented high IQ society encourage teen pregnancy?

The answer is clearly no.

And the Middle Ages Western Europeans were smarter than current America.

And you wonder why the white birth rate is so, so low.

Among women with a history of spontaneous abortion, the reverse tendency was observed; in general, nulliparous women had a higher age specific risk than did parous women (fig ​(fig33).”

Stop getting this wrong. We need to avoid spontaneous abortions (miscarriages) to increase the birth rate. You can’t throw conceptions at the wall to see what sticks.

That’s a male perspective on women’s bodies and it’s demonstrably, mathematically wrong.

Not to mention stressful on the longsuffering wife.

Teens (biological children) have a higher pregnancy risk than adult, mature mothers:

“Under the assumption that only 80% of women with abortions in recognised pregnancies were hospitalised the risk of spontaneous abortion would be: 12-19 years, 13.3%; 20-24, 11.1%; 25-29, 11.9%; 30-34, 15.0%; 35-39, 24.6%; 40-44, 51.0%; and 45 or more, 93.4%.” that’s :-

Minor: 13.3% natural abortions

20s: 11.5% natural abortions

30s: 19.8% natural abortions (average, more variation)

40s: basically at least half. You’d need top tier DNA to survive that.

So stop lying, pedos. Call yourself hebe all you like, a POS by any other name.

This doesn’t factor in the mental trauma of giving birth, PTSD is quite common, discounting obvious cases like episiotomies without cause and C-sections with no pain relief. It happens.

Obviously, traumatising your teenage girls will put them off breeding altogether.

Then what happens to your precious ego birth rate?

The teen ectopic pregnancy rate also peaks in the teens comparable to a near-thirty year old.

DAT J-shape curve.

You mad, pedos?

Wait, there’s more!

Now onto stillbirths:

The rate for minors (teens) peaks at the same level as women in their late 30s.

That’s gotta hurt.

Good luck with your scientism though. I’m sure 1M+ white births are lying.

DAT 20s dip:

and it’s fractions of a percent, hardly apocalyptic is it? They’re such special snowflakes with the bloody victim complex.

“The association between maternal age and stillbirth showed a J-shaped curve, but the effect of age was less than for spontaneous abortions and ectopic pregnancies (fig ​(fig5).5). When restricting the analysis to nulliparous women, we found an identical pattern, although the level was slightly higher. The proportion of stillbirths was substantially increased in teenage pregnancies and was at the same level as for the 35-39 year age group. The incidence of stillbirth was unchanged during the study period.”

Ouch.

I’d also like to see a subdivision of dead babies risk in teen/minor mothers by aged daddy. Maybe next time. I covered paternal age generally beforehand anyway.

It’s funny that the paper writers still try to make it about age though. Nice try. Miscarriage is the biggest factor in future fertility according to their actual data, age is more important for niche risk of ectopic and stillbirth, but less so. And most importantly, NONE OF THIS IS LINEAR. NONE OF IT. The curve is a J. Redpills read the data. I don’t care what the researchers claim to get gibs, read the data itself. It is a non sequitur to claim older = worse outcomes and also a non sequitur to claim younger = better outcomes when the data doesn’t show that, it blatantly shows the opposite, a kind of Goldilocks effect in the 20s.

To put this all on increasing age is false reasoning, as shown, it’s increasing mutant burden. Age is a vector of genetic load, not the cause. Like – Being in a car is a vector of drunk driving, it isn’t the alcohol!

But they wanna get cited so…. they’ll twist their own data. Or try? God forbid anything be genetic, even reproduction!

nb “The increase in risk of ectopic pregnancies in teenage women is most likely caused by pelvic inflammatory disease.”

Teenagers are not women but k. And that’s wrong. The female human reproductive system takes time to fully develop. r/K explains this. Inflammation takes years, it’s literally impossible to blame that or 20s would be still higher.

“The risk of stillbirth was found to be high among teenagers, as previously reported.24 This may be a result of unfavourable social and behavioural conditions among pregnant teenagers, although a biological explanation cannot be excluded. The risk of stillbirth among women aged more than 35 years was increased but to a lesser extent….”

lol

“Conclusion

Our study shows an important increase in the risk of spontaneous abortion and other types of fetal loss among women aged more than 40 years”

Middle-age, then? Duh? The body’s aborting print errors like it should?

Yeah because like I said about the r/K system starting up, it also takes years to wind down?

Why aren’t you getting this?

“increase is already considerable among those in their 30s.”

no it isn’t data varies too much in that decade so you cannot accurately comment

“This increase is observed irrespective of a woman’s reproductive history.”

but that’s the bigger effect size? it’s the objectively more important factor?

Can’t hurt feels or lose those IVF shekels, huh?

The effect is still there but that’s a curious omission of scale.

“For society, such findings would indicate that tendencies to postpone pregnancy increase the overall incidence of fetal loss and possibly the costs of health care.”

ooooh they’re pushing teen pregnancies

damn r-types

“overall” POPULATION is not filial risk (personal risk)

filial risk is genetic, kin based

socialists shouldn’t be allowed to science

postponing in a K-select manner is MATURING

it’s HEALTHIER

higher actual birth rate, higher maternal safety, higher child survival

healthier children! higher IQs!

WHAT IS THE DOWNSIDE

= fewer r-types, I weep!

“these factors are highly correlated” = NOT CAUSATION

for the reproductive equation, you must include the age of BOTH parents at conception

BOTH PARENTS.

That’s the genetic equation of causation. Single parents are not up for discussion here, they didn’t impregnate themselves?!!

12-19 (minor/teen) pregnancies, not aborted: 51,132.

That’s a huge dataset of adverse pregnancy outcomes. How will the hebes recover?

….

….

….

in prison, where they belong.

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.

Nanolipids gather in ovaries, adrenals and liver

Imagine my shock.

https://jnm.snmjournals.org/content/54/11/1996

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

The nanolipids are the modRNA carrier. So where lipids go… I think we have our organ sequester, gentlemen.
NLs are in at least the moderna and Pfizer ‘vaccines’.
https://portal.ct.gov/-/media/Coronavirus/Community_Resources/Vaccinations/Print-Materials/Fact-Sheets/Ingredients_English.pdf

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

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

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

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

COVID, sperm infertility and STD potential

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.

They want to sterilise you (hCGβ)

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

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

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

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

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

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831725/

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

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

ONTO THE STUDIES:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4627648/
“Efforts to produce a contraceptive vaccine targeting human chorionic gonadotropin (hCG) face several important challenges.”

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

Journal of Reproductive Immunology:

https://www.sciencedirect.com/science/article/pii/S0165037809004537
“Gonadotropin-releasing hormone/human chorionic gonadotropin β based recombinant antibodies and vaccines”

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

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

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

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

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

MEN AREN’T IN THE CLEAR.

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

CHEMICAL CASTRATION.

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

Guessing atrophy is permanent? Sounds kinda permanent. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876172/
Linked to ‘adverse prognosis’ (death).

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

https://www.sciencedirect.com/science/article/pii/0167569986900290

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

https://www.sciencedirect.com/science/article/pii/0264410X89900431

Search engine (DDG) description:

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

1989 publication date.

1989

When you click:

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

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

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

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

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

It relates to cancer vaccines
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172635/

Anti-fertility vaccine again
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0897.1981.tb00063.x

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

Chemical human neuter sounds so cruel.

They think they own you.

Target for cancer therapy, apparently? Nice excuse. Sounds so comfy, philanthropy.
https://www.researchgate.net/publication/11500441_Tumor-associated_antigen_human_chorionic_gonadotropin_beta_contains_numerous_antigenic_determinants_recognized_by_in_vitro-induced_CD8_and_CD4_T_lymphocytes

WHO knows?

https://www.researchgate.net/publication/15504700_Functional_and_immunological_relevance_of_the_COOH-terminal_extension_of_human_chorionic_gonadotropin_b_Implications_for_the_WHO_birth_control_vaccine

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

You didn’t wanna breed, right?
How much would you pay for an anti-anti-fertility vaccine?
Task Force on Birth Control Vaccines….. selected…. target… fucking Nazi ‘eugenics’ again.
https://www.ncbi.nlm.nih.gov/pubmed/7693535

Christians are up first.

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

https://www.ncbi.nlm.nih.gov/pubmed/1874951

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

So including chemical abortion, like the Pill.

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

BIRTH CONTROL VACCINES, THE PROGRESS CONTINUES:

https://pubmed.ncbi.nlm.nih.gov/12286012/

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

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

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

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

Immunogenicity
https://www.sciencedirect.com/science/article/pii/S0264410X96000461
“Vaccines based on hCG have been proposed as a means either to prevent metastatic cancr6 or to control fertility’. Approaches to development of such vaccines have been pursued usij either the complete beta sub unit of hCG (hCG-fl) or the 37 amino acid CTP alone”

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

https://academic.oup.com/humrep/article/6/1/166/875911

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

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

Guess the year. Guess. I’ll tell you in a few lines.*

https://www.sciencedirect.com/science/article/pii/0277953695000378
“Immunization to regulate fertility…”

https://medical-dictionary.thefreedictionary.com/Beta-HCG
“produced by placental cells”

*It’s 1991 published above re WHO. 
PDF here: https://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.883.9964&rep=rep1&type=pdf

save save save

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

This one is tricksy.

https://www.nature.com/articles/nm0218-118?draft=marketing

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

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

described in SEO brief

paywalls should be illegal

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

https://scihub.to/

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

https://www.tandfonline.com/doi/pdf/10.1016/S0968-8080%2897%2990087-2

Published 1997.

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

spellings are often deliberate to thwart SEO

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

corrected

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

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

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

you know, pre-replication crisis

scientists often own stock so….. null appeal

2015
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4627648/

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

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

they think you’re stupid

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

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

neutralised, like a threat
neutered you – like a dog

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

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

Blood type is racially determined, like fertility problems

https://www.babymed.com/pregnancy-test/ethnic-distribution-of-blood-types

There are four main blood types: O, A, B, and AB and two Th factors, positive or negative. Most people are either A positive or O positive and the fewest are AB negative. Because blood types are genetic, they are inherited from the parents,  blood types have different racial and ethnic differences. The majority of people in the world and across various ethnicities have Rh+ blood type. Subsaharan African populations have a 97-99% Rh+ factor. East Asian communities have 93-97% Rh+ bloodRh factor is a big determinant in both fertility and pregnancy. If you’re Rh-negative, you will need to take certain precautions during your pregnancy because an Rh positive fetus can conceivably be affected

wait so does Nature abort hybrid babies?

if the RH negative mother has previously been exposed to Rh positve blood and creates antibodies that cross the placenta and attack the fetus’ RH positive blood.

It isn’t our fault Asians need IVF more and more often fail at it, it’s literally in their blood. What are they implying otherwise, a curse?

https://www.babymed.com/pregnancy-test/blood-test-blood-type-and-rh-status-and-antibody-screen

Asian Women & Fertility Problems

Race is biological, see.

Unfortunately, many Asian couples face challenge trying to conceive naturally or using fertility treatment. The decline in natural fertility and the lower success of IUI and IVF in Asian women is documented in The US, UK, China, Japan, Korea and other Asian countries.

Fertility in Asian countries has declined to the population replacement rate 2.1 or lower. Many factors contribute to decline in natural fertility in Asian women;

Not our fault. Not our problem. Nature tends to curb the over-population of r-types by introducing more threats to thin the herd.

It happens to Asians who never lived in the West, stop blaming whites.

Repost on the Asian female infertility problem:

When compared to Caucasian women, Asian women undergoing IVF significantly produce less eggs at all Anti-Mullerian hormone (AMH) levels, even in women with high AMH. AMH is the most accurate marker for ovarian reserve.

Gynecologic and medical disorders that impairs fertility: PCOS, endometriosis and Systemic lupus (SLE) are more common in Asian women.

Vaginismus : may interfere with regular intercourse in some Asian women.

Environmental Factors: Asian women has more exposure to methyl Mercury and vitamin D deficiency.

Culture : surveys of Asian women and men indicate that they are less likely to consent to be contacted for fertility research, are fatalistic about failure to conceive, less informed about fertility issues, only 36 percent knew that chances of getting pregnant declined with age, and are less likely to suspect a male factor.

Asian women are commonly late at seeking care for infertility and overestimate the chance for getting pregnant.

Look at the national IQs, hardly surprising.

Genetics : Many genes are likely involved. FMR1 is a gene on X chromosome responsible for Fragile X syndrome and its variants. High repeats at this gene may reduce ovarian reserve.

It’s literally genetic. R-selection doesn’t keep those repeats low in the populace.

Did pesky white women interfere with their genes?

Yeah we tinkered with the Ts, the Gs, the As, all of it!

Fertility Treatment Outcomes in Asian Couples

  1. Pregnancy and delivery rates are lower in Asian women following ovarian stimulation and IUI compared to white women
  2. IVF: when compared to white women in the US,  31 per cent of the Asian women gave birth successfully compared to 48 per cent of the white women. Asian women were also less likely to become pregnant; 43 percent against 59 per cent even after control for many fertility factors. Endometrial lining was thinner in Asian women compared to Caucasian women.

Shit, is white supremacy real but only for women? We did need to weather the Ice Age.

I think endometrial lining has a connection to T-levels, it gets thinner with higher T, if memory serves.

I didn’t find enough conclusive data on white men v Asian when I linked sperm quality studies. A little but not as clear. There are fewer studies like that on men in general.

Asian women should be aware that fertility treatment may be less successful and seek care of a reproductive endocrinologist and fertility specialist as early as possible.

In addition there are other factors that require attention in Asian women during fertility treatment especially the higher prevalence of chronic hepatitis B infection.

?

After conception, asian women at are a higher risk for gestational diabetes.

https://obi.org/blood-donation/scientific-facts/

Only 18% of people in the U.S. have a negative blood type. Yet, when someone with a negative blood type needs blood, only another person with a negative type can save his or her life.

The blood type correlations to medical conditions like mental problems really trigger SJWs.

Are rh negatives more intelligent?

I may sound conceited but yes, yes we are.

That’s why anglos, who have a lot of Rh-neg, have so many historic geniuses.

From obi

Blood type by race/ethnicity:

O-positive is the most common blood type. Blood types vary by ethnic group. More Hispanic people, for example, have O blood type, while Asian people are more likely to be type B. In 2014, Oklahoma Blood Institute saw this ethnic diversity and blood types in its donors.

The O stats for whites are shockingly different.

Limited by who donated, wish I could find broader data.

Some patients require a closer blood match than that provided by ABO positive/negative blood typing. For example, the risk of a reaction to transfused blood can sometimes be reduced if a patient receives blood that is from a donor with the same ethnicity. That’s why African-American donors may be the best hope for patients with sickle cell disease, 98 percent of whom are of African-American descent.

Why mention this now?

https://www.dailymail.co.uk/health/article-8434167/Study-ties-blood-type-COVID-19-risk-O-help-A-hurt.html

“Why do ‘BAME’ get it more?” Well damn I dunno, maybe look at their blood type?

If they don’t wanna catch it here they can always …. go somewhere else?

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?