The sperm allergy vaccine and genocide by sterilisation

Missed this nugget.

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

Why do under-30s “need” anything, let alone a random new ‘vaccine’ with no ingredients list available?

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

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


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

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

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

The wages of sin – HPV in men and sperm infertility


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

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

-increased miscarriage rate, lower odds of conceiving

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

Yes, this is a dealbreaker to sane women.

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

No abstract available


MRAs: crickets

Human papillomavirus infection and fertility alteration: a systematic review

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

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

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

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

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

The role of human papillomavirus on sperm function

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

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

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

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

-only? a? 100% is a percentage too…

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

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

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

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

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

– no hurt their feefees? NAW

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

– Manosphere fears this topic and all male degenerate accountability.

semen infection may cause infertility and early miscarriage

it’s the sins of the FATHER, you see…

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

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

>DNA quality
>in the germline of
>white men

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

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

TLDR: yes.

HPV is commonly present in semen samples. 

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

The overall rate of HPV positivity was 15.5%

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

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

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

It’s worse for the older men.

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

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

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

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

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

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

what a mystery

The mechanism of ASA cause male infertility is not clear

does it look like HPV?

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


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

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


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

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

-what r the odds?

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

Medicine can’t spare you.

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

 Fifteen samples

-aka HALF

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

no muh scientism and IVF cope

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

-may, LOL

a negative effect on development of the fetus

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

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

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

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

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

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

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

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

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

brace yourselves

guess the result


go on

just guess



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

and all fertile men were HPV-negative

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

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

Player burnout shall henceforth be dubbed HPV-driven infertility?


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

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

-maybe where you live

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

-well the husbands are freshly infecting the wives so

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

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

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

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

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

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

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

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

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

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

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

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

dat p-value


Sperm DNA fragmentation in couples with unexplained recurrent spontaneous abortions


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

– idiopathic? Are you shitting me?


sure it is


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

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

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

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

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

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

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

I mean – where are the STUDIES?!

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

unexplained….. sigh, ok.

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

Known for 20 years.

Human sperm deoxyribonucleic acid fragmentation by specific types of papillomavirus

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


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

-swimming in circles isn’t motility, really

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

it’s a viral abortion, really

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

i.e. no, you won’t just get IVF

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

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

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

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

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

-all trust the EU guys

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

-somebody else look up herpes, I’m lazy

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

-Really, f-ing fascinating!

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

>male fertility disorders


Oh, I’m not done yet.

HPV infection in semen: results from a new molecular approach

Let’s get molecular.

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

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

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

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

Your superpower is probably autism.

MSM push on male impotence and normalization of mutation

Studies are in their description, duplicated below.

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

Decrease in Anogenital Distance among Male Infants with Prenatal Phthalate Exposure

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

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

First trimester phthalate exposure and anogenital distance in newborns

Possible impact of phthalates on infant reproductive health

Prenatal phthalate exposures and anogenital distance in Swedish boys

Endocrine-disrupting chemicals: implications for human health

The Endocrine Disruption of Prenatal Phthalate Exposure in Mother and Offspring

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

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

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

They want to sterilise you (hCGβ)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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


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

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

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

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

Search engine (DDG) description:

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

1989 publication date.


When you click:

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

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

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

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

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

It relates to cancer vaccines

Anti-fertility vaccine again

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

Chemical human neuter sounds so cruel.

They think they own you.

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

WHO knows?

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

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

Christians are up first.

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

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

So including chemical abortion, like the Pill.

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


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

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

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

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

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

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

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

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

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

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

save save save

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

This one is tricksy.

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

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

described in SEO brief

paywalls should be illegal

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

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

Published 1997.

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

spellings are often deliberate to thwart SEO

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


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

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

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

you know, pre-replication crisis

scientists often own stock so….. null appeal


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

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

they think you’re stupid

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

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

neutralised, like a threat
neutered you – like a dog

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

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

Blood type is racially determined, like fertility problems

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

wait so does Nature abort hybrid babies?

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

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

Asian Women & Fertility Problems

Race is biological, see.

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

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

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

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

Repost on the Asian female infertility problem:

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

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

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

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

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

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

Look at the national IQs, hardly surprising.

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

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

Did pesky white women interfere with their genes?

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

Fertility Treatment Outcomes in Asian Couples

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

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

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

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

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

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


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

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

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

Are rh negatives more intelligent?

I may sound conceited but yes, yes we are.

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

From obi

Blood type by race/ethnicity:

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

The O stats for whites are shockingly different.

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

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

Why mention this now?

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

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

Darwin Awards global finale

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

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

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

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

Pandemics always hit the sluts hardest.

repost link;

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

The bioweapon’s coming for yar balls.

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

Orchitis and male infertility

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

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

Some thots are still going shopping in person in London.

It’s called the internet, bitch!

Spoiled rich pricks are complaining they were corona-cancelled.

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

BE OFFENDED. Pandemics are marvelously impersonal.

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

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

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

Adolescent Premature Ovarian Insufficiency Following Human Papillomavirus Vaccination

choice quote:

Vaccine research does not present an ovary histology report of tested rats but does present a testicular histology report. 


Enduring ovarian capacity and duration of function following vaccination is unresearched in preclinical studies, clinical and postlicensure studies.

Unresearched. Injecting it into all the little girls with thick parents, unresearched whether the ovaries still operate or the ORGANS shut down. aka partial organ failure

Since this group includes all prepubertal and pubertal young women, demonstration of ongoing, uncompromised safety for the ovary is urgently required. This matter needs to be resolved for the purposes of population health and public vaccine confidence.


Feminists pushing this shit hate women.

Timely reminder for when they try to force these things on you/r loved ones.

UT Austin Researchers File SARS-CoV-2 Vaccine Patent


“February 19, 2020 – Researchers from The University of Texas at Austin (UT Austin) and the National Institutes of Health (NIH) announced a critical breakthrough toward developing a vaccine for the novel coronavirus 2019 (COVID-19).”

Why DO they want so many immigrants?

case study of a 16yo girl:

and Human papilloma virus vaccine and primary ovarian failure: another facet of the autoimmune/inflammatory syndrome induced by adjuvants.


We documented here the evidence of the potential of the HPV vaccine to trigger a life-disabling autoimmune condition. The increasing number of similar reports of post HPV vaccine-linked autoimmunity and the uncertainty of long-term clinical benefits of HPV vaccination are a matter of public health that warrants further rigorous inquiry.

Great news for misogynists everywhere. Real ones.

All three patients experienced a range of common non-specific post-vaccine symptoms including nausea, headache, sleep disturbances, arthralgia and a range of cognitive and psychiatric disturbances. According to these clinical features, a diagnosis of primary ovarian failure (POF) was determined which also fulfilled the required criteria for the ASIA syndrome.

Explains some women I’ve met.

ASIA = autoimmune/inflammatory syndrome induced by adjuvants (ASIA)

A link between human papilloma virus vaccination and primary ovarian insufficiency: current analysis.


Reviews are good.

The cause of primary ovarian insufficiency (POI) is multifactorial. Known causes include external factors such as chemotherapy, radiotherapy, exposure to endocrine-disrupting chemicals, infections that lead to a permanent insult to the ovary, autoimmune conditions, and genetic causes. An association between the quadrivalent antihuman papilloma vaccine (HPV4) and POI was recently suggested.


The birth rate cult ought not to get their hopes up.

Q is, if the vaccine is so bad, what about the manwhores spreading the ‘organic’ version?

Credit: Master Brew

When do we outlaw sluts on population threat grounds?


An increasing number of cases of POI post-HPV4 are being reported. Possible mechanisms for the suspected effect of HPV on female reproductive function are a toxic effect or an autoimmune response. The trigger could be the vaccine immunogen contents or the adjuvants, the latter are used to increase the immune reaction.

increase, not produce

The adjuvant in HPV4 contains aluminum.

Yeah, still using it. Despite claims.

Animal models have shown aluminum exposure to inhibit expression of female reproductive hormones and to induce histologic changes in the ovaries.

I haz reasons for my quotes.

Specific genetic compositions may be more susceptible to developing an autoinflammatory syndrome after exposure to an environmental factor.

Bioweapon, by any other name.


The mechanisms responsible for POI are not yet fully understood. Although case reports cannot establish causation, awareness of a possible link between HPV4 and POI will help to identify and manage future cases that may arise.

They want people scared right now but don’t lose sight of the facts.

Don’t take any NWO shit. It’s going to be forced anyway. Rape with an object, legally.

They can claim e.g. one single paper from 2018 was “retracted” (impossible once peer-reviewed)

but that doesn’t change the hundreds of other studies documenting the same thing.

This study written by Gayle DeLong,  an associate professor at Baruch College, concluded that ‘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.’ 

Scientism people are stupid. You should want a follow-up.


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.”

Iodine and IQ

aka most of the Thing behind the Flynn effect.

Vegans are deficient.

We assessed the association between maternal iodine status and child IQ at age 8 years and reading ability at age 9 years. We included 21 socioeconomic, parental, and child factors as confounders.

Our results show the importance of adequate iodine status during early gestation and emphasise the risk that iodine deficiency can pose to the developing infant, even in a country classified as only mildly iodine deficient. Iodine deficiency in pregnant women in the UK should be treated as an important public health issue that needs attention.

After adjustment for confounders, children of women with an iodine-to-creatinine ratio of less than 150 μg/g were more likely to have scores in the lowest quartile for verbal IQ (odds ratio 1·58, 95% CI 1·09–2·30; p=0·02), reading accuracy (1·69, 1·15–2·49; p=0·007), and reading comprehension (1·54, 1·06–2·23; p=0·02) than were those of mothers with ratios of 150 μg/g or more.


The present comments are restricted to the role of maternal thyroid hormone on early brain development, and are based mostly on information presently available for the human fetal brain. It emphasizes that maternal hypothyroxinemia – defined as thyroxine (T4) concentrations that are low for the stage of pregnancy – is potentially damaging for neurodevelopment of the fetus throughout pregnancy, but especially so before midgestation, as the mother is then the only source of T4 for the developing brain.

Despite a highly efficient uterine-placental ‘barrier’ to their transfer, very small amounts of T4 and triiodothyronine (T3) of maternal origin are present in the fetal compartment by 4 weeks after conception, with T4 increasing steadily thereafter. A major proportion of T4 in fetal fluids is not protein-bound: the ‘free’ T4 (FT4) available to fetal tissues is determined by the maternal serum T4, and reaches concentrations known to be of biological significance in adults. Despite very low T3 and ‘free’ T3 (FT3) in fetal fluids, the T3 generated locally from T4 in the cerebral cortex reaches adult concentrations by midgestation, and is partly bound to its nuclear receptor. Experimental results in the rat strongly support the conclusion that thyroid hormone is already required for normal corticogenesis very early in pregnancy. The first trimester surge of maternal FT4 is proposed as a biologically relevant event controlled by the conceptus to ensure its developing cerebral cortex is provided with the necessary amounts of substrate for the local generation of adequate amounts of T3 for binding to its nuclear receptor.

Don’t worry, the brain damage was genetic anyway.

Women unable to increase their production of T4 early in pregnancy would constitute a population at risk for neurological disabilities in their children. As mild-moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia in Western societies, the birth of many children with learning disabilities may already be preventable by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible.


This editorial reviews the impact of iodine deficiency (1) on thyroid function in pregnant women and neonates and (2) on the neurointellectual development of infants and children.
All degrees of iodine deficiency (mild: iodine intake of 50-99 µg/day, moderate: 20-49 µg/day, and severe: <20 µg/day) affect thyroid function of the mother and the neonate as well as the mental development of the child. The damage increases with the degree of the deficiency, with overt endemic cretinism as the severest consequence. Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism in cretins.
Iodine deficiency results in a global loss of 10-15 IQ points at a population level and constitutes the world’s greatest single cause of preventable brain damage and mental retardation.

An entire Standard Deviation, no big deal!

Supplements won’t help, you’ll OD.

Iodine is a micronutrient that is essential for the production of thyroid hormones. The primary source of iodine is the diet via consumption of foods that have been fortified with iodine, including salt, dairy products and bread, or that are naturally abundant in the micronutrient, such as seafood. Recommended daily iodine intake is 150 μg in adults who are not pregnant or lactating. Ingestion of iodine or exposure above this threshold is generally well-tolerated. However, in certain susceptible individuals, including those with pre-existing thyroid disease, the elderly, fetuses and neonates, or patients with other risk factors, the risk of developing iodine-induced thyroid dysfunction might be increased. Hypothyroidism or hyperthyroidism as a result of supraphysiologic iodine exposure might be either subclinical or overt, and the source of the excess iodine might not be readily apparent.

The Great Iodine Debate


Iodine is critical to human health. It forms the basis of thyroid hormones and plays many other roles in human biochemistry. While the thyroid gland contains the body’s highest concentration of iodine, the salivary glands, brain, cerebrospinal fluid, gastric mucosea, breasts, ovaries and a part of the eye also concentrate iodine. In the brain, iodine is found in the choroid plexus, the area on the ventricles of the brain where cerebrospinal fluid (CSF) is produced, and in the substantia nigra, an area associated with Parkinson’s disease.

Iodine is essential to normal growth and development. Iodine deficiency in utero and during growth can result in cretinism, a condition of severely stunted physical and mental growth due to prolonged nutritional deficiency of iodine or from untreated congenital deficiency of thyroid hormones (hypothyroidism). The condition is characterized by short stature, delayed bone maturation and puberty, infertility, neurological impairment and cognitive impairment ranging from mild to severe. Iodine deficiency also causes goiter, the gradual enlargement of the thyroid gland. Both conditions have led to public health campaigns of iodine administration in many countries. The addition of iodine compounds to table salt or water represents the first attempt to provide nutrient supplementation via “fortification” of common foods.

At least they won’t have grandkids.

China paper here:

Click to access 32.pdf

also here

IQ so unreal it tracks brain damage.

The level of iodine nutrition plays a crucial role in the intellectual development of children. The intelligence damage of children exposed to severe ID was profound, demonstrated by 12.45 IQ points loss and they recovered 8.7 IQ points with iodine supplementation or IS before and during pregnancy. Iodine supplementation before and during pregnancy to women living in severe ID areas could prevent their children from intelligence deficit. This effect becomes evident in children born 3.5 years after the iodine supplementation program was introduced.

And now… we wait.

Waist-Hip Ratio and female beauty

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

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

Hello sexual selection, tied intimately to natural selection.

PDF here:

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

so K-type women may have better WHR.

Normal weight women have the most positive attributes associated.

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

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

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

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

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

So there’s that. Nobody’s jealous.

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

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

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

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

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

This chart drags you harder than I ever could.

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

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

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

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

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

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

What does a foetus feed from?

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


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

Suck on that, soyboys.

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

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

Not womanly. Remember that word? This:

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

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

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

If you only care for other male opinions.

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

Ya don’t say?

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

Distribution varies by race.

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

Am I imagining all of this?

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

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

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


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

Normal men aren’t pedos.

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

Stick with health.

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

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

Not really.

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

crazed pointing-

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

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


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

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

Study 2, rubbing salt in that fact.

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

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

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


Study 3

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

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

This is why we need studies on men too.

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

Study 4

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

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


Let’s look historically. Study 5

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

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

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

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

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

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

Something in the food?

More history, prehistoric. Study 6

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

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

Should’ve controlled for race.

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

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

Latter requires time.

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

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

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

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

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

Yet they don’t tell men this information.

Back to women

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

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


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

Asia is weird for dimorphism studies.

Hence the focus on health.

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

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

Click to access nihms827194.pdf

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

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