Aged, post-Wall men when childless more likely to die young

and their r-select offspring, too, if they have them. Quantity over quality doesn’t work in the long run, see, so don’t worry about immigrants that much. Low fitness cannot win, long-term.
Mother Nature culls bachelors.

Slight repost for SEO. Nature, this year.

Impact of genetic risk score on the association between male childlessness and cardiovascular disease and mortality

Men need purpose of family or wither away. Believe no copes.

Childless men are reported to have a higher risk of cardiovascular disease (CVD) and mortality. Information on inherited genetic risk for CVD has improved the predictive models. Presuming that childlessness is a proxy of infertility we aimed to investigate if childless men inherit more often genetic traits for CVD and if combining genetic and parenthood information improves predictive models for CVD morbidity and mortality. Data was sourced from a large prospective population-based cohort where genetic risk score (GRS) was calculated using two sets of either 27 (GRS 27) or 50 (GRS 50) single nucleotide polymorphisms (SNPs) previously found to be associated with CVD. Part of the participants (n = 2572 men) were randomly assigned to a sub-cohort with focus on CVD which served as an exploratory cohort. The obtained statistically significant results were tested in the remaining (confirmatory) part of the cohort (n = 9548 men). GRS distribution did not differ between childless men and fathers (p-values for interaction between 0.29 and 0.76). However, when using fathers with low GRS as reference high GRS was a strong predictor for CVD mortality, the HR (95% CI) increasing from 1.92 (1.10–3.36) for GRS 50 and 1.54 (0.87–2.75) for GRS 27 in fathers to 3.12 (1.39–7.04) for GRS50 and 3.73 (1.75–7.99) for GRS27 in childless men. The confirmatory analysis showed similar trend. Algorithms including paternal information and GRS were more predictive for CVD mortality at 5 and 10 years follow-ups when compared to algorithms including GRS only (AUC 0.88 (95% CI 0.84–0.92) and 0.86 (95% CI 0.84–0.90), and, AUC 0.81 (95% CI 0.75–0.87) and 0.78 (95% CI 0.73–0.82), respectively). Combining information on parental status and GRS for CVD may improve the predictive power of risk algorithms in middle-aged men. Childless men and those with severe infertility problem may be an important target group for prevention of CVD.

The Wall literally kills men. It’s undeniable. The MGTOW types are an anti-natal death cult as much as SJWs, except spinsters live longer, actually.
There is no accounting for this but genetics, as we see in the premature mortality of children if they do have them.

Risk of childhood mortality in family members of men with poor semen quality

Men who wait until postWall to have kids, tend to have dead kids. It isn’t just paternal age, it’s poor genetic quality or fitness.
Stop lying to men about this, they don’t have immortal sperm. No such thing. Don’t tell them to leave it too late while you hock them playa e-books.
So the kids they do manage to have will die early, this is also seen among the mixed with rare genetic conditions.

What is known already: Semen quality is an established predictor of men’s somatic health. We can gain a better understanding of possible genetic or environmental determinants of the infertility phenotype by exploring familial aggregation of childhood mortality in relatives of men with poor semen quality.


Get rekt, you’re already dead. So are your r-type kids.
This is why r-types evolved to have children as early as humanly possible, and as often. The high quality K strategy is genetically barred from them, no wonder they hate happy families, it’s like fat women hating thin ones. The kids don’t live long enough to act like a K, long-term. This is why fake Ks make me laugh and largely don’t concern me. You can’t cheat your own inferior genetic quality. Go ahead, have expensive medical bills for likely retarded or mentally ill kids, that will die before you get grandkids. See if I care.

The Lord works in mysterious ways. Or maybe you aren’t listening to Him.
The sins of the father…..

You say, ‘God stores away a man’s iniquity for his sons.’
Let God repay him so that he may know it.

“Prepare for his sons a place of slaughter
Because of the iniquity of their fathers.
They must not arise and take possession of the earth
And fill the face of the world with cities.”

Sounds like early mortality to me!

There are many studies on weak sperm and premature mortality in men, I’m surprised really. Nature has the gold standard one because I know they’ll try to cherrypick around it.
They never discuss real redpills like this, do they?

If something cut a childless woman’s lifespan in HALF, you’d be sure they’d talk about it.

Men are, at best, dying of a broken heart in the mid-30s, early-40s because they have no family, and you hear crickets from the con artists who don’t really care about men, only wish to profiteer from them.

It directly contradicts their pure copium that ALL men have magical sexy singleton 30s (as K-type high fitness men might exclusively*), despite going outside, touching some grass and seeing how many let themselves go into grotesque swamp monsters. It isn’t just the women. Speaking to some Americans, I attributed a full decade or two onto their claimed age. I don’t think they were lying. The GMO carbs and booze age them like shit. The diabeetus fairy sprinkles them with powdered sugar.

*but Ks don’t sleep around, so it’s redundant to be hot. Rs want to be Ks so badly but slut genes lose.

CVD is the leading cause of morbidity and mortality in the US as well as in the European Union to a cost of hundreds of billion €, and responsible for 400,000 annual US deaths and 1.8 million EU deaths11,12,13. Therefore, improving CVD risk prediction and prevention is an important public health goal and is embedded in the Action Plan for the Prevention and Control of Non-Communicable Diseases in the WHO European Region for the time period 2016 to 202514.

This risk was most pronounced in childless men with high genetic risk scores having up to more than three times increased risk of CVD mortality, as compared to fathers with low GRS. Furthermore, we showed that adding information on paternal status to the GRS-based risk algorithm increases the predictive power for CVD mortality during 5- and 10-years follow-up.

Previously, by using data from a prospective cohort of 22,000 men with long follow-up from the same urban population, we were able to show that childlessness can be regarded as an independent risk marker for CVD along with other well-known risk factors2, an association previously reported by other authors4,26,27,28. In the current study we used a similar cohort from the same region of southern Sweden which provided genetic data and was specifically designed to study CVD risk. We were able to show the same effect of paternal status on CVD mortality estimates as previously published2. To the best of our knowledge this is the first study which evaluates the impact of established genetic risk scores for CVD on the association between parental status and the risk of CAD and CVD mortality.

Family size can be directly linked to the male fertility status29 and therefore male infertility is most likely overrepresented among childless men. Similarly, increased mortality and morbidity risk have been associated with impaired semen quality2 suggesting biological factors related to fertility to also play an important role for the risk of adverse health events in those men—association already established for women30.

The hypothesis of shared genetic traits for CVD and male infertility is based on the model proposed by Skakkebaek et al.18. It suggests a common mechanism, involving a combination of prenatal life exposures and adverse genetic factors to affect the future health of male fetuses making them more prone to develop subfertility as well as various diseases in adult life and to have shorter life span16,17,18,19. The mechanism suggests a primary testicular dysfunction including low testosterone—hypogonadism—as a possible mediator for the aforementioned risks31,32. Since up to 15% of the genome is directly involved in the physiology of reproduction16, disruption of non-reproductive, including metabolic, pathways likely impacts reproductive function and vice versa. However, the lack of interaction between parental status and inherited genetic risk for CVD reported by us suggests independent mechanisms when using childlessness as proxy for infertility.

Our study has several strengths but also some limitations. Comprehensive information from Swedish national registries allows for precise information on date and cause of death, emigration, disease diagnosis and represents men from all socioeconomic backgrounds. The meticulous data collection at baseline provides an opportunity to adjust for a large number of well-known risk factors for CVD. Furthermore, the genetic scores used in the analysis were previously verified as a risk factor using data from more than 55,000 individuals15, thus making it a reliable factor in risk estimation.

The robustness of our findings is underlined by confirmation of the findings based on MDC-CVC sub-cohort in the analysis of data from the remaining MDC subjects. In the latter analysis some additional GRS 27 subgroups showed statistically significantly increased CAD HRs, probably due to larger sample size.

therefore the risk of our cohort to reflect voluntary childlessness is low.

TLDR: Genetic r.

Solution? Simple. Compel hot people to breed like military service and ban the ugly.

Deformed sperm sub-fertility ‘baffles’ researchers

I wonder what these guys recently all had in common?

No date on this:

What did I say? Depopulation shots, if I were to design them, would target overall fertility in women, and mutate the sperm in the men.

Nobody was checking the men, I’ve been blowing this whistle all year.

“All participants have never suffered from infertility and have not been treated for it. The semen samples were tested for parameters and immune factors.”

Did they have herp? That causes infertility in men. It’s hugely covered up though.

I’ve posted about it.

These guys were dead, so let’s consider this a win for natural selection. Maybe sub-fertility in general predicts premature mortality for men? (see below, checked) HOWEVER: If disease-ridden manwhores are most likely to die of coof, I’ll personally send a thank you letter to Pfizer.

THE WAGES OF SIN ARE STILL DEATH. Das the real redpill, and white.

Thus, we were able to observe the disruption of sperm production, which can be partially explained by the result of an increased immune response from the testes.

Inflammation? Like from modRNA?

In addition to this, autoimmune inflammation of the testicles occurred in some COVID-19 patients.

Specifically WHAT PERCENTAGE had received a modRNA injection of any variety?

NO data? Seriously? You believe that? If they had pure blood, they’d be screeching told ya so.

from June 25th

Is it the disease or symptoms of a reaction to the jabs?

The current study observed a significant impact on male fertility and pathological changes in male gonads that might impact healthy reproductive well-being in male COVID-19 patients in the long-term. It is connected with impaired spermatogenesis with low sperm count, inflammatory responses in the testes and epididymis, and altered markers of seminal immunity indicating impaired immunity due to COVID-19 disease.

Why not tell us the percentages?

Research funded by China, this is a cover-up.

Impaired human spermatogenesis and delayed sperm maturation may be the result of an immune response in the testes and epididymis of COVID-19 patients, these factors are vital and determinant for healthy male fertility. It requires further care and support of males infected with SARS-CoV-2. It may indicate an increase in male infertility as a consequence.

Or immune response to the clot shots, since it impaired the tubes, which viruses don’t actually do?

“COVID-19 affects men more than women compared to its original form. SARS-CoV-2 can stay in human bodies longer than SARS-CoV. Its clinical characteristics are similar to SARS, but the male reproductive system is seriously affected by it. The male reproductive system is vulnerable to viral infections, and previous viral epidemics had documented varying impacts on male reproductive functions.

Depop by design.

There is substantial recorded evidence that the male reproductive system is vulnerable to viral infections like MUMPS, ZIKA, Hepatitis B virus (HBV), Hepatitis C Virus (HCV), Human Immunodeficiency Virus (HIV), Human papillomavirus (HPV), Herpes, EBOLA.

It’s a bioweapon. Chinese ball bleach. But let them marry into your family, sure.

As such, the manosphere, as primary vectors of birth-rate killing disease, should be banned from any traditional society. Banishment is holy. God did it.
A lot of hebe/pedo guys you’d think are Chads, like Henry Cavill, are mostly infertile (sub-fertile) due to their HPV, herp, etc. Watch that scandal break, the wages of sin…. HC had a John Doe case in Canada for failing to inform a woman prior to sex that he had herp and passing it on, ruining her fertility. Due to the medical damage, she won because they are spreading infertility via their STDs, we didn’t lynch cads without just cause. Patriarchy was right. Soon it’ll be prosecuted as rape by fraud, like a tranny lying to a man. Here here.

re epididymis

The clot shot will target the epithelial cells in it.

The mammalian epididymis is a highly specialized region of the male reproductive tract that is lined with a continuous layer of epithelial cells that display a remarkable level of regionalized secretory and absorptive activity. The luminal environment created by this combined secretory and absorptive activity is directly responsible for promoting the functional maturation of spermatozoa and their maintenance in a quiescent and viable state prior to ejaculation. This study was designed to identify the complement of microRNAs (miRNAs) that are expressed within the mouse epididymal epithelial cells and the maturing populations of spermatozoa. Through the use of Next Generation Sequencing technology we have demonstrated that both epididymal epithelial cells and spermatozoa harbour a complex repertoire of miRNAs that have substantially different expression profiles along the length of the tract. These data, deposited in the Gene Expression Omnibus (GEO) with the accession numbers GSE70197 and GSE70198, afford valuable insight into the posttranscriptional control of gene expression within the epididymis and provide the first evidence for the dynamic transformation of the miRNA content of maturing sperm cells. Ultimately such information promises to inform our understanding of the aetiology of male infertility. Herein we provide a detailed description of the methodology used to generate these important data.

It applies to sperm in other mammals too.

Mutant sperm causes miscarriages.

So the side effect of women miscarrying may not have been THEIR clot shot.

But some research over the past decade suggests that this might not always be the case. Some cases of recurrent miscarriages seem to involve the father having a high incidence of abnormal chromosomes in his sperm.

There aren’t any real estimates for how frequently the sperm is a factor in recurrent miscarriages, and chromosome problems in sperm aren’t believed to be a major cause of repeat losses. It does seem to be a possibility—especially in men whose sperm showed abnormal morphology or other markers of low fertility.

Sperm cannot repair cell damage like other cells in the body and this is a leading cause of male infertility. The damage also affects the DNA structure within the sperm and if it fertilizes an egg, this can potentially lead to miscarriage.

One study compared couples who experienced multiple miscarriages to couples with infertile men and fertile men. The result is that the sperm involved in the miscarriages was more likely to have signs of fragmentation at nearly the same rate as that of the infertile men.

TLDR: Stop blaming the women.

These sorts of results suggest that the correlation between SDF and fertility—both the inability to conceive and miscarriages—can be a factor. However, researchers are cautious to note that SDF alone cannot predict a couple’s risk of miscarriage.

Miscarriage is the woman’s body rejecting him because her mind was too dumb to. Like female weebs.

Unhealthy choices can lead to the many factors that decrease the chances of a successful pregnancy. This includes decreased sperm mobility and vitality, lower sperm counts, and abnormal morphology (the size and shape of sperm). It can also lead to physical damage. Any damage to sperm can cause fertility problems and, if an egg is fertilized, it may also lead to a miscarriage.

Test men early. No reason not to.

Don’t wait until miscarriage number 3.

Some physicians may recommend that men undergo tests for sperm quality when no other cause for recurrent miscarriages is found. The standard test is a sperm analysis, which looks at the shape, mobility, and sperm count in the sample.

Or test them FIRST prior to the trauma that’s 100% preventable by them jizzing in a cup?
The trauma that puts women off trying more?

Childless men more likely to die, as I suspected.

Manosphere get rekt.

It’s likely the sperm mutation is also affecting the brain by similar disease vectors like herp, causing childlessness but also early death. Like the rats attracted to cats.

They sense their low quality and hence, don’t bother to invest. Self-selection of genetic suicide. This is why the Spartans had a bachelor tax, it was a tax on the genetic dregs. All healthy men have a paternal instinct.

Men who wait until post-Wall to have kids, tend to have dead kids.

Risk of childhood mortality in family members of men with poor semen quality

So the kids they do have will die early, this is also seen among the mixed with rare genetic conditions.

What is known already: Semen quality is an established predictor of men’s somatic health. We can gain a better understanding of possible genetic or environmental determinants of the infertility phenotype by exploring familial aggregation of childhood mortality in relatives of men with poor semen quality.

Wider implications of the findings: We are not the first study to show a relationship between fertility and CMs. Children conceived through ART may be at higher risk of birth defects, however it is not known if the relationship is causal or if there is some underlying factor linking infertility and birth outcomes. This study provides further evidence that the increased risk of congenital birth defects may not be due to the ART, but rather genetic or environmental factors that link the two outcomes. We encourage further research in order to confirm a relationship between semen quality and increased risk for CM.

R-type children, like the fathers, age like shit.

COVID, sperm infertility and STD potential
COVID-19 and human spermatozoa—Potential risks for infertility and sexual transmission?

TLDR: scroll to end

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

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

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

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

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

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

If only someone warned you.

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

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

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

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

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

to put it in terms you degenerates can understand

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

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

now I am fucking with you yes indeedy do

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

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

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

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

From top paper:

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

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

Big Pharma Balls? Mutant metaplasia.

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

How many times must I try to save your nuts?

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

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

Why did you think they wanted to inject college kids?

also see

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

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

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

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

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

…Shut down Tinder.

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

The wages of sin – HPV in men and sperm infertility


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.

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


MRAs: crickets

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.

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.

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…

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?

>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.

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.

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.


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.


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.

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.

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.

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

brace yourselves

guess the result


go on

just guess



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?


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

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

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.

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


Sperm DNA fragmentation in couples with unexplained recurrent spontaneous abortions


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?


sure it is


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.

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?!

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.

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.


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

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

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


Oh, I’m not done yet.

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.

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

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

I can’t wait until October, all the “influencers” are pushing this online NOW. Ethically, I must put my ego aside.
A lot of Pill failures are actually in the hippy chicks taking plant “extracts”. That’s why doctors now ask young women about supplements and herbal remedies immediately after the contraception question. It wouldn’t be ethical to study pill failures but they know there’s a link.

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

so you cannot blame poverty, Karen.

Remember, they’re now encouraging wine moms to drink while pregnant.
They used to claim nicotine was a “safe” plant extract because the addictive property was removed, supposedly.
“CBD, THC use during early pregnancy can disrupt fetal development”
Nicotine was justified as anti-inflammatory too, and it is:
Still addictive!

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

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

Let’s trust those guys!

“muh no public health risks”

Buckle up, I found a LOT.

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

trans. minimal.

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

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

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

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

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

That came out after this:

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

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

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

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

The hippy Karens must be stopped.

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

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

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

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

The advice to women must account for this.
It’s called dope for a reason.

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

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

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

I knew this so I had to post.

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

re above study:

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

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

You also see sluggish cerebral flow in the low IQ. That’s why they call it dope. It has a dopifying effect.
Stupidity is bliss? It’s diagnostic.

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

CBF = cerebral blood flow

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

This has a lot of studies linked:

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

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


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

Aimed at minors.

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

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



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

I think this is the one:

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

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

4 =

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

5 =

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


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

How are these products on the market? HOW?

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

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

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

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

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

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

And it does.

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

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

IVF high in Denmark, wonder why?

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

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

Men are lied to and the SJWs love it.

From the sol link:

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

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

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

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

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

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

The method was flawless, before AND after.

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

Zoomers aren’t stupid, they’re polluted.

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

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

Superstitious minds

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

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

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

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

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

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

2015 Birth Defects in the Newborn Population: Race and Ethnicity

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

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

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

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

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

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

Craniofacial = ugly. 

Musculoskeletal = ugly. Well, dumpy.

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

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

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

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

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

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

Some superstitions have a basis in fact.

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

To see if you’re a SINNER!

[inc Thou shalt not adulterate]

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

We’re looking for spiteful mutants.

Now the post gets huge.

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

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

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

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

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

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

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

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

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


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

Do not hold information my lily-white arse.

Table link:

“Page does not exist”.

It’s this paper.

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

In an ONS report. They know.

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

(Black, 54%;

Mixed, Chinese and any other group, 44%;

White, 43%;

For a majority, that’s incredibly low.

and those where ethnicity was

not stated, 49%).

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

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

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

read: racially

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

Smaller brains too. Inbreeding depression but also group average by nation. Look at national IQ.
Bangladesh 82
Over one whole standard deviation below. According to the likes of Peterson, useless to a Western economy. The average Bangladeshi.
India 82
Recall regression to the mean. Also, friendliness correlates more to low IQ. Do not be fooled.
Pakistan 84
Thailand 91
Philippines 86
Nigeria 84
Jamaica 71, where we’re picking up new NHS nurses.

Enjoy that decline.

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

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

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

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

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

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

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

Something’s off.

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

Do you see what I see?

For non-statistically minded people:

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

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

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

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

Table 10 screen-capped, do your own charts.

Related studies, I do have a point about measurement error.
2009 Fertility by ethnic and religious groups in the UK, trends in a multi-cultural context

Asian tsunami in USA too

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

Ethnicity and IVF

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

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

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

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

We’ll see why.

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

Seriously. Measurement bias much?

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

We did that.

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

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

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

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

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

Genetics is the ONLY difference now.

You have NOTHING.

DNA causes germline DNA, really? Maybe?

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

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

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

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

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

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

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

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

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


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

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

The Ice Age killed the boyish ones.


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

I wonder which way.
Inbreeding or outbreeding depression?


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

Dudebros like “where’s da studies?”

I’m like “Have you even looked?”

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


TIL Wombs iz white supremacist.

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

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

Learn to read, weebs.

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

aka nice way of calling out deception

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

They know. It’s a cover-up.

Category errors galore.

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


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

What DO these studies have in common? [Asians]

Could also be child of rape as a confound.

You’ll see.

2012 Biracial couples and adverse birth outcomes: a systematic review and meta-analyses.

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

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

Your Third World surrogate plan may need retouching.

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

Why is it so hard to find studies about the most populous race on the planet?
What is associated with IQ and other development issues? Pre-term birth.

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

It’s mentioned along with smoking.

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

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

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

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

Their own women.

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

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

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

Clear defect evidence in the genes- study it!

But surely, you say, genetic issues would be also hormonal (hormones regulate genes as well) and apply to men?
Yes. Yes it would.

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

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

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

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

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

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

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

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


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

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

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

In the interest of intellectual honesty.


We literally have the studies. e.g. It’s metabolic.

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

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

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

Old expression.

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

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

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

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

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

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

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

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

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

NOBODY is jealous. You keep your secret fatty.

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

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

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

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

Hips don’t lie because biochemistry.

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

Waist-Hip Ratio and female beauty

The sexual dimorphism for this metric is obviously lowest on Asians.

Evidence is presented showing that body fat distribution as measured by waist-to-hip ratio (WHR) is correlated with youthfulness, reproductive endocrinologic status, and long-term health risk in women. Three studies show that men judge women with low WHR as attractive. Study 1 documents that minor changes in WHRs of Miss America winners and Playboy playmates have occurred over the past 30-60 years. Study 2 shows that college-age men find female figures with low WHR more attractive, healthier, and of greater reproductive value than figures with a higher WHR. In Study 3, 25- to 85-year-old men were found to prefer female figures with lower WHR and assign them higher ratings of attractiveness and reproductive potential. It is suggested that WHR represents an important bodily feature associated with physical attractiveness as well as with health and reproductive potential. A hypothesis is proposed to explain how WHR influences female attractiveness and its role in mate selection.

Hello sexual selection, tied intimately to natural selection.

PDF here:

also connected to “desire and capability for having childrenp7 or 299.

so K-type women may have better WHR.

Normal weight women have the most positive attributes associated.

Overweight category was universally unattractive.
It’d be nice to see a male study on this. I think Western women would want more children if fewer men were obese.

Why Asians are considered youthful but not sexy (they’d usually fall in the underweight group):

The variables of attractiveness, sexiness, and good health were located close to each other, suggesting that subjects perceived them to be closely related.

Attributes of desire and capability for having children were located close to each other in the solution space but farther from attractiveness, sexiness, and good health, implying that subjects did not perceive a great similarity between these two sets of attributes.

Finally, the attribute of youthfulness was located alone and away from both sets of other attributes. Thus, subjects apparently did not perceive youthfulness to be related to any other measured attributes of good health, sexiness, attractiveness, and desire and capability for having children.

So there’s that. Nobody’s jealous.

Figure N7 was located closer to attractiveness, sexiness, and good health as well as desire and capability for having children than any other Figure.

Normal weight for frame (and race) + most nubile WHR would make sense.
More of those genes survived.

Figure N9 was located closest to desire and capability for having children, whereas Figure N8 was located between Figure N7 and Figure N9. The figure N10 was grouped along with overweight figures, which were not perceived to be closely associated with any of the attributes under investigation. Underweight female figures, U7 and U8, were associated only with youthfulness. However, underweight figures with high WHR (U9 and U10) were perceived as neither youthful nor healthy, in spite of the fact that their depicted body weight was quite similar to figures with lower WHR.

Women with an atrocious WHR (boy hips, no waist) and under or overweight for their skeleton are objectively unattractive from an evolutionary standpoint. This would apply whether it’s a Jap, a Ruskie or an American.

Stop calling sexy science ‘racist’ because it doesn’t share your fetish.

This chart drags you harder than I ever could.

Your Asian girlfriend with the boy hips is approximately as attractive to the world as the average WHR white fat chick. That’s your level, accept it.

It’s also a fact we cannot accurately perceive attractiveness of the racial outgroup as well as our own, so an awareness of ingroup flaws changes nothing.

Most modern women straight up don’t look healthy, whether they’re American, European or, yes, Asian.

Stop trying to make boy hips = sexy happen. It’s not going to happen.

Look at the damn gradient on that underweight thing. The solution to fat women isn’t anorexia. That also suggests bad genes. In fact, at least the fat percentage on slightly overweight 0.7 WHR women suggests femininity and fertility.

“Overall, it seems that subjects inferred reproductive capability from body fat”

What does a foetus feed from?

“Thus, it seems that although WHR is related to health and attractiveness, body weight is perceived to be related to reproductive capability”


“As a group, underweight figures were assigned the lowest reproductive capability, followed by overweight figures and then normal weight figures.”

Suck on that, soyboys.

You actually tend to downgrade. That’s why the Democrat-voting soyboys all want an Asian girlfriend and expressly don’t want kids with it.

“Overall, it appears that both fatness and thinness are perceived as unattractive, and such figures are not perceived as having especially high reproductive potential. “

Not womanly. Remember that word? This:

Not girly, not sexy, not cute, not hot. Womanly.

You can’t discuss women in a reproductive, evolutionary context without it.

Thus, consistent with the present findings, men did not find thin or underweight figures attractive.

If you only care for other male opinions.

There is some evidence that suggests that being extremely underweight or overweight can have adverse effects on female reproductive functions.

Ya don’t say?

A critical body mass has been shown to be significantly related to the onset of menstrual cycle and its maintenance (Frisch & McCarthur, 1974), although recent evidence (DeRidder et al., 1990) suggests that it is the body fat distribution, rather than body fat mass or body weight, that is related to early pubertal development.

Distribution varies by race.

Africans are the most pronounced in women then Europeans shapely but delicate then Asians last – no shape, very yang flesh (broad but flat or full in the middle like cortisol fat) and almost nothing to distribute.

Am I imagining all of this?

Underweight females (15% below ideal body weight) have been reported to have a higher incidence of oligomenorrhea (menses 35 days or more apart) and amenorrhea and to have a higher prevalence of ovu-latory infertility than normal weight females (Green, Weiss, & Daling, 1986).

Underweight women also give birth to infants who are small and growth delayed, and such infants often have permanently impaired intellectual and physical development (Supy, Steer, McCusker, Steele, & Jacobs, 1988).

Menstrual dysfunction and ovulatory infertility also occur more often in females who are 20% above ideal body weight (Green et al., 1986). Morbid obesity in females with high WHR has been shown to increase the degree of androgenicity (increased percentage of free testosterone) and associated menstrual and ovulatory problems (Kirschner & Samojilik, 1991). Thus, the reproductive success of a woman may be low in spite of a high level of fat deposits if the regional distribution of fat is not appropriate, that is, gynoid.


Finally, the finding that underweight figures were assigned high rankings for youthfulness but not for attractiveness (or other attributes related to reproductive potential) is difficult to reconcile with some evolutionarily based mate selection hypotheses.

Normal men aren’t pedos.

Youthfulness and health have been proprosed as absolute criteria for female attractiveness (Symons, 1987).

Stick with health.

Health has good or bad, you have no negative way to assess youth e.g. immature.

Features of physical appearance associated with youth supposedly provide the strongest and most reliable cues for female reproductive potential. The present finding illustrates that the relationship of youthfulness and attractiveness is quite complex.

Not really.

A woman who is judged to be attractive is also found to be youthful; however, youthfulness alone does not make a woman attractive. Apparently, youthfulness is a necessary, but not a sufficient condition, for determination of female physical attractiveness.

crazed pointing-

also, don’t try to chalk this up to taste:

“Furthermore, if the ideal of female attractiveness is arbitrary and ever changing, no evidence of transgenerational stability in the meaning of WHR should be found, as older men are more likely to be exposed to different ideals of attractiveness than are younger men.”


“Older men did not associate health with underweight figures, including those with lower WHR.”

TLDR: Pedos are wrong. Underweight, waistless wonders are not attractive.

Study 2, rubbing salt in that fact.

Optimal Waist-to-Hip Ratios in Women Activate Neural Reward Centers in Men

Secondary sexual characteristics convey information about reproductive potential. In the same way that facial symmetry and masculinity, and shoulder-to-hip ratio convey information about reproductive/genetic quality in males, waist-to-hip-ratio (WHR) is a phenotypic cue to fertility, fecundity, neurodevelopmental resources in offspring, and overall health, and is indicative of “good genes” in women. Here, using fMRI, we found that males show activation in brain reward centers in response to naked female bodies when surgically altered to express an optimal (∼0.7) WHR with redistributed body fat, but relatively unaffected body mass index (BMI). Relative to presurgical bodies, brain activation to postsurgical bodies was observed in bilateral orbital frontal cortex. While changes in BMI only revealed activation in visual brain substrates, changes in WHR revealed activation in the anterior cingulate cortex, an area associated with reward processing and decision-making. When regressing ratings of attractiveness on brain activation, we observed activation in forebrain substrates, notably the nucleus accumbens, a forebrain nucleus highly involved in reward processes.

These findings suggest that an hourglass figure (i.e., an optimal WHR) activates brain centers that drive appetitive sociality/attention toward females that represent the highest-quality reproductive partners. This is the first description of a neural correlate implicating WHR as a putative honest biological signal of female reproductive viability and its effects on men’s neurological processing.


Study 3

Men report stronger attraction to femininity in women’s faces when their testosterone levels are high

Many studies have shown that women’s judgments of men’s attractiveness are affected by changes in levels of sex hormones. However, no studies have tested for associations between changes in levels of sex hormones and men’s judgments of women’s attractiveness. To investigate this issue, we compared men’s attractiveness judgments of feminized and masculinized women’s and men’s faces in test sessions where salivary testosterone was high and test sessions where salivary testosterone was relatively low.

This is why we need studies on men too.

Men reported stronger attraction to femininity in women’s faces in test sessions where salivary testosterone was high than in test sessions where salivary testosterone was low. This effect was found to be specific to judgments of opposite-sex faces. The strength of men’s reported attraction to femininity in men’s faces did not differ between high and low testosterone test sessions, suggesting that the effect of testosterone that we observed for judgments of women’s faces was not due to a general response bias. Collectively, these findings suggest that changes in testosterone levels contribute to the strength of men’s reported attraction to femininity in women’s faces and complement previous findings showing that testosterone modulates men’s interest in sexual stimuli.

Study 4

Beauty is in the eye of the plastic surgeon: Waist–hip ratio (WHR) and women’s attractiveness

Attractiveness conveys reliable information about a woman’s age, health, and fertility. Body fat distribution, as measured by waist-to-hip ratio (WHR), is a reliable cue to a woman’s age, health, and fertility, and affects judgment of women’s attractiveness. WHR is positively correlated with overall body weight or body mass index (BMI). Some researchers have argued that BMI, rather than WHR, affects judgments of female attractiveness. To evaluate the role of WHR, independent of BMI, we secured photographs of pre- and post-operative women who have undergone micro-fat grafting surgery. In this surgery, surgeons harvest fat tissue from the waist region and implant it on the buttocks. Post-operatively, all women have a lower WHR but some gain weight whereas others lose body weight. Results indicate that participants judge post-operative photographs as more attractive than pre-operative photographs, independent of post-operative changes in body weight or BMI. These results indicate that WHR is a key feature of women’s attractiveness.


Let’s look historically. Study 5

Trends in waist-to-hip ratio and its determinants in adults in Finland from 1987 to 1997

Background: Although abdominal obesity has been shown to be an important risk factor for cardiovascular disease and a variety of other diseases, secular changes in fat distribution in populations have rarely been documented.

Objective: Our objective was to assess trends in waist-to-hip ratio (WHR) in the Finnish population during a 10-y period. In addition, we investigated the associations of WHR with body mass index (BMI), age, education, and lifestyle factors.

Design: Three independent cross-sectional surveys were carried out at 5-y intervals between 1987 and 1997. Altogether, 15096 randomly selected men and women aged 25–64 y participated in these surveys.

Results: The WHR increased in both men and women during the 10-y period (P< 0.0001). In men, the strongest upward trend took place in the first 5-y period and then seemed to plateau; in women, the WHR continued to increase into the 1990s. In both sexes, the most prominent increase was observed in subjects aged ≥45 y. The WHR increased in all education-level groups, the lowest WHR being among those with the highest education. Age (18% in men, 12% in women) and BMI (33% in men, 25% in women) accounted for most of the variation in WHR, whereas only 3% was explained by education and lifestyle factors.

Conclusions: Abdominal obesity is a growing problem in Finland, especially in persons aged ≥45 y. These adverse changes in body shape continued to take place, particularly in women, in the 1990s.

Something in the food?

More history, prehistoric. Study 6

Preferred Women’s Waist-to-Hip Ratio Variation over the Last 2,500 Years

The ratio between the body circumference at the waist and the hips (or WHR) is a secondary sexual trait that is unique to humans and is well known to influence men’s mate preferences. Because a woman’s WHR also provides information about her age, health and fertility, men’s preference concerning this physical feature may possibly be a cognitive adaptation selected in the human lineage. However, it is unclear whether the preferred WHR in western countries reflects a universal ideal, as geographic variation in non-western areas has been found, and discordances about its temporal consistency remain in the literature. We analyzed the WHR of women considered as ideally beautiful who were depicted in western artworks from 500 BCE to the present. These vestiges of the past feminine ideal were then compared to more recent symbols of beauty: Playboy models and winners of several Miss pageants from 1920 to 2014. We found that the ideal WHR has changed over time in western societies: it was constant during almost a millennium in antiquity (from 500 BCE to 400 CE) and has decreased from the 15th century to the present. Then, based on Playboy models and Miss pageants winners, this decrease appears to slow down or even reverse during the second half of the 20th century. The universality of an ideal WHR is thus challenged, and historical changes in western societies could have caused these variations in men’s preferences. The potential adaptive explanations for these results are discussed.

Should’ve controlled for race.

Why not look at male WHR? Plus sperm health? Found:

  • The volume of ejaculate decreases in a linear fashion with increasing BMI (suggesting an inverse relationship).
  • The sperm quality and viability declines with increasing waist circumference.
  • Investigators also discovered that quality of semen decreases (such as sperm viability, motility, semen volume) with increasing body size; however, no relationship was observed between sperm DNA fragmentation index and physical activity or obesity.

Latter requires time.

Various research and clinical studies suggests that subfertility in men is multifactorial i.e. several factors can impact the quality of reproductive health.

  • Abnormal sperm production: Study conducted by Jensen and associates (2) suggested that abnormal BMI is very strongly linked to impaired sperm production. One of the many reasons is, abnormal metabolism of testosterone (which plays a key role in the production of healthy and viable sperms).
  • Abdominal obesity and risk of metabolic disorders: According to a new study reported in the Human Reproduction (3), investigators provided statistical evidence that abnormal BMI and abdominal obesity is very strongly linked to a number of health issues (such as cardiovascular dysfunction, atherosclerosis, type 2 diabetes, hypertension and others). Needless to say that these health issues have a deleterious effect on the sexual health regardless of the body-mass index (or BMI).
  • Obesity, physical activity and testosterone: Testosterone levels tends to decline in males who have a sedentary lifestyle. Various research and clinical studies indicates that aerobic activity or exercise can improve testosterone metabolism in males significantly.

1. Eisenberg, M. L., Kim, S., Chen, Z., Sundaram, R., Schisterman, E. F., & Louis, G. M. B. (2014). The relationship between male BMI and waist circumference on semen quality: data from the LIFE study. Human Reproduction, 29(2), 193-200.

2. Jensen, T. K., Andersson, A. M., Jørgensen, N., Andersen, A. G., Carlsen, E., & Skakkebæk, N. E. (2004). Body mass index in relation to semen quality and reproductive hormones among 1,558 Danish men. Fertility and sterility, 82(4), 863-870.

3. Hammiche, F., Laven, J. S., Twigt, J. M., Boellaard, W. P., Steegers, E. A., & Steegers-Theunissen, R. P. (2012). Body mass index and central adiposity are associated with sperm quality in men of subfertile couples. Human reproduction, 27(8), 2365-2372.

Yet they don’t tell men this information.

Back to women

Cross-cultural variation in men’s preference for sexual dimorphism in women’s faces.

Both attractiveness judgements and mate preferences vary considerably cross-culturally.


We investigated whether men’s preference for femininity in women’s faces varies between 28 countries with diverse health conditions by analysing responses of 1972 heterosexual participants. Although men in all countries preferred feminized over masculinized female faces, we found substantial differences between countries in the magnitude of men’s preferences. Using an average femininity preference for each country, we found men’s facial femininity preferences correlated positively with the health of the nation, which explained 50.4% of the variation among countries. The weakest preferences for femininity were found in Nepal and strongest in Japan. As high femininity in women is associated with lower success in competition for resources and lower dominance, it is possible that in harsher environments, men prefer cues to resource holding potential over high fecundity.

Asia is weird for dimorphism studies.

Hence the focus on health.

While the economy is bad, it isn’t surprising men prefer manly looking women.

It’s temporary. There’ll be a flood of divorces as the economy improves. Men will suddenly see how mannish the wife has been and be repulsed. Menopause also makes women look more mannish, including higher WHR. So much for a youth argument there.

Click to access nihms827194.pdf

Factors Underlying the Temporal Increase in Maternal Mortality in the United States

They don’t say more non-white mothers or more mixed race babies, so it’s wrong. They guess.

Unvaccinated mortality rate and scapegoating

Rhetoric: “If you don’t vaccinate, you’re much more likely to die.”

Title: “Evidence of Increase in Mortality After the Introduction of Diphtheria–Tetanus–Pertussis Vaccine to Children Aged 6–35 Months in Guinea-Bissau: A Time for Reflection?” 2018

35 months? A decent study length, for once.

I could leave it at this but since “cherrypicked” is the next goalpost position they slide to, shamelessly, after claiming “no valid empirical studies”, this’ll be a slightly longish post. It’s a doozy. Bring tea. 8k words.

When studies are available, there is a range of errors in the method.
A range of “errors”. I also debunk the myth at the end of unvaccinated children being ‘dangerous’. It’s the biggest font, can’t miss it and also the “ahrp” link, if you text search.

You can ignore me, but not your loud conscience.

Mawson, published April 2017. STILL available, contrary to lies. Abstract:

Vaccinations have prevented millions of infectious illnesses, hospitalizations and deaths among U.S. children, yet the long-term health outcomes of the vaccination schedule remain uncertain. Studies have been recommended by the U.S. Institute of Medicine to address this question. This study aimed 1) to compare vaccinated and unvaccinated children on a broad range of health outcomes, and 2) to determine whether an association found between vaccination and neurodevelopmental disorders (NDD), if any, remained significant after adjustment for other measured factors. A cross-sectional study of mothers of children educated at home was carried out in collaboration with homeschool organizations in four U.S. states: Florida, Louisiana, Mississippi and Oregon. Mothers were asked to complete an anonymous online questionnaire on their 6- to 12-year-old biological children with respect to pregnancy-related factors, birth history, vaccinations, physician-diagnosed illnesses, medications used, and health services. NDD, a derived diagnostic measure, was defined as having one or more of the following three closely-related diagnoses: a learning disability, Attention Deficient Hyperactivity Disorder, and Autism Spectrum Disorder. A convenience sample of 666 children was obtained, of which 261 (39%) were unvaccinated. The vaccinated were less likely than the unvaccinated to have been diagnosed with chickenpox and pertussis, but more likely to have been diagnosed with pneumonia, otitis media, allergies and NDD. After adjustment, vaccination, male gender, and preterm birth remained significantly associated with NDD. However, in a final adjusted model with interaction, vaccination but not preterm birth remained associated with NDD, while the interaction of preterm birth and vaccination was associated with a 6.6-fold increased odds of NDD (95% CI: 2.8, 15.5). In conclusion, vaccinated homeschool children were found to have a higher rate of allergies and NDD than unvaccinated homeschool children. While vaccination remained significantly associated with NDD after controlling for other factors, preterm birth coupled with vaccination was associated with an apparent synergistic increase in the odds of NDD. Further research involving larger, independent samples and stronger research designs is needed to verify and understand these unexpected findings in order to optimize the impact of vaccines on children’s health.


Let’s quote, shall we? I didn’t list everything sig, just the big findings.

Under ‘results’, 92% of the children studied were white, as a liar tries to claim later, race cannot be a factor preventing such studies. 8.5% high school or less, no SES confound. 91.2% Christian, other categories unlisted. 93.7% married women.

Table 3 contains chronic conditions.
ADHD 4.7% vacc 1% NOT – p=0.013
ASD 4.7% vacc 1% NOT – p=0.013
Learning disability 5.7% vacc, 1.2% NOT – p=0.003
Neurodevelopment Disorder 10.5% vacc, 3.1% NOT – p=< 0.001
Any Chronic Condition (inc minor) 44% vacc, 24.9% NOT – p=< 0.001.

Table 6
Used antibiotics in the past 12 months p=< 0.001
Sick visit to doctor in the past year p=< 0.001
Seen doctor for checkup in past 12 months p=< 0.001

The figure shows that the single largest group of diagnoses was learning disability (n=15) followed by ASD (n=9), and ADHD (n=9), with smaller numbers comprising combinations of the three diagnoses.”

NDD “Two factors that almost reached statistical significance were vaccination during pregnancy (OR 2.5, 95% CI: 1.0, 6.3) and three or more fetal ultrasounds (OR 3.2, 95% CI: 0.92, 11.5).”

Table 7 NDD and vaccination status p=<0.001

Following a recommendation of the Institute of Medicine [19] for studies comparing the health outcomes of vaccinated and unvaccinated children, this study focused on homeschool children ages 6 to 12 years”
“Data from the survey were also used to determine whether vaccination was associated specifically with NDDs, a derived diagnostic category combining children with the diagnoses of learning disability, ASD and/or ADHD.”


“With regard to acute and chronic conditions, vaccinated children were significantly less likely than the unvaccinated to have had chickenpox and pertussis but, contrary to expectation, were significantly more likely to have been diagnosed with otitis media, pneumonia, allergic rhinitis, eczema, and NDD.”

The vaccinated were also more likely to have used antibiotics, allergy and fever medications; to have been fitted with ventilation ear tubes; visited a doctor for a health issue in the previous year, and been hospitalized.”

“The reason for hospitalization and the age of the child at the time were not determined, but the latter finding appears consistent with a study of 38,801 reports to the VAERS of infants who were hospitalized or had died after receiving vaccinations.

I don’t think they included deceased children (no) in this one so the numbers would go up.

The study reported a linear relationship between the number of vaccine doses administered at one time and the rate of hospitalization and death; moreover, the younger the infant at the time of vaccination, the higher was the rate of hospitalization and death [55]. The hospitalization rate increased from 11% for 2 vaccine doses to 23.5% for 8 doses (r2 = 0.91), while the case fatality rate increased significantly from 3.6% for those receiving from 1-4 doses to 5.4 % for those receiving from 5-8 doses.”

Informed consent?

“However, the ASD prevalence of 2.24% from a CDC parent survey is lower than the study rate of 3.3%. Vaccinated males were significantly more likely than vaccinated females to have been diagnosed with allergic rhinitis, and NDD. The percentage of vaccinated males with an NDD in this study (14.4%) is consistent with national findings based on parental responses to survey questions, indicating that 15% of U.S. children ages 3 to 17 years in the years 2006-2008 had an NDD [28].”

“Vaccination was strongly associated with both otitis media and pneumonia, which are among the most common complications of measles infection [56,57]. The odds of otitis media were almost four-fold higher among the vaccinated (OR 3.8, 95% CI: 2.1, 6.6) and the odds of myringotomy with tube placement were eight-fold higher than those of unvaccinated children (OR 8.0, 95% CI: 1.0, 66.1).”

“found an increased frequency of M. catarrhalis colonization in the vaccinated group compared to the partly immunized and control groups (76% vs. 62% and 56%, respectively). A high rate of Moraxella catarrhalis colonization is associated with an increased risk of AOM [65].”
“These observations have suggested that eradication of vaccine serotype pneumococci can be followed by colonization of other bacterial species in the vacant nasopharyngeal niche, leading to disequilibria of bacterial composition (dysbiosis) and increased risks of otitis media. Long-term monitoring has been recommended as essential for understanding the full implications of vaccination-induced changes in microbiota structure [67].”

After adjustment, the factors that remained significantly associated with NDD were vaccination, nonwhite race, male gender, and preterm birth.”

“The present study suggests that vaccination could be a contributing factor in the pathogenesis of NDD but also that preterm birth by itself may have a lesser or much reduced role in NDD (defined here as ASD, ADHD and/or a learning disability) than currently believed. The findings also suggest that vaccination coupled with preterm birth could increase the odds of NDD beyond that of vaccination alone.”

Assessment of the long-term effects of the vaccination schedule on morbidity and mortality has been limited [71]. In this pilot study of vaccinated and unvaccinated homeschool children, reduced odds of chickenpox and whooping cough were found among the vaccinated, as expected, but unexpectedly increased odds were found for many other physician-diagnosed conditions. Although the cross-sectional design of the study limits causal interpretation, the strength and consistency of the findings, the apparent “dose-response” relationship between vaccination status and several forms of chronic illness, and the significant association between vaccination and NDDs all support the possibility that some aspect of the current vaccination program could be contributing to risks of childhood morbidity.

Vaccination also remained significantly associated with NDD after controlling for other factors, whereas preterm birth, long considered a major risk factor for NDD, was not associated with NDD after controlling for the interaction between preterm birth and vaccination. In addition, preterm birth coupled with vaccination was associated with an apparent synergistic increase in the odds of NDD above that of vaccination alone. Nevertheless, the study findings should be interpreted with caution. First, additional research is needed to replicate the findings in studies with larger samples and stronger research designs. Second, subject to replication, potentially detrimental factors associated with the vaccination schedule should be identified and addressed and underlying mechanisms better understood. Such studies are essential in order to optimize the impact of vaccination of children’s health.”

True. Tell Gorski that. Further reading.

55 Goldman GS, Miller NZ (2012) Relative trends in hospitalizations and mortality among infants by the number of vaccine doses and age, based on the Vaccine Adverse Event Reporting System (VAERS), 1990-2010. Hum Exp Toxicol 31: 1012-1021
71 Fisker AB, Hornshøj L, Rodrigues A, Balde I, Fernandes M, et al. (2014) Effects of the introduction of new vaccines in Guinea-Bissau on vaccine coverage, vaccine timeliness, and child survival: an observational study. Lancet Glob Health 2: e478-e487.

However, tetanus might be a good one to get, if you are likely to be exposed.

Preferably before pregnancy.

The foreign death rate for rotavirus doesn’t actually check if vaccines decrease deaths?

Flu benefit lies

<10% elderly deaths from flu in USA, claimed benefit five-fold.

Infant mortality:
In conclusion “These findings demonstrate a counter-intuitive relationship: nations that require more vaccine doses tend to have higher infant mortality rates.”
“A closer inspection of correlations between vaccine doses, biochemical or synergistic toxicity, and IMRs, is essential. All nations—rich and poor, advanced and developing—have an obligation to determine whether their immunization schedules are achieving their desired goals.”

Vaccination and All-Cause Child Mortality From 1985 to 2011: Global Evidence From the Demographic and Health Surveys
“Childhood vaccination, and in particular measles and tetanus vaccination, is associated with substantial reductions in childhood mortality.”
Nobody really dies from measles anymore.
Their estimations, not a real study.
“The results indicate that measles vaccination is associated with a relative risk of mortality of 0.83, whereas maternal tetanus vaccination is associated with a relative risk of 0.92
Really? So little. I retract the tetanus thing.
“Generally, it is not possible to estimate the association between vaccination status and mortality at the individual level in household survey data, such as the DHS, because the vaccination status of children who have died is not usually reported (36)”
Lying directly. So just get the data?
“An additional advantage of this aggregate analysis is that it allows us to capture potential herd immunity (37–39), which would not typically be observed in an individual-level analysis.”

36 Cutts FT, Izurieta HS, Rhoda DA. Measuring coverage in MNCH: design, implementation, and interpretation challenges associated with tracking vaccination coverage using household surveys. PLoS Med. 2013;105:e1001404.
I hope I’m including enough references, wouldn’t want to disappoint anyone.
Measles study method issues.

Growing infertility epidemic, CDC:

“Although some perceive infertility as a quality-of-life issue, the American Society for Reproductive Medicine (ASRM) regards infertility as a disease (3). A U.S. Supreme Court opinion agreed with a lower court statement that reproduction is a major life activity and confirmed that conditions that interfere with reproduction should be regarded as disabilities, as defined in the Americans with Disabilities Act (4).”

And according to international law, deliberately bringing about impaired fertility is GENOCIDE, see d.

Wait, is preventing reproduction (a “major life activity”) by forced poverty, thanks to tax redistribution so others CAN have kids, illegal? Seems so.

“Although the focus of research and services has traditionally been on women (and, as a consequence, much of this article reflects it), fertility impairments may be just as common among men (6). The statistics cited above distinguish impaired fecundity from infertility. In this article we refer to infertility more broadly, including all fertility impairments. Recurrent pregnancy loss (miscarriage) is a component of impaired fecundity, distinct from infertility (ASRM, unpublished data) and is not included in this presentation.”

It started with Boomers, the free love generation, putting off reproduction. I wonder if STDs might be a cause?

“African American women had a twofold increase in odds of reporting a history of infertility (9).”

Mixed women? Is the same true in full African immigrants?

“Different subgroups may have infertility of different etiology.”

“In 2006, reported chlamydia rates were eight times higher among African Americans than among whites, highlighting the large disparities in this important risk factor for infertility (13).”

“Other modifiable factors contribute to the burden of infertility. Although the proportion of male factor infertility due to varicocele is unknown, this common condition is reported in approximately half of the inpatient surgery services and approximately two thirds of office visits for male factor infertility in the United States (14)”

“Although the proportion of infertility that is due to tobacco smoking is unknown, infertility specialists are increasingly aware that exposure to tobacco products can cause infertility”

Including secondhand?
The ban moaners have explaining to do.

“Obesity in men is associated with erectile dysfunction and decreased androgen production, but its effects on male fertility are not as clear (30).”

“A public health strategy focusing on primary prevention (e.g., through removal of risk factors for infertility such as those described above) would reduce the prevalence of infertility,”

Why do I mention that? Here.
“A lowered probability of pregnancy in females in the USA aged 25–29 who received a human papillomavirus vaccine injection” 2018

“Shortly after the vaccine was licensed, several reports of recipients experiencing primary ovarian failure emerged.”

trans. Instant shutdown.

“Using logistic regression to analyze the data, the probability of having been pregnant was estimated for females who received an HPV vaccine compared with females who did not receive the shot. Results suggest that females who received the HPV shot were less likely to have ever been pregnant than women in the same age group who did not receive the shot. If 100% of females in this study had received the HPV vaccine, data suggest the number of women having ever conceived would have fallen by 2 million. Further study into the influence of HPV vaccine on fertility is thus warranted.”


“If the association is causation, however, DeLong’s math suggests that if all the females in this study had received the HPV vaccine, the number of women having ever conceived would have fallen by two million. That’s not two million missing children. That’s two million women who can’t conceive one, two, or any children.”

Less contraceptive use should translate to more babies among the vaccinated.”

“Male sperm counts have nosedived in recent decades – scientists published data last year showing that globally, they have dropped 50 percent in just the past 40 years – signalling serious unidentified environmental hazards.”

They should look at whether r or K-types have higher or lower than normal fertility.

HPV vaccination – as well as tetanus vaccination – has been linked in medical literature to a condition called anti-phospholipid syndrome which is a poorly defined disease caused when the immune system erroneously manufactures antibodies against certain lipid proteins found in membranes that are in a host of tissues — eyes, heart, brain, nerves, skin – and the reproductive system. One 2012 study by Serbian researchers at the Institute for Virology, Vaccines and Ser “Torlak” found that “hyperimmunisation” of the immune system with different adjuvants, including aluminum, in mice, resulted in induction of antiphospholipid syndrome and the tandem lowering of fertility.””

That study:

You cannot discuss female fertility without male.

“Other research has implicated aluminum in conception problems. French infertility researcher Jean-Philippe Klein and his colleagues at the University of Lyon published the results of their 2014 study of the sperm of men seeking assistance at a French infertility clinic.”

That study:

From it:

This study provided unequivocal evidence of high concentrations of aluminum in human semen and suggested possible implications for spermatogenesis and sperm count.

I recommend chelation therapy studies, for all concerned with what I think.

And back:

Merck’s HPV vaccine test ““placebos” contained both the high doses of aluminium as well as another scary ingredient, polysorbate 80. This chemical has exhibited delayed ovarian toxicity to rat ovaries at all injected doses tested over a tenfold range.”

I’m sure they aren’t planning to make you infertile. (Scroll down).

“None of the trials accurately assessed the long-term impact of the vaccine on the reproductive health of girls”

Actually many brought that up at the time it was pushed.

“Why make a vaccine for a disease that afflicts less than 0.3% of people in their lifetime?”

It’s now being pushed on men like they’re gay (anal cancer risk). Penile cancer may go up though thanks to anal sex.


increase of 23% of this rare cancer alone since early 90s, when porn use was lower]

Actually, decided to look up anal cancer, look at this:
“Since the early 1990s, anal cancer incidence rates have increased by almost two-thirds (63%) in the UK. Rates in males have increased by a fifth (20%), and rates in females have increased by almost two times (99%).”
What could possibly account for such a huge sex difference? I wonder…
“91% of anal cancer cases in the UK are caused by HPV infection.
Around 91% of anal cancers in women and 75% in men are HPV-positive, a meta-analysis showed.
Anal cancer risk may be higher in people participating in anal sexual behaviours (including but not limited to receptive anal intercourse)”


“In the case of heterosexual anal intercourse it is the woman who is at risk to develop fecal incontinence.”
Lovely way to treat the wife.

“The American Cancer Society reports, “Receptive anal intercourse also increases the risk of anal cancer in both men and women, particularly in those younger than 30.” 7 HPV (human papillomavirus) is the main cause of anal cancer; but apparently, anal intercourse in particular increases the likelihood that the virus will attack the anus or rectum.”

Why does this remind me of the Pill?
Relevance of immuno-contraceptive vaccines for population control

Gates Foundation own vaccine stock

High-titre measles vaccine and female mortality
“Hence, the new hypothesis has created increasing consistency in existing data, which suggest that causal processes might be involved. This consistency across different studies should reduce the likelihood of chance as an explanation.”
Underreporting Vaccine Adverse Events
“How can they dismiss placebo-controlled trials that raise serious possibilities of vaccine-caused illness?”

No comment.

“Whatever their previous menstrual history women, especially the nulliparous, who are concerned about their future fertility should be recommended oral contraception in preference to an intrauterine device.”
Compared to?
2018 Discrepancies in the evaluation of the safety of the human papillomavirus vaccine
“In this article we bring the attention on certain adverse effects of the vaccine against HPV that have not been well studied as they are not well defined.”
It seems the WHO lied.
“We also compare the different approaches on HPV vaccine policies regarding its adverse reactions in countries like Japan and Colombia, vs. the recommendations issued by the WHO.”
“Pandemic mortality rates in 1918 and in 2009 were highest among those with the lowest socioeconomic status (SES). Despite this, low SES groups are not included in the list of groups prioritized for pandemic vaccination, and the ambition to reduce social inequality in health does not feature in international and national pandemic preparedness plans. We describe plans for a systematic review and meta-analysis of the association between SES and pandemic outcomes during the last five pandemics.”
Estimating the annual attack rate of seasonal influenza among unvaccinated individuals: A systematic review and meta-analysis
Overall, we found that approximately 1 in 5 unvaccinated children and 1 in 10 unvaccinated adults were estimated to be infected by seasonal influenza annually, with rates of symptomatic influenza roughly half of these estimates. Our findings help to establish the background risk of seasonal influenza infection in unvaccinated individuals.”
Okay, compared to? Why not look at vaccinated?
2018 Does consecutive influenza vaccination reduce protection against influenza: A systematic review and meta-analysis
“Dose-response results (≥3 consecutive vaccinations) did show a reduction in effectiveness.
Certainty in the evidence is very low due to inconsistency and imprecision.
The findings do not rule out the possibility of reduced effectiveness.”
2018 Influenza vaccine effectiveness in older adults compared with younger adults over five seasons
Over 5 seasons, influenza vaccination provided similar levels of protection among older and younger adults, with lower levels of protection against influenza A(H3N2) in all ages.”
Effectiveness of MF59-adjuvanted seasonal influenza vaccine in the elderly: A systematic review and meta-analysis
“Adjuvantation with MF59 may increase vaccine effectiveness among seniors.”

Lucky them.
Read the whole thing for this link, it’s short. Quoting in case it gets taken down.


“In the last few days there have been multiple news articles and testimonies in the Maine and Vermont legislatures about the need to impose vaccine mandates to protect immunocompromised children.[1] [2] I attended the vaccine bills’ hearing in Augusta, Maine on May 11, which lasted into the night. I also attended the Vermont Senate hearing 3 weeks earlier. The Vermont Senate committee said it would only hear testimony from physicians, which is why I was invited. Not very many doctors are familiar with the vaccine literature. Vaccines are, surprisingly, an arcane area of medicine.

I feel safe.

Unfortunately, I heard not a single expert (at either hearing) provide any data about the magnitude of the problem that vaccine mandates are supposed to fix. In fact, I was quite surprised to learn that helping the immunocompromised seemed to be the major justification to remove vaccine exemptions.

I heard no one mention the fact that vaccine efficacies of 40%, 60%, 80% (approximately correct for influenza, diphtheria, mumps vaccines) might also pose some risk to the immunodeficient. (These are just examples; most other vaccines have efficacy in the 60-90% range.) Actually, any statistician could tell you that low efficacy poses considerably more risk than exemption rates of 1-5% in Maine (depending on which required vaccine we are discussing). Vaccines with low efficacy make the claim of herd immunity a joke–but did even one “expert” at the hearings know or care?

Herd immunity of 100% (impossible) wouldn’t prevent mortality.

Herd immunity is a myth. The extreme case’s claim is demonstrably false.

How much risk is actually posed by “vaccine-preventable” diseases to the immunocompromised? I reviewed the most common infections seen in those at highest risk: stem cell transplant recipients[3] and leukemia patients.[4]

Here is what I found….”

Shit, someone who cares.

“The limited data show that community acquired respiratory viruses (CARVs) and herpesviruses are the most common pathogens.”
“The reports on human herpes virus (HHV)-6 diseases are increasing…”
“Herpesvirus pneumonia is usually caused by reactivation of latent viruses which occurs in severe immunosuppression.”
“… viral encephalitis was mainly caused by human herpes virus (HHV)-6, followed by EBV, HSV, JC virus, CMV, VZV in the recipients of allo-HSCT. Our data showed that herpesvirus-associated encephalitis was mainly caused by EBV followed by HSV, CMV and VZV…
The most frequent pathogens of viral hepatitis are hepatitis B virus (HBV) and hepatitis C virus (HCV). Besides these, other viruses such as CMV and HSV may also result in hepatitis. Hepatitis B and C can be caused by either virus reactivation or blood transmission…””

There are also many bacterial and fungal infections they may develop: too many to list. Of the many infections these patients tend to develop, the only 3 infections commonly seen, for which there exists a vaccine and which spread between children, are chickenpox (varicella zoster virus or VZV), influenza, and rotavirus.

Rotavirus is a relatively mild gastrointestinal virus and mortality, even in those with impaired immunity, is rare.[5]

Influenza is a real concern, but influenza vaccines are notoriously ineffective. This year, CDC said the vaccine had 19% efficacy.[6] (A Canadian study found no efficacy for this year’s flu vaccine.) Over the past ten years, CDC’s efficacy estimates for influenza vaccines averaged 40%.[7] So even if everyone in America was vaccinated, you could not generate herd immunity for influenza. You could not achieve the desired “cocoon” for those most vulnerable.

Remember the word cocoon, please.

Chickenpox is caused by a virus that, once you have been infected, will live forever in your nerve cells. The vaccine virus also does this. Immunocompromised patients developing chickenpox/VZV infections are usually reactivating latent virus long present in their own bodies. Only very rarely are they “catching” chickenpox virus from someone else. Fortunately, we have antiviral drugs and immune globulin to prevent and treat these common reactivations.”

Her bold in this paragraph:

“Let me repeat: vulnerable, immunodeficient children are susceptible to many viral, bacterial and fungal infections, but these are very rarely caused by child to child spread of microorganisms for which we have vaccines. They are listed in footnotes 3 and 4.



For those who want to waste my time digging up a never-ending stream of references.

It is troubling that vulnerable families have been encouraged to fear and stigmatize unvaccinated children, when the rates of primary and secondary vaccine failures (i.e., number of vaccinated kids who lack immunity despite their vaccinations) are far greater than the rates of children lacking vaccinations. [CDC’s 2012-13 kindergarten vaccine exemption rates by state ranged from a low of 0.1% to a high of 6.5%.]

In fact, the vaccine failures pose a much larger risk. But are the immunocompromised suffering and dying due to other childrens’ vaccine failures? We are not hearing about it.


If the vulnerable are not being harmed by vaccinated children who lack immunity, then it follows they are not suffering from exposure to the unvaccinated, either.


You have no right to forbid children their education on medical grounds, it is a right.

Low IQ is medical too, you heap those ghetto kids in. Being stabbed is a more prevalent danger.

Don’t vulnerable families have enough real problems, without adding unfounded and unjustified fears? Isn’t it time to drop this canard?

But then how will they emotionally blackmail us into buying their products?

The gaslighting of “you’re killing babies” – seldom levied at the aborting parents?

As I said in an earlier post, the last measles deaths in the United States (there were 2) occurred in 2003. One was elderly; the other was aged 13 and had had a bone marrow transplant. I was unable to learn if his infection was from a vaccine strain or wild-type measles virus. Not a single American has died from measles since.

We need to know if vulnerable, immunocompromised children are catching and dying from vaccine-preventable diseases, and from whom they are catching these diseases: from the vaccinated, from the unvaccinated, or from their own latent viruses? From vaccine strains or wild-type infections?

from WHOM indeed

test the genetics of what they come down with, check for a match to the vaccine genes

if they don’t match, they’d have something to brag about

How many children are affected? Where are they? Which diseases are killing them? I am not finding evidence of a problem in the medical literature.”

Listen and obey.

Fine, let’s look up the strawman victims being used to push this.

“In the above regard, vaccines play an important role in preventing infections in the immunocompromised host. Prevention can be achieved by a combination of strategies. Besides vaccination of the immunocompromised patient (in whom immune responses might be suboptimal), there is a recognition of the importance of the “cocoon strategy” that is widely used in protecting susceptible patients from specific vaccine-preventable diseases (Forsyth et al. 2015). In the context of immunocompromised patients, one vaccinates parents, caregivers, and other close contacts, which provides indirect protection by preventing disease in those in close proximity to the immunocompromised person.”

Parents are the primary disease vector (risk) to their immunocompromised children.

Proven by the cocoon strategy designed specifically for compromised children.

Given the frequent physical interactions, this is quite obvious.

They don’t get to blame the world for their mistakes. If the kid catches something, they should immediately test the parent and drain some antibodies.

The latest data claims immunocompromised children MUST STILL BE VACCINATED.

As in, no, your child is not exempt.


Indirect protection is provided by ensuring that all household members and other close contacts are immunized against infections that they may transmit to the immunocompromised child”

Inactivated vaccines may be given safely to immunocompromised patients, but responses may be diminished or absent, and increases in dose or in number of doses may be indicated (e.g., hepatitis B, conjugate pneumococcal vaccines) [1]–[4].”

Live vaccines may cause disease by uncontrolled replication and are usually contraindicated in immunocompromised individuals, with the exception of those with isolated IgA deficiency, IgG subclass deficiency, complement deficiency, or anatomical or functional asplenia. Another exception is that live viral vaccines are safe for most children with phagocyte or neutrophil disorders (including chronic granulomatous disease) but live bacterial vaccines (e.g., BGG, live typhoid vaccine) are contraindicated [1][3]. Live vaccines may be given to individuals with HIV infection who are not severely immunocompromised [1]–[3].”


Who do you have to hide behind now?

Don’t blame the world for your kid getting sick, scapegoating doesn’t reduce your personal culpability.
Scapegoating is disgusting.
Sacrificing other people’s kids doesn’t make you exempt.

Additional vaccines: Immunocompromised children may require vaccines that are not routinely recommended for all children (e.g., 23-valent pneumococcal polysaccharide), or not routinely given beyond a certain age (e.g., Haemophilus influenzae type b).”


Assuming other people can do your job for you is ass-backwards wrong!

Even if everyone in the world got vaccinated, your child would still need vaccines, according to the authorities you appeal to!

“The duration of the immune response may be diminished, necessitating extra booster doses (e.g., children at ongoing risk of hepatitis B exposure should undergo annual testing for hepatitis B antibody and receive booster doses if indicated) [2].”
When long-term immunosuppression is required, inactivated vaccines are given when the patient is on the lowest anticipated dose of immunosuppressive agents. Also, if feasible, immunosuppression is held or reduced temporarily to maximize response.”

MUH Medication – NOT AN EXCUSE.

“Response to a vaccine should not be assumed”

Refusing to listen to these OFFICIAL MEDICAL GUIDELINES makes you an abusive parent, according to the Canadian government.

General antibody production problem?

“No delay is required for live oral or intranasal vaccines or for inactivated vaccines [5].”

u r WRONG, Karens. Mz ‘my kid can’t get any’. Not a barrier.

But, I hear you cry, what about the cancer patients?

Low, but K. I am willing…. to go there. This once.

OT “reactivation infection with herpes group viruses”
where would children get that?
More evidence in favour of slut shaming.

You might notice something odd, a paper on managing infection risk in cancer patients doesn’t mention vaccines.
At all.

Conclusion “Infection in immunocompromised patients offers a particular clinical challenge because the pathogens are often unusual, and appropriate treatment must begin early in the course of the illness. These patients also must receive the highest tolerated dosages of antimicrobial agents and for maximum durations. Prophylactic antibiotics should also be given based on the pathogens likely to reactivate during the time of more severe immunosuppression.”

They’re commonly struck down by unusual microbes, not the ones we’re told to vaccinate for!

To close, here is a paranoid misogynistic shill telling us we’re evil for wanting the standard of proof in medicine, and anyway, it would cost money. Can’t put the breaks on the gravy train!

“The low vaccination rates in ultra-Orthodox neighborhoods have been attributed to a faulty perception that fervently religious Jews are protected from infection by the insulated nature of their communities, as well as discredited rumors that the life-saving practice is dangerous.”

(((Gorski))) has no conflict of interest at all, as you’ll see.

“However, there is one trait of the anti-vaccine movement that, however its camouflaging plumage may evolve, never, ever changes. It is as immutable as believers say that God is. That trait is that, whatever other claims, the anti-vaccine movement makes, at its core it is always about the vaccines. Always…
at its core the anti-vaccine movement is about fear and loathing of vaccines. Always. When inconvenient science doesn’t support their views, anti-vaccine activists either ignore the science, distort the science, or launch ad hominems against the people doing the science or citing the science. And, as I said before, the claims of the anti-vaccine movement evolve. Never again will the anti-vaccine movement make the horrific mistake of yoking itself to a hypothesis that is as easily testable”

Just do the studies, shill.
That bolded contradicts his conclusion. We noticed.

“Thimerosal was removed from nearly all childhood vaccines (the sole exception being some flu vaccines),”

Wait, mercury is in childhood vaccines still, known neurotoxin?
It’s also in the adult flu jab, which others? That explains why the elderly here pop their clogs after getting one.
We all know people.

“This “too many too soon” chant has lead to a demand by the anti-vaccine movement that the government conduct a large study of “unvaccinated” versus the “vaccinated” children to compare them for health outcomes and, especially, the prevalence of autism.”

They refuse despite that being the gold standard.

How queer.

“I don’t think that people like J.B. Handley realize how risky their gambit is.”

It isn’t just the gravy train, it’s the crazy train!

What echo chamber?

The Ivory Tower sure can echo!

“Such a study would have a very high risk of torpedoing virtually everything the anti-vaccine movement has been working toward in terms of promoting their message of fear about vaccines as being somehow credible (or at least not unreasonable) and based on science (more on that later).”

Then do it.

They want to be proven wrong, huh? Like… scientists?
Shit, if only that were your job. If you only received taxpayer money from these people too.
We live in a society – where you need to do what people pay you for.

Comparisons allowed on a single vaccine basis are clear (top link) so I’d expect a compounded, huge differential between the complete schedule and none whatsoever. The former is sufficient evidence to conduct the latter.

Of course, Ms. Tamaro is either ignorant or disingenuous herself in that some anti-vaccine advocates do indeed call for just such a study, even going so far as to demand a randomized, double-blinded study. J.B. Handley himself has attacked people who correctly call demands for such a study “unethical.””

Correctly? First harm none. Burden of proof.
Are you sure correctly is your word of choice?
He completely dismisses the woman on no grounds.

She says:

“Research studies are divided into two categories, observational studies and experimental studies. An observational study observes individuals and measures variables of interest but does not attempt to influence the responses. (The “epidemiological” studies to which Dr. Insel refers are actually observational studies.) An experimental study, on the other hand, deliberately imposes some treatment on individuals in order to observe their responses; the purpose of an experiment is to study whether the treatment causes a change in the response.”

True, you could find plenty of volunteers to submit data of what they were GOING TO DO ANYWAY.
Why not collect the evidence?

“This paragraph just goes to show how a little knowledge is a dangerous thing.”

but no observational study has been done comparing the prevalence of autism diagnoses in a vaccinated human population compared to an unvaccinated human population. When Dan Olmsted points out that he has identified large populations of unvaccinated children in the United States and asks why a study has not been done on them, he is actually asking why an observational study has not been done.”

She is being perfectly reasonable.

He ignores this question.

“When Senator Harkin asks Dr. Insel why a study has not been done on vaccinated vs. unvaccinated American children, he too is actually asking why an observational study has not been done to date. Dr. Insel, however, chooses to respond by saying that an experimental study would be required in order to resolve the issue.”

Get someone else to do it and pull his funding.
This is fraud. They are refusing to do their job.

Playing shell games means you are not qualified.

“ignoring the fact that there have been calls from the anti-vaccine movement for experimental studies, which, of course, would be highly unethical because they would leave large numbers of children completely unvaccinated and thus vulnerable to vaccine-preventable diseases”

that is your hypothesis, NOT a fact
this is WHY we need studies
the vaccine failure children are vulnerable, not biologically bulletproof
these intellectually dishonest douches, e.g.

“In any case, here’s where Tamara goes right off the deep end:

He…. he literally says that. Go look.

“”I would like to point out the epidemiological similarity between smoking/lung cancer and vaccines/autism. Smoking has been proven to cause lung cancer, yet not a single experimental study on humans was ever done – all of the human studies proving that smoking causes lung cancer were observational. The experimental studies were performed on research animals only. Attached at the end of this letter is a lesson taken verbatim from an introductory course in college statistics describing how the connection between smoking and lung cancer was made.””

Proven fact?
Proven fact is ‘off the deep end’?

Introductory course on statistics – she has a sense of humour, this is basic.

“Both Prometheus and Autism Diva enumerated the numerous flaws and ethical lapses in that experiment.”

So what? Try to replicate it or STFU.
Ethical lapses – for data we ALREADY HAVE.

Does Gorski own a time machine?
Let’s all entrust the safety of American children to one ‘autism diva’.

“Then there was the more recent (and even more unethical) Laura Hewitson experiment looking at vaccinated and unvaccinated Macaque monkey infants. I was appalled at how badly designed and grossly unethical that experiment was, not to mention at the enormous undisclosed conflicts of interest of the investigators.”

In your opinion.
Screeching about ethics won’t change biology.

“The problem, of course, is that there is not yet a good animal model of autism”

In your opinion.

So all your method ‘flaws’ you spot make it impossible to meet your standard. Wow.

“Moreover, the history of such research (i.e., Hornig and Hewitson) is not exactly cause for optimism, given how badly done these studies were.”

In your opinion.
The weasel words in this should be studied.

So the gist of this ENTIRE LENGTHY POST is “don’t try, don’t note data that already exists, the method is always wrong, the models aren’t good enough and whatever you do, IT’S UNETHICAL” as if that’s ever stopped science before.
Didn’t the vaccination guy abuse his children?


Where’s the kitchen sink? Oh, it comes. At the end.

“While she is correct to say that an experimental (i.e., randomized, blinded) study is not always necessary to provide sufficient evidence of causation to conclude that there is causation, she’s picked the wrong example for a number of reasons.”

He’s beating his strawmen hard.

In any case, Ms. Tamara is also wrong when she says that a study of the vaccinated and unvaccinated has never been undertaken.”

She’s right but she’s wrong, guys!

The study he discusses blames RACIAL DIFFERENCES for why his comparison ‘didn’t count’.

But, you said about how it hasn’t been done earlier and later you say it hasn’t been done because statistics?

He doesn’t have the Mawson study above.

It’s this study he is referring to and weirdly, if you follow his link nothing comes up.
PAYWALL. I smelled bullshit before but linking the wrong URL?
Here it is, the right link.

Parts he didn’t quote:

“Unvaccinated children are at increased risk of acquiring and transmitting vaccine-preventable diseases.”

What bias? And as opposed to what? Increased compared to….?

The largest numbers of unvaccinated children lived in counties in California, Illinois, New York, Washington, Pennsylvania, Texas, Oklahoma, Colorado, Utah, and Michigan.”
“Unvaccinated children have characteristics that are distinctly different from those of undervaccinated children. Unvaccinated children are clustered geographically, increasing the risk of transmitting vaccine-preventable diseases to both unvaccinated and undervaccinated children.”

So it just says who they are (and Jews are white here) and nothing whatsoever about HEALTH OUTCOMES, as he implied it did.

He LIED. Please, check. I implore you.
Lie of omission is still a lie. Blatant intellectual dishonesty.

The topic is health outcomes, Gorski. We could compare the hair colour of the vaccinated/not (that study essentially does) and it’s irrelevant to the topic at hand. Clutching at straws, why?

I can only conclude that Ms. Tamara is also quite naive in that she clearly has no clue just how much money and how many children an observational study of the vaccinated versus unvaccinated would require to do properly, much less how tricky it would be to control for confounders, given that the unvaccinated vary in significant ways from the vaccinated.”

Shocker. Sounds like he’s holding you to ransom.

But he knows there are huge differences. Huh.

“Skeptical blogger extraordinaire Prometheus tells the tale. First, he points out how few completely unvaccinated children there are to study, perhaps around 50,000 in the entire U.S., in the 3-6 year old age cohort that would be most fruitful to do a study looking at autism incidence in the vaccinated and unvaccinated.”


What, so let’s not bother? Yes, let’s listen to a blogger.
A ‘skeptic’, no less. Saying no to everything isn’t hard.

Well, plugging those numbers in – along with the current 1 in 150 autism prevalence – we find that we need over 360,000 children in each group to detect a 10% difference (you can try it yourself here). Unfortunately, that is more than the total number of unvaccinated children in the US, so that’s not going to happen.”

Wait, numbers you literally just made up? And the highest, most unlikely prevalence?
84% of statistics are made up, including that one.
Again, don’t bother is the best you can come up with? Over time you’d get enough data.
A 1% increased risk is medically valid, their significance in medicine is 0.001%.

What can we get with our “sample” of 49,652 unvaccinated children? If we manage to include each and every unvaccinated child in the US in the study, we could detect a 26% or more difference in autism prevalence.”

Why not do it, the kids already exist in that condition?

The data is RIGHT THERE.

Of course, it’s not even remotely practical to expect to get 100% of the unvaccinated children in the country into a study.”

So don’t try?

“How more about a practical number – say, 10% of them?”

Bullshit artist literally making up “samples” with quote marks is the best argument they have.

“That would allow us to detect a 70% or greater difference – about a three-fold difference in autism prevalence between the fully vaccinated and unvaccinated groups.”

Okay, so at least conduct A study?
Why not?
Why say, oh, let’s not bother, we know the results?
That is not science, but faith. Fuck these baby-killers.
If you know it’s safe, why not check?

Shut your critics up?

Does anyone here think that parents who fervently believe that vaccines cause autism would accept negative results from a study that’s only powered to detect a three-fold difference in autism rates between the vaccinated and unvaccinated as sufficiently reassuring to accept the current vaccination as safe?”

Sure, you won’t do it because the people who want it wouldn’t like the results.
Not you. The people who want it.
You’d definitely accept results that show you’ve been encouraging child abuse for years?

Appeal to incredulity. Someone else’s.

“Given the religious fervor with which the anti-vaccine movement clings to the myth that vaccines cause autism, I doubt that it would accept a negative result from a study powered to detect a 1% difference in autism rates as sufficiently reassuring to abandon its fear.”

If it’s a myth, settle it with the study. It doesn’t have to be specific to autism. Health outcomes.

Any percentage is better than nothing!

“Moreover, as Prometheus tells us, even the study described above would be inordinately expensive and difficult to do.”

Who cares is we’re advocating the harm of children, it’s expensive to prove this thing is safe?

Wasn’t Prometheus tortured?

“Finally, let’s “run the numbers” on a more practical study – one where we are able to enroll 500 unvaccinated children and 5000 fully vaccinated controls”

Made up numbers, again.
You said there are thousands of unvaccinated in America.
Why not 5000/5000? Why not even groups? That would be ‘practical’.

“I can’t help but note that the study described by Prometheus would probably fail to find the well-known increased risk of lung cancer and heart disease due to smoking, the more so since the incidence of lung cancer in nonsmokers is considerably lower than 1 in 150, which is how many children are estimated to be autistic.”

So it’s let’s not ever look or bother because the made-up numbers of a blogger say it wouldn’t find anything?

“The only way to get around the problems inherent in designing a study …would be to expand the study to multiple nations. Of course, doing such a study would be even more enormously expensive, take several years, and, because funding for autism research is pretty much a zero sum game, would divert huge amounts of money from more promising research to chasing down a highly implausible hypothesis that has virtually no credible empirical support behind it, either from basic science, epidemiology, or other evidence, certainly nowhere near enough evidence to justify such a huge expenditure and effort.”

Yep. He’s lying.

Virtually no?

Nowhere near enough – in his opinion.

I hope these people go to prison for fraud, when this study is eventually conducted. Obstruction.

“Certainly the government does, hence its reluctance to spend all sorts of money chasing a highly improbable hypothesis….

Not Pharma Super PACs?

In reality, the “vaccinated versus unvaccinated” gambit is just that–a gambit. The leaders of the anti-vaccine movement probably know that doing a study with sufficient power and numbers to exclude even a modest risk of autism due to the current vaccine schedule is so expensive and impractical that it would probably never be done and that smaller studies that are feasible will have too little power to reassure those who believe that vaccines cause autism that vaccines are in fact safe. Why do it then?

So, conspiracy now?
The researchers won’t do their job and it ‘won’t’ be done, instead of can’t?

Here’s the kitchen sink:

In fact, I rather suspect that the smarter among the anti-vaccinationists know all the problems”

That’s an insane conspiracy. Everyone deserves to know the results. Public interest.

“On the other hand, antivaccinationists should be very careful what they ask for. They may just make enough of a pain of themselves to get it.”


Worse, if the government ever did spend the money on such an enormous study and it was resoundingly negative, it’s easy to predict that it would make no difference.”

You don’t discuss what would happen if they’re right.
This article of yours was an old whore, windbagging about how impractical, expensive and unethical it is to hold you accountable. The projected paranoia is exquisite, it would be their worst nightmare – but they suggested it?

“As they have done before for other large studies, anti-vaccinationists would discount the results and cry bias.”

Would you accept it if you’re wrong?
If it’s a good study, solid statistically, that wouldn’t be an argument. And you couldn’t find fault with it either, if YOU didn’t like the result.

Kinda why it’s done? Objectivity?

not the dubious study

custom designed

to have the maximal chance of a false positive result,

which is

of course

what the anti-vaccine movement really wants.”

Conspiracy theorist. By all means, do the most accurate study, I’d love to write about it.

He’s literally attacking a study he says is impossible. Nothing to fear, nothing to hide.

Male beauty predicts sperm quality


It’s called fitness, smarter people are also naturally more attractive.
Who we’re told is (((smart))) in the modern world is just educated, a different variable, natural IQ correlates to beauty. It’s an established, permanent correlation. Appealing to exception doesn’t work.

Facial attractiveness has been related to health in both men and women. Certain psychological, physiological, and secondary sex characteristics have been used as accurate markers of hormonal and developmental health. The main objective of this study was to investigate the capacity of women to select males of high reproductive quality based on their facial attractiveness. A total of 66 males were included in the study. Each of them provides a semen sample, and frontal and lateral photographs were taken. Semen analysis was made according to standard WHO (1999) guidelines for morphology, motility, and concentration. Moreover, a Sperm Index (SI) was calculated as the principal component of these parameters. In Study 1, 66 women rated the attractiveness, as a possible permanent couple, of pictures of all 66 men. In Study 2, the pictures of a subset of 12 males were randomly selected from three semen quality subgroups (terciles named good, normal, and bad, according to the value of the SI). These 12 pictures were rated on attractiveness by two independent sets of women (N=88 and N=76). Facial attractiveness ratings were significantly (P<.05) and positively correlated with sperm morphology, motility, and SI, but not with concentration, for all the women sets.

Fitness and reproductive success, bound.

Darwin wins again.

And naturally, with age men are less attractive and sperm quality tanks (i.e. paternal age and miscarriage go up).

Abnormal brain function after drugs

And lower IQ.


Since the time of Oscar Wilde, the media has tried to push drugs as something only intelligent people “try”. OK, “Try”, first off, that’s not possible.

You are a biochemical in/out machine. There is no Try. This isn’t a fucking cheese sample.

Try to put porridge in your gas tank. It isn’t supposed to be there. It throws the otherwise working parts off. Can you arrange a deep clean for your brain? No.

One meal can give you food poisoning or an infection that won’t quit. This is easy to diagnose because it’s gut. One instance of drug use can and does damage you. It may not kill you, but like puffing on one fag doesn’t instantly KaPow you with lung cancer, it does always damage you.

Something something artistic 2deep4u Byron. I’m sure the pre-existing mental illness and self-medication had nothing to do with it.

Nope. There is no evidence for that ‘genius’ connection, it’s purely anecdotal. The lazy people want to blame the drugs for less-than-ideal performance failure, a common form of self-sabotage. Do smart people sabotage out of peer pressure?

They commonly cite openness, a personality trait that smart people can be ever so slightly higher on. This is because it basically looks for intellectual curiosity, it’s a confound of the variable.

No, it doesn’t mean that ‘open’ people are smart, it isn’t truly connected.

Not to mention, but I’m gonna-

People self-rate on openness, can you imagine if we did that with IQ?

Relatively little is known about the neural bases of the Big Five personality trait Openness/Intellect. This trait is composed of two related but separable aspects

Intellect was also correlated significantly with scores on tests of intelligence and working memory capacity, but the association of Intellect with brain activity could not be entirely explained by cognitive ability.


Look at a related variable, something easy to measure. e.g.

The higher someone’s IQ, the older they are when they lose their virginity.

I don’t think they’re smoking pot. Somehow. This is just the new trendy thing to smoke anyway, look at tobacco rates for how much Millennials despise something with health warnings attached. Tricked their grandparents though.

Look at the cluster of finding. Look at related variables.

They might just say, Oh that’s it, no other effects on a person?

In adults you can damage the frontal connections. This happens with any addiction including porn and is called hypofrontality, there is reduced activity in the reasoning… levels (which are where most of the IQ stuff happens).

Well, why would pro-abortion anti-natalists be telling us to do it?

This along with advanced paternal age.

Both increase mutations.

It isn’t women trying to conceive who need to be teetotal and off drugs for as long as possible (ideally never starting), there is far more cause for men to do it. Look up advice for men trying to conceive, it says exactly this.

If anything, the rules are more stringent for men.


Because it’s their sole contribution to the baby-making process.

The work comes years beforehand.

This is genetic.

Since men process sperm repeatedly, constantly, any damage from any point in their life is present and consequent on their present sperm. However, it’s hard to discern clear medical causation beyond a few months because we’ve yet to find a suitable method, not because it isn’t there. FYI, you can’t really use sperm beyond ten years, more like five would be pushing it. It isn’t a magical technology.

Sperm is purely epigenetic in men because it is one of the few body parts that constantly refreshes with a completely new code, new switches off or on. It would be immoral to damage and mutate babies deliberately to prove this.

 published in the Human Reproduction journal — researchers looked at sperm samples of 1,970 men from various fertility clinics in the United Kingdom. The scientists examined how smoking and drinking habits, as well as other lifestyle factors, such as BMI, medical history and the type of underwear worn, affected sperm

Okay, you might think, but most of them are fine?

You don’t have any particular medical problems? You can afford to?

Not so.

Of the men studied, 1,652 produced “normal” samples of sperm, meaning that more than 4 percent of their sperm was the right shape and size. The remaining men’s sperm was shown as “abnormal.”

A lot of men have rendered themselves infertile and don’t even know it.

There’s no such thing as free love, look at the Boomers suddenly getting pathogenic cancers.

Is it any coincidence that such drug use is common among already-low IQ populations?

How about the undeniable link to high time preference, inversely associated with IQ?


The ONLY link found of IQ to drug use is childhood IQ.

Yep, they’re basically lobotomising themselves.

Fridge horror?

Once the neurons are pruned, they’re dead. They’re gone. You cannot get them back.

Is that because drugs=good or some other explanation, like a society that hates smarts and teaching systems that imprison them until they’re eighteen?

Where’s the adult (25+, in brain terms) IQ connection?