The wages of sin – HPV in men and sperm infertility

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

TLDR – NOT HARMLESS

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

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

-increased miscarriage rate, lower odds of conceiving

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

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

Yes, this is a dealbreaker to sane women.

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

No abstract available

irony

MRAs: crickets

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

Human papillomavirus infection and fertility alteration: a systematic review

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

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

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

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

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

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

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

The role of human papillomavirus on sperm function

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

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

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

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

-only? a? 100% is a percentage too…

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

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

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

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

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

– no hurt their feefees? NAW

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

– Manosphere fears this topic and all male degenerate accountability.

semen infection may cause infertility and early miscarriage

it’s the sins of the FATHER, you see…

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

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

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

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

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

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

TLDR: yes.

HPV is commonly present in semen samples. 

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

The overall rate of HPV positivity was 15.5%

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

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

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

It’s worse for the older men.

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

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

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

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

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

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

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

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

what a mystery

The mechanism of ASA cause male infertility is not clear

does it look like HPV?

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

yes

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

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

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

duh?

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

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

-what r the odds?

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

Medicine can’t spare you.

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

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

 Fifteen samples

-aka HALF

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

no muh scientism and IVF cope

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

-may, LOL

a negative effect on development of the fetus

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

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

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

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

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

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

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

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

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

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

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

brace yourselves

guess the result

c’mon

go on
think

just guess

….

ready?

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

and all fertile men were HPV-negative

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

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

Player burnout shall henceforth be dubbed HPV-driven infertility?

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

2021

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

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

-maybe where you live

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

-well the husbands are freshly infecting the wives so

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

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

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

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

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

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

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

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

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

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

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

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

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

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

dat p-value

MORE STUDIES

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

Sperm DNA fragmentation in couples with unexplained recurrent spontaneous abortions

(((((“”unexplained“”)))))

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

– idiopathic? Are you shitting me?

(((idiopathic)))

sure it is

sure

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

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

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

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

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

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

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

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

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

I mean – where are the STUDIES?!

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

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

unexplained….. sigh, ok.

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

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

Known for 20 years.

Human sperm deoxyribonucleic acid fragmentation by specific types of papillomavirus

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

CAUSED

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

-swimming in circles isn’t motility, really

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

it’s a viral abortion, really

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

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

i.e. no, you won’t just get IVF

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

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

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

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

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

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

-all trust the EU guys

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

-somebody else look up herpes, I’m lazy

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

-Really, f-ing fascinating!

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

>male fertility disorders

k.

Oh, I’m not done yet.

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

HPV infection in semen: results from a new molecular approach

Let’s get molecular.

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

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

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

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

Your superpower is probably autism.

Superstitious minds

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

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


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

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

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

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

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

2015 Birth Defects in the Newborn Population: Race and Ethnicity

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

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

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

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

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

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

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

Craniofacial = ugly. 

Musculoskeletal = ugly. Well, dumpy.

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

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

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

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

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

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

Some superstitions have a basis in fact.

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

To see if you’re a SINNER!

[inc Thou shalt not adulterate]

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

We’re looking for spiteful mutants.

Now the post gets huge.

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

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

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

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

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

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

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

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

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

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

Reply:

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

Do not hold information my lily-white arse.

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

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

“Page does not exist”.

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

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

In an ONS report. They know.

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

(Black, 54%;

Mixed, Chinese and any other group, 44%;

White, 43%;

For a majority, that’s incredibly low.

and those where ethnicity was

not stated, 49%).

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

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

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

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

read: racially

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

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

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

Enjoy that decline.

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

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

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

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

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

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

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

Something’s off.

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

Do you see what I see?

For non-statistically minded people:

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

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

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

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

Table 10 screen-capped, do your own charts.

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

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

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

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

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

Ethnicity and IVF

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

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

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

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

We’ll see why.

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

Seriously. Measurement bias much?

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

We did that.

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

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

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

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

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

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

Genetics is the ONLY difference now.

You have NOTHING.

DNA causes germline DNA, really? Maybe?

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

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

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

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

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

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

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

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

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

Nope!

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

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

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

The Ice Age killed the boyish ones.

MORE:

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

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

I wonder which way.
Inbreeding or outbreeding depression?

Guess.

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

Dudebros like “where’s da studies?”

I’m like “Have you even looked?”

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

DING DING DING DING DING

TIL Wombs iz white supremacist.

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

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

Learn to read, weebs.

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

aka nice way of calling out deception

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

They know. It’s a cover-up.

Category errors galore.

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

Relevant!

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

What DO these studies have in common? [Asians]

Could also be child of rape as a confound.

You’ll see.

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

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

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

Your Third World surrogate plan may need retouching.

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

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

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

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

It’s mentioned along with smoking.

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

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

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

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

Their own women.

Pre-term study and IQ:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

In the interest of intellectual honesty.

WHR

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

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

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

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

Old expression.

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

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

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

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

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

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

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

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

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

NOBODY is jealous. You keep your secret fatty.

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

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

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

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

Hips don’t lie because biochemistry.

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

Pot smokers have sicklier babies

https://www.ncbi.nlm.nih.gov/pubmed/16458631
“If men smoked marijuana 11 to 90 times in their lifetime, there was a 15% decrease in infant birth weight (P = .03); if this increased to more than 90 times, there was a 23% decrease (P = .01). Timing also played a role.”
“Women and men who smoked in the past 15 years, had 12% (P = .04) and 16% (P = .03) smaller infants, respectively.”

This is why ((they)) want to legalize.

Such a change in one generation is huge news.

Related

https://www.ncbi.nlm.nih.gov/pubmed/15343228

Paternal age increases pregnancy failure and miscarriage rate in IVF

Brave New Eugenics: officially making fatherless babies

article

In full;

Britain is to get its first NHS-funded national [socialist] sperm bank to make it easier for lesbian couples and single women to have children. [DS: boys without any father at all]

For as little as £300 – less than half the cost [???] of the service at a private clinic –  they will be able to search an online database and choose an anonymous donor on the basis of his ethnicity, height, profession and even hobbies.

The bank, which is due to open in October, will then send out that donor’s sperm to a clinic of the client’s choice for use in trying for a baby. [IVF is too expensive and causes birth defects and retardation]

Heterosexual couples will also be able to benefit, but the move – funded by the Department of Health – is largely designed to meet the increasing demand from thousands of women who want to start a family without having a relationship with a man.

Critics last night called it a ‘dangerous social experiment’ that could result in hundreds of fatherless ‘designer families’.

The former Bishop of Rochester, Michael Nazir-Ali, said last night: ‘It is the welfare of the child that must come first and not the fact that people want a particular kind of baby.’ [or any baby, you don’t have a right to another human being, that’s called slavery]

Bishop Michael, who once chaired the ethics committee of Britain’s fertility watchdog, added: ‘This is social experimentation. It’s one thing for a child not to have a mother or father through tragedy, but it is another to plan children to come into the world without a father.’ [who wants to tell the Children’s Rights people?]

The National Sperm Bank will be based at Birmingham Women’s NHS Foundation Trust, which currently runs an existing NHS fertility clinic and recruits sperm donors from the local population. [who are liable for 18 years of Child Support payments]

Funded by a £77,000 Government grant, the bank will be run by the National Gamete Donation Trust (NGDT) which this year received  an additional £120,000 of public money to organise egg and sperm donation.

Over the next three years the NGDT aims to recruit at least 1,000 men and collect sufficient  donations for the sperm bank to meet demand.

Laura Witjens, NGDT chief executive, said: ‘There are people who  are medically infertile or practically infertile [you mean they can’t have children because of their lifestyle choices, their choices] – they want to use donation services in the UK but can’t do so because there isn’t enough donated sperm. [blame Child Support laws]

‘The demand from same-sex couples and single women has grown exponentially. It’s become more socially acceptable to say, I haven’t found a guy yet, don’t want to wait for him, still want a child.’

She added: ‘The aim is that we will have enough surplus sperm so that we will be able to set up a service for people like single women and same-sex couples.’

She described this group as ‘customers rather than patients’. [Then they can fucking pay for private.]

Britain has a major shortage of sperm donors, whose anonymity is preserved until any children they father reach the age of 18. [not really, the kid can track them down – Facebook? Google?]

Women who want to have a baby using donated sperm have been routinely waiting for up to two years, with many eventually forced to seek donors abroad. [what a shame]

Treatment resulted in the births of 161 babies to lesbian couples.

Ms Witjens rejected suggestions that children suffer adverse consequences from lacking a father figure. [abuse charges?] ‘There is no evidence to suggest that children are better off with or without a father,’ she said. ‘There’s never been a call – from us or the Department of Health – to reduce the access to sperm for same-sex or single women. That’s a non-issue.’

Ms Witjens pointed to the removal of the reference to a ‘need for a father’ in the Human Fertilisation and Embryology Act, when taking account of a child’s welfare when providing fertility treatment. [equality!]

She added that the National Sperm Bank would also help prevent desperate women using murky unregulated services and going online to buy sperm. [or save up and pay private. If they can’t save enough they can’t be good parents.]

Heterosexual couples with fertility problems who need donations as part of IVF treatment will be among the customers of the new bank.

But a large percentage are predicted to be professional, single females who decide to have a baby without a man.

And based on current trends, more than a quarter of all the recipients are likely to be gay women.

Latest available figures from the Human Fertilisation and Embryology Authority show that in 2011, 4,101 cycles of donor insemination were carried out in the UK.

Of these, 1,271 related to women registered with a female partner. That figure represents more than  a quarter of the total and was a  23 per cent increase from the  previous year.

There are currently just two clinics in the UK where women can choose donors from an online list.  Both are private and charge around £850 for the service.

NHS funding for fertility services, including donor insemination, is decided by regional Clinical Commissioning Groups and varies widely. [same NHS which has been refusing cancer treatments to cut costs, including to children]

CCGs are typically more likely to fund heterosexual couples struggling to conceive rather than lesbians or single women because they are considered to have more of a medical need. [duh] The NGDT hopes the sperm bank will be self-funding after a year.

A spokeswoman for the HFEA said: ‘We welcome the new National Sperm Bank which will help to ensure that the recruitment of donors and the availability of donor sperm is better organised.’

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COMMENT: Designer babies are a disaster for society, writes Bishop Michael Nazir-Ali

This announcement raises some important questions about the future of our children and the role of men in our families  and communities.

The most important thing to say is that the needs of  any child must be primary. It is the upbringing, welfare and education of the child that should be the prior consideration. It is not enough to ‘want’ a child, let alone one with particular characteristics.

This bank will allow women to choose from profiles of donors, which will include educational attainment and ‘attractiveness’ criteria, [DISCRIMINATION!] raising the spectre of ‘designer babies’, born to the parents’ specifications. [this was predicted. Holy Shit, someone tell CH!]

What if  the process of pregnancy and birth ‘interferes’ with the desired outcomes? Will such babies then  be rejected? [yes, they already are]

Research shows that children are best brought up in families where a mum and dad are present. The role of fathers in the nurture of their children is unique and cannot be replaced by other so-called ‘male role-models’ or, indeed, an extra ‘mother’.

Research tells us that children relate to their fathers differently than to their mothers, and this is important in developing a sense of their own identity.

In particular, boys need closeness to their fathers for a sense of security and in developing their own identity, including appropriate patterns of masculine behaviour.

The results of ‘father-hunger’ can be seen in educational achievement and on our streets, where it contributes to delinquency.

None of this should detract from the heroism of single parents. They should be provided with every support by the State and by local communities.

There is, however,  a big difference between children growing up without fathers because of death or family breakdown, and actively planning to bring children into the world who will not know one of their biological parents and where such a parent will never be part of the nurture of these children. [violation of a human right, actually]

Research tells us that children relate to their fathers differently than to their mothers, and this is important in developing a sense of their own identity, writes Bishop Nazir-Ali

This also brings the question of anonymity to the fore. The change in the law, so people could, at a certain age, find out who their biological father is, has certainly contributed to the ‘shortage’ of donors in response to which the sperm bank has been set up. [and the big bill, say, for University tuition, 18+?]

If there is no anonymity, will potential donors come forward, or will the bank face these same ‘shortages’?