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).

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.”

Right-wingers are different

It’s that time of year for a study-dump. Read until the end.

Better-looking (on AVERAGE):

“Good-looking individuals are more likely to have right-wing political views than less physically attractive people, according to a university study.
The authors of the report, Rolfe D. Peterson from the US Susquehanna University and Carl L. Palmer from the Illinois State University, examined the connection between physical attractiveness and political beliefs, applying multiple surveys measuring people’s attractiveness.
“More attractive individuals are more politically efficacious than their peers and more likely to identify as conservative and Republican than less physically attractive citizens of comparable demographic backgrounds,” the report read.”

Comparable demographic background, an important control.

Better-looking again:
PDF at:

“Controlling for socioeconomic status, we find that more attractive individuals are more likely to report higher levels of political efficacy, identify as conservative, and identify as Republican.”

SES control is important.


“Politicians on the right look more beautiful in Europe, the U.S. and Australia.”

How to tell May isn’t really right-wing.

They should also study disease load (emphasizing STDs, which do affect appearance) compared to partisanship.

Support meritocracy, oppose the cult of equalism:

“Higher self-perceived attractiveness (SPA) increased support for inequality.”

Self-perceived, relative.

Have a ‘look’:

“The political sympathies of scholars can be accurately assessed from photographs.”
“In contrast to politicians, Right-leaning scholars were not more attractive.”

The scholars haven’t hired image consultants.

What, do you think a man buys an expensive suit just for the suit?

“Right-leaning scholars were better groomed.
Controlling for grooming, Left-leaning scholars were more attractive”

This is supposed to be looking at genetic attractiveness, true attractiveness, not clothing/haircare/make-up?
Okay, I’ll let them have that one. They’re better at faking it, a trait of narcissism.

Less likely to cheat when expected to cooperate:

Neurologically different:

“Political Orientations Are Correlated with Brain Structure in Young Adults”
We found that greater liberalism was associated with increased gray matter volume in the anterior cingulate cortex, whereas greater conservatism was associated with increased volume of the right amygdala.”

So they’re more gender neutral in the brain?
Because the same IQ can still be produced by structural differences between the sexes.

“Researchers found major differences in the amount of gray and white matter in the brains of men and women of the same intelligence, suggesting that men and women may derive their intelligence in different ways.”

“”These findings suggest that human evolution has created two different types of brains designed for equally intelligent behavior,” says researcher Richard Haier, professor of psychology at the University of California, Irvine, in a news release. “In addition, by pinpointing these gender-based intelligence areas, the study has the potential to aid research on dementia and other cognitive impairment diseases in the brain”

Again, the same IQ score.


Man Card isn’t a MENSA card, accomplish something.

Sexual dimorphism didn’t stop at the neck.

But white matter is generally more important for HIGH IQ:
White matter could only be imaged recently.

“They found a strong correlation between the integrity of the white matter and performance on a standard IQ test.”

Although grey matter can matter too, white matter cannot be denied EITHER:

Positive relationships were found between FSIQ and intracranial gray and white matter but not cerebrospinal fluid volumes. Significant associations with cortical thickness were evident bilaterally in prefrontal (Brodmann’s areas [BAs] 10/11, 47)

IQ so real you can scan someone’s brain, almost.

and posterior temporal cortices (BA 36/37) and proximal regions.

Sex influenced regional relationships;

Before any sexist bitch goes to twist this, different does not mean inferior. This is a study of intelligence, NOT stupidity.

You can’t prove a negative and individuals are not groups?

The obvious pointed out? Okay, let’s continue.

women showed correlations in prefrontal and temporal association cortices, whereas men exhibited correlations primarily in temporal–occipital association cortices.


An idiot reading that would assume women are smarter, prefrontal doesn’t always mean smarter, necessarily, it’s just a group-level skew of structural difference. However, it does explain the higher female average.

Again, average.

In healthy adults,

important distinction, many brain studies are conducted on the undeveloped (teens) or pathologies

neither of which generalize to a HEALTHY, ADULT population

[sorry for the smart people tuning in, idiots twist what I type]

greater intelligence is associated with larger intracranial gray matter and to a lesser extent with white matter.

Plot twist: both matter.

Almost like we evolved.

Variations in prefrontal and posterior temporal cortical thickness are particularly linked with intellectual ability.

PF – registered as female strength, generally.
PT – registered as male and female strengths, generally.

This isn’t better/worse, it’s apples/oranges.

Even race overwhelms sex as a confound in IQ (so does class, education etc).

Sex moderates regional relationships that may index dimorphisms in cognitive abilities, overall processing strategies, or differences in structural organization.”

Trans. sex differences real yo.

Overall, key word.

Moderates, may index, differences. As in, these processes still occur but like a road trip, each take different paths different enough to map but not distinct enough to be unrecognizable.


Estrogen, which men also NATURALLY produce, also boosts brainpower.
Study here but my commentary explains it:
Whereas, everyone knows, testosterone (which women also produce) correlates to violence.
Nothing is all-good, all-bad in hormones.
“A moment of silence for all the women in history who married dumber men.”

They should study political economic wing and compare it to natural/un-supplemented hormone levels.
As in, a man who ‘needs’ steroids for vanity is less of a man.

They should also look at whether men going onto steroids drop in IQ score because it competes with their organic estrogen that makes them handle stressors better.

[Update: after checking, they did. Here it is.]

“long-term high-dose AAS exposure may cause cognitive deficits, notably in visuospatial memory.”

“These results remained stable in sensitivity analyses addressing potential confounding factors.”
The dumb jock stereotype is true!


It gets better!

Actually, it causes brain damage!
This is amazing!

Fake masculinity is really bad for men. You can’t cheat code becoming a man.


Long-term AAS use is associated with right amygdala enlargement and reduced right amygdala rsFC with brain areas involved in cognitive control and spatial memory, which could contribute to the psychiatric effects and cognitive dysfunction associated with AAS use.

The MRS abnormalities we detected could reflect enhanced glutamate turnover and increased vulnerability to neurotoxic or neurodegenerative processes, which could contribute to AAS-associated cognitive dysfunction.

Now the right amygdala enlargement sounds like the natural conservative difference but understand it’s rooted, not in experience and genuine masculine virtue, but chemical dependence. Without the drugs, it’ll shrink right back and possibly atrophy.

This would be like congratulating a tall guy who took HGH for his superior genetics. No. It’s a superficial, fake result.

The cognitive control is impaired, that’s regression. The meat head stereotype is true, biologically. Useless.

I wonder how many male suicides were on steroids? Both groups happen to be middle-aged men in fear of the Wall.

Whatever the details, it makes them biologically vulnerable compared to their natural state, the opposite of fitness.

Ironically, they’re more vulnerable to microplastics and xenoestrogens. 

To further screw the point in… that brain region explicitly mentioned?

Right amygdala rsFC study:
“In high HA scorers, we also observed stronger right amygdala rsFC with the dorsomedial prefrontal cortex (dmPFC), which is implicated in negative affect regulation.”
It’s a girly brain thing to do with harm avoidance. [aka common sense]
“may represent a vulnerability marker for sensitivity to stress and anxiety (disorders).”
So the meat head with reduced volume (therefore not conservative*) is dumber, senses dulled by drugs and more likely to fail to get the brain signals to avoid trouble. Sounds like a future in handcuffs. They can’t perceive danger nor regulate negative emotions like anger or shame after rejection. Basically, they’re future chimp-outs waiting to happen, whatever their race**. Less able to CONTROL emotions, the broflakes.***

Hair-trigger temper calling out people for looking at him.

The guy who picks on people but never actually expects to get hit.

Will grab a woman and be shocked she slaps him. That’s the one.

*because, again “greater conservatism was associated with increased volume of the right amygdala.”

[as referenced above]

yet they have less?

So steroids make men more left wing. It isn’t the correct area and type to be considered otherwise.



My guess is it messes with their sexual reward system and produces impotence, porn addiction, dissatisfaction.

Steroids do cause impotence (PC term is ED). Does it lower sperm count?


“Anabolic steroids abuse and male infertility”

I am good at this.

“Infertility is defined by the WHO as the failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse and a male factor is present in up to 50 % of all infertile couples. Several conditions may be related to male infertility.

Substance abuse, including AAS, is commonly associated to transient or persistent impairment on male reproductive function, through different pathways. Herein, a brief overview on AAS is offered. Steroids biochemistry, patterns of use, physiological and clinical issues are enlightened. A further review about fertility outcomes among male AAS abusers is also presented, including the classic reports on transient anabolic steroid-induced hypogonadism (ASIH), and the more recent experimental reports on structural and genetic sperm damage.”

hypogonadism = tiny balls

“In layman’s terms, it is sometimes called interrupted stage 1 puberty”

You’d have to be a moron already to think supplementing that shit makes you manly.

Nice muscles bro, shame you hit rewind on puberty!

They impair their body’s ability to naturally produce testosterone in future…. idiots.

Darwin Award category?

Big Pharma’s best customer? Like Israel’s Viagra use. Israel and America, top consumers.


**Logically we should restrict steroid use to lower the crime rate. We can’t have gorilla people chimping out and blaming da drugs.

***There are few things less masculine than a man who throws tantrums because Hulk RAGE entitlement. The mantrum has neurological correlates, as we can see.

As for the ACC lefty brain finding:

..I didn’t forget.

“Through these connections, the ACC is thought to be involved with a number of functions related to emotion including the regulation of overall affect, assigning emotions to internal and external stimuli, and making vocalizations associated with the expression of states or desires.

No comment.

The ACC also seems to contribute to the regulation of autonomic and endocrine responses, pain perception, and the selection and initiation of motor movements. Additionally, there are other areas of the ACC that are involved in various aspects of cognition ranging from decision-making to the management of social behavior.”

And about sexual potency….

I order these for a reason.

Right-wingers more sexually satisfied:

“A new YouGov survey, which asked over 19,000 participants from the UK, France, Germany, Sweden and Denmark about both their politics and their sex lives, has found conservatives to be happier in the bedroom than liberals, with those identifying as “very right-wing” found to be the happiest.”

So much for the benefits of slutting. Muh experience. Yes, experiencing a burning sensation.

If you want a better sex life, don’t be a manwhore.
Chastity is a virtue. Less stress when single, hot sex when married.

Sluts reee.

I deserve an Ig Nobel for all this connection-making. It could save the West.

While I’m putting out fires imagined by shrill men.

Click through.


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.

How long can they deny HBD?

Waiting to be a father is irresponsible, imagine my shock.

“The records showed that children born to men aged 45 and over had a 14% greater risk of premature birth, low birth weight and being admitted to neonatal intensive care compared with babies born to younger fathers.”

Geriatric fathers, yes.
If you’re past middle-age (36-7 in men) and old enough to be a grandfather.

Infants born to men aged 45 and over also scored lower on the Apgar newborn health test, and were 18% more likely to have seizures compared with infants born to fathers aged 25 to 34 years, according to the study in the British Medical Journal.

Why not state all the findings, including compared with <25?

Boomer readership, that’s why. 60 is the new 40 though, sure.

For women, the risk of gestational diabetes was greater when they had children with older men.”

Paternal age as a medical risk factor is long known, I’ve posted on it.

Their study.

“This is something else to take into consideration,” he said. “There are potential risks with waiting. Men should not think that they have an unlimited runway.”

Why isn’t male fertility and issues like impotence mentioned in biology class? Men deserve to know, it’s important life planning. Modern men don’t realise their fertility is dropping steeply until they eventually go to conceive or get a random sperm count for other reasons.

I’d go so far as to call it a public health issue.

They are not fully informed, the information is withheld from them. Where’s the full consent for that wait, if they don’t understand what it might entail?

Obviously the man commenting on the study tries to downplay it but other studies I’ve posted didn’t find mild differences, in some cases extreme (such as psychiatric risk) and that’s without looking at whether the child is mixed-race, that includes the risk even further. Good luck getting that published.

“increases in health risks might have across populations as paternal age continues to rise.”

If it’s a risk across a population, it is also a risk for the individuals within it, showing up his earlier weasel words about ‘individuals’ to be a lie. You don’t have medical complications as a population, it’s personal.

“When I talk to couples about health risks, I use the lottery as an analogy,”

You use a con about people who can’t do maths to… lie to people who can’t do maths.

“Even if your risk for something goes up 10-20%, the absolute risk for an individual

doesn’t change

At all?

that much.”

Hear that gentlemen?

Who gives a shit about your individual risk going up by 20%? Not this guy! He’d rather not offend you but let you slowly become infertile because, by the time you figure it out, you’ll be powerless to do anything about it. White men need to have fewer children, as other Guardian articles have informed us.

You aren’t entitled to oppressive white male fertility.

The researchers calculating risk across the field (here a part of gerontology) know more maths than the doctors downplaying it.

“Eisenberg and his colleagues suggest changes in the DNA of older men’s sperm might explain their findings.”

Berg-berg-berg-berg et al.

“The concern is backed up by previous work, including a Harvard study last year that found births through IVF fell as the fathers’ age increased.”


IVF isn’t magic.

“Studies have shown that advanced paternal age is associated with negative health behaviours such as smoking and frequent alcohol consumption, obesity, chronic disease, mental illness, and sub-fertility,” she writes, adding that all are linked to health problems in newborns.”

Sub-fertility, which many clueless men have and they don’t care to warn you about.

It’s almost like men evolved to have children while they were healthier.

From the BMJ article itself:

“Though the effects of advanced maternal age on perinatal outcomes have been extensively studied,

can’t blame women, credits on that excuse are maxed out

research on the impact of older fathers on the health of offspring has been limited mostly to the risk of congenital disease.345678

we’re scared of offending old guys with money

The high number of male germ cell divisions in aging fathers has been proposed to increase the risk of autism, genetic abnormalities, psychiatric morbidity, and neoplasia in offspring, but recent studies have also suggested a potential paternal effect on perinatal morbidity.691011121314

I didn’t call my article Old fathers, sick babies for nothing.
Can’t get sicker than dead or disabled.

This passes down the germline so one bad breeding decision will affect all their offspring’s fitness too (I think the children will eventually sue for epigenetic damages, on poor lifestyle choices prior to conception as well).

I’ve love to see a study comparing older fathers with younger and recording sexual history (partners and diseases) because you know that has an effect. A medical effect. They’re too chickenshit to do it (and record the same in women but paternal factors into their sperm donation are more likely modified by those behavioural factors, his baby-making factory is the testes area so its prior health and the delivery vehicle’s are especially important).

One common explanation arises from the epigenetic changes that occur within spermatocytes; specifically modifications to histone and DNA methylation in spermatozoa of older men. These alterations occur in regions of the genome that are responsible for several diseases in offspring.15 Disruption of histone methylation in developing male germ cells might be a precursor to aberrant embryonic and placental development, with studies suggesting that paternal imprinting of aging could affect both fetal growth and maternal health during pregnancy.”

Degenerate DNA gets so offended when people stop filtering about it.

No prizes why they didn’t quote this part.

I wonder if their boys (because paternal factors would be stronger to another male) are more or less effeminate than the average? Again, they don’t dare do that study.

Paternal imprinting, that’s a nice word for degeneration on a genetic level.

At least they’re acknowledging men age, I suppose.

Looking at non-Guardian approved science:

“Studies of human populations and animal models suggest that a father’s experiences such as diet or environmental stress can influence the health and development of his descendants. How these effects are transmitted across generations, however, remains mysterious.”

I’m guessing the sperm.


Just a random, wild guess.

“Epigenetic changes do not alter the DNA sequences of genes, but instead involve chemical modifications to either the DNA itself or the histone proteins with which DNA is packaged in the chromosomes. These modifications influence gene expression, turning genes on or off in different cells and at different stages of development. The idea that epigenetic modifications can cause changes in gene expression that are transmitted from one generation to the next, known as “transgenerational epigenetic inheritance,” is now the focus of intense scientific investigation.

For many years, it was thought that sperm do not retain any histone packaging and therefore could not transmit histone-based epigenetic information to offspring. Recent studies, however, have shown that about 10 percent of histone packaging is retained in both human and mouse sperm.”

So …more lying to men.
Get obese, it’s fine! Drink like a fish! Your kids will be fine!

Our ancestors never knew that vice… had a price.

They didn’t have iPhones, we’re so much wiser than them.

“The LORD is slow to anger, abounding in love and forgiving sin and rebellion. Yet he does not leave the guilty unpunished; he punishes the children for the sin of the parents to the third and fourth generation.‘”

What does that even mean? Nature can’t see what you’re doing.

Trust the “experts” who profiteer from fertility treatments and hate white men!

“”Furthermore, where the chromosomes retain histone packaging of DNA is in developmentally important regions, so those findings raised awareness of the possibility that sperm may transmit important epigenetic information to embryos,” Strome said.”

Wait, could rednecks be even smarter if they drank less?

Was Prohibition, pro-white?

“These findings show that the DNA packaging in sperm is important, because offspring that did not inherit normal sperm epigenetic marks were sterile, and it is sufficient for normal germline development,” Strome said.”

Money shot?

Sinner father, no grandchildren?

That is a divinely calculated revenge, all their paternal investment wasted.


“The presumption of female defect is confirmed in a letter to the Ugarit king about a woman who failed to produce any children for her husband after an extended period of time. The letter relates how the husband used the infertility as an occasion to take a second wife. It was only when he failed to produce children with the second woman that he was then considered to be the defective one”


“While monogamy was probably the norm in antiquity,”

louder for cucks at the back

“childlessness was one of the most common reasons that a man would resort to a bigynous marriage”

But God is punishing them, going around that in favour of dysgenic reproduction is a sin.

Women could divorce infertile or impotent men under the Catholic church, it was so important.

“The goal is to analyze how the chromatin packaging changes in the parent,” she said. “Whatever gets passed on to the offspring has to go through the germ cells. We want to know which cells experience the environmental factors, how they transmit that information to the germ cells, what changes in the germ cells, and how that impacts the offspring.”

I doubt it’s for the greater good.

Could addiction be genetic?

Lawyers are celebrating just thinking of it.

By demonstrating the importance of epigenetic information carried by sperm, the current study establishes that if the environment experienced by the father changes the epigenetics of sperm chromosomes, it could affect the offspring.”


A few others, while I’m here.

Your genes affect your nose shape.

Ya gotta have chutzpah to believe the science.

“The colour of a person’s hair is one of the most heritable features of their appearance, with studies on twins suggesting that genetics explains up to 97% of hair colour.”

Race explains 100%. Subrace especially.

They’re right that hair colour isn’t a matter of sexual preference …but race is.

““Pigments are far more than just cosmetic – they are important for the immune system and play a role in many diseases,” said Spector. “Understanding the genetics could lead to new therapies.”

They tried that with African heart medication, it was taken off the label.

They’d rather let black men keel over and die than admit they’re genetically different.

K-shift in mice:

“Intriguingly, the experience of winning appeared to leave an imprint on the mice, making them more assertive, even when their brains’ were no longer being artificially controlled. They were found to be more combative in a second scenario in which they competed to occupy the warm corner in a cage with an ice-cold floor.”

So you see, they can’t let men grow up. There’d be no politically useful regression then.
Buy stock in pajamas.
They can knock out that part of the brain too. They don’t mention this. This makes me suspicious.

“The findings, they suggest, could have applications in understanding a variety of psychiatric conditions where people exhibit overly dominant behaviours, or lack motivation to compete socially.”

Psychopathy and depression (or r-selection, as a trait).
Psychopaths are immune to depression. What makes others sad, makes them mad.
The study itself has nothing to do with “alpha” as Americans consider it, an alpha is never single in biology but part of a breeding pair.

The study is really about psychopathy in the extreme form (genetic engineering, useful for the military) and social dominance in prosocial, milder forms (K) which cannot be undone (even in GE mice) as a natural maturation process. Its absence of activation (say, from the amygala circuits) could explain effete males. Again, they gloss over that.

I noticed.

Genes influence subject choice.

Not IQ?
Isn’t that a huge confound that should be studied?
And why force children to study languages then? Isn’t that oppression when they could study something else?

“Birney warns that the findings do not imply that it is possible to predict a student’s subject choice, or achievement, from their genome.”

trans. Don’t look in the race box, please, don’t look in the race box. I don’t want to get the sack.

“As schooling and other factors vary greatly from person to person it is unlikely that genetics is the dominant factor in A-level choice.”

The likelihood was calculated.

“The scientists found that this was indeed the case, with 50-80% of subject choice down to genetic influences.”

Academic ability …. not IQ?

How is GPA not a reliable proxy for IQ, on that point?

GPA is basically just the PC term for IQ. Mathematically.

Cheats are brain-damaged

Once a cheat, always a cheat = If someone makes that choice once, they’ll make it again.

Behavioural genetics is confirming what the traditionalists already knew.

As for the neurochemistry of vasopressin, low levels of any count as pathological (see depression, OCD etc).

If the K-types wanted a surer mating game in future, a simple genetics test to distinguish the short allele (K-selected, monogamous) types from the deceptive hedons with a long-form allele (r-selected, high infidelity risk) would cut the latter off at the heels. It isn’t an excuse, but again, if they make that choice once, they’re tainted and should be divorced.

Imagine short-listing the prospects for your daughter’s hand, and your grandchildren’s genetics, based on this, oh the wonders of technology! Simply cutting them out from social circles would be a genetic death. Why do you think slutty people congregate in urban areas, where nobody knows them and they’d have to be dismal to build a reputation among their own? Why do you think we collect alcoholism, drug and sexual information as a bundle?

This isn’t just a marital issue, it covers social deception, this is just one sexual application of it i.e. K-selected males would be unwise to accept an r-male into their group, because he’ll screw you over metaphorically. And you shouldn’t leave him with a free house (some stay-at-home fathers) because he’ll invite over your wife too.

Most sperm are destroyed by white blood cells. However, here’s a horrifying fact about where it can escape;

“Once sperm cells reach the end of the oviducts they are free to swim out of the end of the tube and into the body cavity, where they are eventually destroyed. So many women walking around today will have sperm cells swimming around the interstitial fluid that surrounds their body organs. The female reproductive tract does not finish in a dead end.”

err what wut wtf scared rdj

Shocker as fathers’ bad habits hurt their future babies

Father’s bad habits directly impact child’s genetic quality

“We did not expect to see such important changes in epigenetic information due to environmental pressure,” says Barrès. “Discovering that lifestyle and environmental factors, such as a person’s nutritional state, can shape the information in our gametes and thereby modify the eating behaviour of the next generation is, to my mind, an important find,” he adds.’

Bad lifestyle too

These results suggest that the parents living conditions before conception may directly impact the health of their children.

“We’ve known for a very long time that preventive care among expectant mothers is critical to the health and well-being of their children,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “Now, we’re learning that fathers don’t get a free pass. How they take care of themselves — even before conception — affects the genetic makeup of their children, for better or worse.”

cracking up dawn french
Sperm carries environmental information about the father’s weight
All this information is technically under male fertility btw. Since it’s germline.
Male interest in babies hormone-mediated

“These results suggest that even before young men make actual decisions about marriage and children, one can distinguish between individuals who are more fatherhood-oriented and those who are less fatherhood-oriented.”

Do I sense a test for r/K? Dare I dream?

I would like to see sexual history included as a poor lifestyle factor. Cue the howls against biological responsibility from the manwhores. Hey, what are you afraid of? Your germline can’t escape your biology, the way you treat your body. Can’t blame that one on women.

toasting raising glass cheers leonardo da vinci congrats well done demons

Why am I mocking them? There are still males who blame the females for any issue with a baby (including miscarriage) as if it’s all on us. It’s a Henry VIII Complex. They refuse to believe it could be them.

Correlation between high IQ and superior sperm

yes lestat dancing happy cheery morbid black comedy

Social Darwinism 1

Social Justice 0

I love everything about this paper. I want to make a small altar and light a candle for this paper.


General intelligence itself is correlated with many important health outcomes including cardio-vascular function and longevity.

lestat rat judgemental

Pretend it’s a rabbit.


Intelligent people aren’t done for! We simply need a really, really, REALLY big freezer!

Male fertility drops too

” In essence, as men age, they experience a decrease in hormone levels which of course affect everything from sperm production, quantity, and quality to sexual drive. Although the greatest impact is seen over age 40, they experience a continuous decline throughout the lifetime. What is interesting, though, is that supplementing testosterone did not improve sperm function in one study of men who were experiencing infertility. (This may explain why making a male hormonal birth control is challenging as their system just doesn’t respond in the expected way, but that’s a digression.) However, much like the statistics for women, the majority of men are still fertile after age 40. It may simply take longer to achieve a pregnancy. “

Women go downhill after ~30 in quality, for men it seems to be ~40 for the healthiest possible offspring.

“You may have also heard that birth outcomes are not as hot for the older dad set and this was confirmed in a 2013 review in The Journal of Family Planning and Reproductive Health Care which showed that autism, schizophrenia, bipolar, and stillbirth are more common amongst children of older fathers. Before you panic, the overall risk of any of these conditions is still extremely low. Low enough that the researchers questioned if the actual risk of these outcomes outweighed the emotional and social benefits of having fathers who were more mature and established in life. “