“It might sound strange, but its true, this remedy has been passed around the feminist community since the 70’s, appearing in many grassroots publications, some of which are cited here. There are also numerous reports of women using it successfully from this era, I’ve heard many stories, but never saw any kind of documentation, which isn’t surprising in a time, where a woman’s right to choose an abortion and have access to safe legal abortion services was just being won.”
Great for ye olde days of gang rape though. Useful if the Red Army comes around town. Abortion does make sense where continuing would kill the mother so there is an ethical grey area e.g. ectopic. I acknowledge that. We also must know what kills a baby so all mothers know to AVOID it. This is why keeping women ignorant leaves them vulnerable to such evil. Parts of nature hate us. Wiccans are imbeciles.
This is why I don’t supplement liposomal Vitamin C, as I suggested for OLDER people.
“The scientists who conducted the research, Samborskaia and Ferdman came to the conclusion that high doses of Ascorbic Acid appeared to increase estrogen levels which contributed to the interruption of an otherwise normal pregnancy. 20 women who approached doctors requesting an abortion participated in the study. Research was conducted by ob/gyn L.I. Ivanyuta. The women ranged from 20 to 40 years of age. The article does not say if a positive pregnancy test was obtained from the participating women. We also don’t know how much ascorbic acid the women were given. They did however measure estrogen levels before and after treatment with ascorbic acid, finding that estrogen levels were higher after taking the ascorbic acid. Of the 20 women, 16 began menstrual type bleeding within 1 to 3 days from administration of ascorbic acid.”
It makes giving kids lemonade real sinister. Mountain Dew, Sunny D, the works.
“Vitamin C works to produce an unfavorable climate within the uterus so that the egg does not implant, or if implantation has already occurred, Vitamin C can weaken the fertilized ovum’s grip on the uterine wall. Possibly by stimulating estrogen, and interfering with progesterone. This also makes it useful as an emergency contraceptive, when taken before implantation occurs on the 6th day following ovulation. The hormone, progesterone is essential for pregnancy, its function is to prepare a nourishing bed for the fertilized egg, if there is not enough progesterone the uterus becomes less supportive to the egg. Which is desirable when the goal is to end pregnancy.”
Progesterone means pro-gestation. Anything that reduces that and/or increases oestrogen causes miscarriage, including xenoestrogens. BPA also causes genetic defects inc. Downs, and can cause abnormal egg development in a female fetus, which can go on to experience many miscarriages (modern rates?) and Downs children themselves.
Also NO parsley. Yes, it kill babies. Viva Italia some other time. Can be used to induce labour, ironically.
History will view the use of xenos as pure evil*. I think endometriosis is caused by it, like a poisoning. Explains the miscarriage common to it. Most common cause of infertility in women. Pure progesterone creams hard to come by, easier to patent a toxic variety close enough. Even pure creams can include preservatives that are oestrogenic! Vegan love of vit C may cause vegan menopause, imho. Xenos also cause premature puberty in girls as young as ONE, especially seen in high-estro skin products used by American blacks and not found in African ones. Xenos (including hops in beer**) also cause a small penis and breast development in boys/men. This shit should be BANNED forever in all skincare vehicles (10x more potent, bypassing liver filter). The amount required (parts per billion) is rarely tested for but maintains estrogenic effect at this level. Parabens were disused in some products due to this. Others like SLS and phthalates also. It isn’t hype, it’s killing men/women hormonally and babies silently. A silent killer in shampoo, lotion, food etc. No wonder American rates of miscarriage are so high. Test ALL skin products for endocrine disruption, especially those that break down into it (XENOS), in rats. Xenos can bio-accumulate for decades in the body (heard of DDT?) and stay for decades too. I share this hoping people won’t abuse the info.
*file under Molech
**how Anglos have gotten softer and softer and softer… literally and morally.
Synthetic perfume is also a xeno. Sorry. I’m sad about it too. They’re aiming this at teen girls and boys, who get fat. And in the case of girls, look sexual. The boys look twinkish. I’m sure the traffickers love that.
They blame kids for being fat when they’re hormonally drugged from seemingly everywhere. They cannot lose weight! The environment is too polluted!
Phyto-estrogen can bind protectively and reduce the capacity of xeno to attach. This is limited. It’s less potent but still oestrogenic and thus reduces progesterone. Can detox from the body in a matter of days since it’s natural.
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.
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
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.
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.
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.
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.
Semen washing procedures do not eliminate human papilloma virus sperm infection in infertile patients
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.
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
guess the result
go on think
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.
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.
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).
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.
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.
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.
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.
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.
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
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.
The impact of male age on fecundity remains controversial. Here, a large population study was used to investigate the effect of paternal age on time to conception. All couples in the Avon Health district expecting a baby between 1 April 1991 and 31 December 1992 were eligible. Questionnaires completed by both the man and the woman at 18 weeks gestation covered specific fertility factors, e.g. parity, paternity, cohabitation and oral contraception; and non-specific factors, e.g. educational achievement, housing, cigarette smoking, alcohol consumption, obesity. Logistic regression was used to identify factors independently related to conception in ≤6 or ≤12 months. Of 8515 planned pregnancies, 74% were conceived in ≤6 months, 14% in the second 6 months and 12% after more than a year. Nine variables, including the age of the woman, were independently related to time to conception. After adjustment for these, the likelihood of conception within 6 or 12 months was lower in older men. Compared to men <25 years old, the adjusted odds ratios (95% confidence interval) for conception in ≤12 months were 0.62 (0.40, 0.98), 0.50 (0.31, 0.81) and 0.51 (0.31, 0.86) in men aged 30–34, 35–39 and ≥40 years respectively.
That might explain Harry. And the kale smoothie diet. Good for sperm.
When people wait too long on purpose, with the right person, and find out they can’t have kids any more, I like to think it’s Mother Nature flipping them off with one hand and punching them in the balls with the other.
Why, you ask?
“the overall association with age was highly statistically significant. If the man’s age was treated as a continuous variable there was a significant linear relationship: the odds ratio for conception in ≤6 months decreased by 2% per year of age (P < 0.01) and for conception in ≤12 months by 3% (P < 0.001).”
Every year a man goes over 25, his likelihood of easy conception drops by 2%.
“These results suggest that there is a larger decline in male fecundity with advancing age than reported in earlier population studies (see above).”
That is all pretty funny considering the guys who think they have Thor-immortal sperm.
More like thaw.
“Therefore our conclusions would remain valid even if the most fertile of the older men had been eliminated from the study group because they achieved unplanned pregnancies. If the opposite bias predominated and the less fertile couples were lost from the older groups, we would underestimate the effect of age on male fecundity. It is unlikely that a substantial number of men aged ≤24 years would believe themselves to be sub-fertile….
Please call it virility. Men don’t give birth, they can’t be fecund. Just call the impotence, impotence. There are levels.
Were this true of older men, it would again lead to an underestimate of the effect of age on fecundity.”
“…However, they do not exclude the possibility that the greater fecundity of young relative to older men was more marked in the past.
….It is also possible that more fertile men complete their families sooner, and less often try to father children in their thirties or forties.”
It gets worse. You can’t supplement your way out of ball shrinkage.
Although most data come from elderly men changes can be detected in middle age (Erfurth and Hagmar, 1995; Bonavera et al., 1997). There are a number of morphological changes in the ageing testis, including a decrease in the number of Leydig cells (Neaves et al., 1985), a decline in Sertoli cell numbers and daily sperm production (Johnson et al., 1984a,b) and an increase in the involution of seminiferous tubules (Paniagua et al., 1987). Spermatozoa from older men are less fertile after intrauterine insemination (Mathieu et al., 1995; Brzechffa and Buyalos, 1997) or in donor insemination (Lansac, 1995). These observations support the conclusion that the effects of paternal age on a couple’s fecundity are real and may be greater than previously believed. After adjustment for other factors, the probability that an ultimately fertile couple will take >12 months to conceive nearly doubles from ~8% when the man is <25 years to ~15% when he is >35 years and paternal age is a further factor to take into account when deciding the prognosis for infertile couples.
Doubles in ten years. That’s worse than any female stat. It tanks!
Reduced fertility typically occurs among women in their late 30s, but increasing evidence indicates that advanced paternal age is associated with changes in reproduction as well. Numerous studies have investigated age-based declines in semen traits, but the impact of paternal age on semen parameter values remains inconclusive.
Clear rationale, nice.
Using data from 90 studies (93,839 subjects), we conducted a systematic review and meta-analysis to quantify the effect of male age on seven ejaculate traits (semen volume, sperm concentration, total sperm count, morphology, total motility, progressive motility and DNA fragmentation). Age-associated declines in semen volume, percentage motility, progressive motility, normal morphology and unfragmented cells were statistically significant and results generally seemed to be robust against confounding factors. Unexpectedly, sperm concentration did not decline with increasing male age, even though we found that sperm concentration declined over time.
More chance of mutant sperm, future psychiatrist patient babies! Lucky you!
It would be better if they made less but retained quality than risk stillbirth.
Our findings indicate that male age needs more recognition as a potential contributor to the negative pregnancy outcomes and reduced offspring health associated with delayed first reproduction. We suggest that greater focus on collection of DNA fragmentation and progressive motility in a clinical setting may lead to better patient outcomes during fertility treatments of aging couples.
Ouch. Thirties is now aging? Well, I guess in medicine, it is.
Really, 40 is the age where male fertility tanks severely.
Like, you’d be better off not conceiving than risk the cost of a disabled kid.
Result(s): The odds ratio of failure to conceive for paternal age 40 years was 2.00 (95% confidence interval [CI]: 1.10–3.61) when the woman was 35–37 years old, 2.03 (95% CI: 1.12–3.68) for age 38–40 years, and 5.74 (95% CI: 2.16, 15.23) for age 41 years and over.
Conclusion(s): As an increasing number of couples choose to postpone childbearing, they should be informed that paternal age over 40 years is an important risk factor for failure to conceive.
This marked maternal age effect led to the conclusion that 35 years is the “amber light” in the reproductive life of women (4). Paternal age was long almost ignored in studies of age effect on reproductive outcomes, but its potential role has recently been investigated. Some works have shown that increasing paternal age is accompanied by greater risk of delay in achieving pregnancy, of miscarriage and of late fetal death (5–8). In a recent review of the literature, we considered that 40 years could be the “amber light” in male reproductive life, as is 35 years for women’s reproductive life (9)
Wow, five years. Almost the average difference of successful marital unions. (Wait, exactly that, the man is five years older). Now I know why it’s Mother Nature.
…. To analyze paternal age effect mediated by biological aging alone, data on medically assisted cycles provide a very interesting model
Our results provide, for the first time, strong evidence for a paternal age effect on failure to conceive that is linked only to biological male aging (without confusion with sexual activity). We observed a clear tendency to increased risk of failure to conceive, especially when the fathers were over 40 years old. Results in the first and last classes in Table 2 (older woman with young man or young woman with older man) should be interpreted with caution because of the small number of couples in these classes. We thus analyzed Table 2 by concentrating on classes with at least 30 couples. This revealed a clear increase in risk of failure to conceive with paternal age.
Our results on a paternal age effect after 40 years are in accordance with results recently published concerning the general population. In a European population-based study of
couples attempting to conceive naturally, a significant odds ratio of 2.99 (95% CI: 2.77, 7.55) for the risk of not having conceived after 12 months of attempting to achieve pregnancy was observed when the woman was 35–39 years old and the man 40 years old and over (7). A similar tendency was observed in another European study of 782 couples, which showed a decrease in the daily probability of conception in couples composed of a woman 35–39 years old and of a man in his late thirties or older (8).
It has been demonstrated that couples having difficulty in conceiving also have an increased risk of miscarriage (19). Thus, the association between paternal age and failure to conceive raised the question of a possible association between paternal age and miscarriage. In the literature, an increased risk of miscarriage was observed in couples composed of a woman 35 years old and over and of a man 40 years old and over (OR 6.73; 95% CI: 3.50, 12.95) (6).
What about 50+? Obvious grandfather territory.
More recently, in a large Danish cohort, a twofold increase of the risk of early fetal death was found when the father was 50 years old and over compared with fathers 25–29 years old, after controlling for various confounders and especially for maternal age (5). In the same cohort, the authors showed a paternal age effect as early as 45 years when considering late fetal deaths.
Yet they’ll still try to blame it on the women….
….The authors concluded that elevated paternal age (35 years) increased the risk of spontaneous abortion during the first trimester and at the beginning of the second trimester, with a suggestion that the association was stronger for deaths occurring during the first trimester.
large genetic abnormalities
Interestingly, a remarkable concordance exists among all these studies, stressing the fact that older fathers (40–45 years old) have a key impact on both reproductive issues, failure to conceive, and miscarriage.
When a man conceives, his sperm quality is all he contributes. Male age will be a much larger factor than anything female, all things considered. Try making a decent omelette with stale eggs. Try fertilizing an ovum with old sperm. The single ingredient on that side of equation becomes very. very important.
Women in that case are trying to compensate for the errors of men.
The mechanism for the paternal age effect remains to be explained.
Aging germline DNA is not better DNA.
Previously, as for maternal age, the genetic hypothesis had been emphasized (21, 22). After analysis of 11,535 pregnancies obtained by artificial insemination using donor spermatozoa, an increased risk of trisomy 21 for the fetus when the donor was 38 years old has been suggested (23).
A lot of my generation thinking they can wait will be sorely mistaken.
Gambling your future, literally.
In reproduction, age must no longer be considered as the concern of the woman, but as that of the couple. Similar to maternal age over 35 years, paternal age over 40 years is a key risk factor in reproduction.
The results showed that maternal age was closely linked to decreased pregnancy rate, which was 8.9 per cent in women over 35 compared to 14.5 per cent in younger women.
But the scientists also found that the father’s age was also important, not only on pregnancy rates, but perhaps more surprisingly, on the rate of miscarriage, with a pronounced negative effect once the father was over 35 years of age…
A representative of the Eylau Centre also said on an interview with the BBC aired early this morning that the likely cause of the decrease in male fertility after 35 was DNA fragmentation. He said that DNA fragmentation was not unusual in male sperm and often this is repaired “by the woman”, but when it is too fragmented it is beyond repair, leading to pregnancy failure and miscarriage, he said.
They’ll still blame the woman.
There’s a reason all of Henry VIII’s kids died childless.
Frozen sperm is only good for about ten years, by the way.
Maybe instead of proving their manliness by submitting to 23andMe, these guys should be getting their sperm quality checked and post those results.
Speciation is an ongoing process, it’s part of evolution, also an ongoing force. As members of a sub-species, better known as race, continue to diverge over time, the characteristic event will be infertility, fertility issues, birth defects and miscarriage. Once it is born, a failure to thrive and reproduce itself would also count as an adverse selection pressure.
My simple question: do we see this?
Oh, boy. Grab a drink, tall one.
The mixed-race dating pool is limited, to the other mixed-race, for example.
This lowers the potential fitness of the organism, compared to its parents’ baseline.
I’ll take a biomedical approach, from the limited information available.
Asians have a lower median birth weight, a racial difference as real as shorter African gestation periods compared to Whites.
“Although past studies have looked at ethnic differences in perinatal outcomes, the majority of research has focused on white- African-American couples. Few studies have focused specifically on Asian-white couples, said El-Sayed, who is also associate chief of maternal-fetal medicine.
More specifically, the researchers found that white mother/Asian father couples had the lowest rate (23 percent) of caesarean delivery, while Asian mother/white father couples had the highest rate (33.2 percent). Because birth weights between these two groups were similar, the researchers say the findings suggest that the average Asian woman’s pelvis may be smaller than the average white woman’s and less able to accommodate babies of a certain size.”
“El-Sayed and his colleagues also found that the incidence of gestational diabetes was lowest among white couples at 1.61 percent and highest among Asian couples at 5.73 percent – and just under 4 percent for Asian-white couples. These findings weren’t altogether surprising: past studies have shown an increased risk of diabetes among Asian couples, which researchers attribute to an underlying genetic predisposition. But the interesting finding, El-Sayed said, was that the risk for interracial couples was about the same regardless of which parent was Asian.”
Dominant genes? No!
“Because of the results on Caesarean section rates they adduce that there is a pelvic size difference between Asian women and white women. Objective male observer acquaintances of mine have generally tended to back up this phenotypic difference between the populations.”
They’re shaped like pre-pubescent boys. Why else get surgery?
You should study it formally though. Asians have the lowest sexual dimorphism and it’s important to know the numbers.
“Although births of multiracial and multiethnic infants are becoming more common in the United States, little is known about birth outcomes and risks for adverse events. We evaluated risk of fetal death for mixed race couples compared with same race couples and examined the role of prematurity and low birth weight as potential mediating risk factors.”
Miscegenation doesn’t work, even with modern medicine.
This applies to black-white pairings too.
It is a disgrace adults are marrying without knowledge of the biology involved.
“Mixed race black and white couples face higher odds of prematurity and low birth weight, which appear to contribute to the substantially higher demonstrated risk for stillbirth. There are likely additional unmeasured factors that influence birth outcomes for mixed race couples.”
I cannot find a stillbirth study for Asian-White pairings, I’m sorry. Is it so common they need not study it?
We have anecdotes? https://www.temptasian.com/fyooz/after-3-miscarriages-the-zuckerbergs-are-finally-expecting-a-girl/
“Most people don’t discuss miscarriages because you worry your problems will distance you or reflect upon you — as if you’re defective or did something to cause this.” Mate choice is something you did. The baby didn’t choose to be conceived by you two. Part of your biology must be defective because miscarriage is an outcome of defective conception and/or pregnancy (there are many possible reasons, some environmental, a few random plus ‘stress’). It sounds cruel but yes, medically, something is wrong.
When trying really hard, the only evidence for hybrid vigour in White Americans vs. mulattos, which they sought to prove (scientism) is “relatively small.” …Is it present or not? https://www.nature.com/articles/nature14618
“this study provides evidence [DS: the evidence isn’t proof?] that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been.”
That’s bullshit, everyone is getting taller and getting better grades.
May not have been? In Nature?
Listen to the twisting in this: http://www.medicaldaily.com/g00/interracial-couples-may-make-taller-smarter-children-due-greater-genetic-diversity-341348 “Meanwhile, human evolution is more focused on the ability to create healthy offspring and have them survive infancy to continue raising them.” Yes.
…Yes, it is.
“Whether you come from a genetically diverse background or not, in the end even the most common medical ailments that affect society will affect everyone, with genetic diversity having little to no impact.”
No, genes. The most common fatal medical ailments aren’t a cold, they’re genetic-based, it’s established fact. And if it had no impact, why push it?
“It combines the parents’ genetic material, resulting in offspring that possess a unique set of genetic blueprints that increase their chances of surviving and thriving compared to a population with limited genetic variability.”
No such thing. Limited genetic variability? No such thing. Where is this thing?
They’re just talking absolute crap to cover how their study was a non-result. Every genome is unique, between twins even. Thriving and surviving varies by individual genome, that should be studied by the natal people. You know this. You hide the scant data that is there with delusions. This is propaganda. It continues:
“This encapsulates Charles Darwin’s theory of natural selection,”
No, he wrote a whole book. Look at the subtitle to The Origin of the Species.
Natural selection is about death and mortality, which you have not studied. Disease is not death.
“where individuals with characteristics that increase their probability of survival”
how? like being able to give birth?
“will have more opportunities to reproduce,”
in a limited dating pool
“according to the University of California, Berkeley’s Understanding Evolution.”
If California understood evolution, it would be Alaska.
“As a result, their offspring will benefit from the variants,”
no, not if they’re the more common disadvantageous mutations or if the combination is novel and fatal
“which will spread throughout the population.”
No, you’re assuming they breed. Infertility exists, and it exists on a spectrum.
“This is an increased risk equivalent to smoking, advanced maternal age or obesity.”
“While other research has found the mother’s ethnicity places a role in the risk of a stillbirth, this has largely been put down to factors related to migration and social disadvantage. What our research shows is women born in South Asia and giving birth in Australia are at increased risk even when other factors are taken into account.”
“There is growing evidence to suggest a mother’s ethnicity influences how fast her placenta ages as her pregnancy progresses.”
Asian placenta is old, got it.
“For some women, they can go into spontaneous labour sooner. In our study, we found South Asian-born women went into labour a median one week earlier than Australian- or New Zealand-born women.”
Racial differences in gestation duration, again.
“However, for others, an ageing placenta cannot meet the fetus’ increasing metabolic needs at term and beyond. And this increases the risk of stillbirth.”
Infertility, insufficient maternal resources for the fetus. That’s a kind of infertility. Considering how skinny they are and how those female curves are supposed to feed a baby, historically, this is not surprising.
Nature is aborting babies that would starve. Before it kills the mother too.
“And the length of telomeres in placentas from pregnancies ending in stillbirth are two times shorter than those from live births. In other words, the placental cells had aged faster.”
Superior Asian genetics people might wanna cover their innocent eyes.
“Some researchers have also studied ethnic differences in placental telomere length.
In an American study, placental telomeres from pregnancies in black women were significantly shorter than from pregnancies in white women (the ethnic backgrounds of the women were not further defined in the study).”
Superior European placentas. As you’d expect for the one race hit hard by an Ice Age. Perhaps this is an unknown r/K variable.
“Whether telomeres are shorter in placentas from pregnancies in South Asian-born women is unknown.”
“However, BMI does not take into account the relative proportions of fat and lean tissue and cannot distinguish the location of fat distribution”
“However, these are based on information derived from the general population, based on risk of mortality, without consideration for racial or ethnic specificity and were not determined to specifically identify those at risk for diabetes. Recently, the U.S. Centers for Disease Control and Prevention presented initial findings from an oversampling of Asian Americans in the 2011–2012 National Health and Nutrition Examination Survey. These data, utilizing general population criteria for obesity, showed the prevalence of obesity in Asian Americans was only 10.8% compared with 34.9% in all U.S. adults (13). Paradoxically, many studies from Asia, as well as research conducted in several Asian American populations, have shown that diabetes risk has increased remarkably in populations of Asian origin, although in general these populations have a mean BMI significantly lower than defined at-risk BMI levels (14,15). Moreover, U.S. clinicians who care for Asian patients have noticed that many with diabetes do not meet the published criteria for obesity or even overweight.”
“In women, the connection between WHR and health measures appears to be hormonal. It is known that ratios of estrogen, progesterone, and prolactin affect all of these features. The “right” balance promotes both health and low WHR. One version of the “attractiveness theory” posits that our attraction to this body shape developed as an indicator of overall health.”
“Another crucial part of the attractiveness theory of wait-hip-ratio (WHR) is that this body shape has to be indicative of something related to fertility, or else it wouldn’t have any evolutionary value.
The key feature in a potential mate is biological fitness, that is, the potential to give birth to many healthy and successful offspring.
Desirable females, in the evolutionary sense, are those that are likely to be healthy, fertile, and robust.
Robust = pelvis, btw.
Venus was never a narrow-hipped vixen.
The body acceptance people should really focus on the hips.
A low WHR, it is thought, must correlate with fertility (ability to have children) and/or fecundity (tendency to have large numbers of children).”
There is such a thing as too low. Boyish figures have less fat, fewer curves and narrower hips.
They’re confusing women who have obesity and babies for State money with natural attractiveness, fecundity in the state of nature and blurring BMI with WHR. Nobody said unhealthy (low) WHR is wealthy, for fecundity. That’s a strawman. The hormones and other details, medical details, are better profiled in the most nubile WHR range. It is a range. Don’t line graph me, study.
It doesn’t mention race although many women in the world do not have a figure. Unless you count a figure of 1.
“The waist is one of the distinguishing human features, such as speech, making tools and a sense of humour,’ says Professor Singh. ‘No other primate has one. We developed it as a result of another unique feature – standing upright. We needed bigger buttock muscles for walking on two legs.”
If the waist makes the human, a lot of women are fucked.
“The ideal ratio in healthy pre- menopausal women ranges between 0.67 and 0.8. In terms of the tape measure, this is produced by waists between 24in and 28in with 36in hips, and waists between 27in and 31in with 40in hips.”
…How many Asian women have a 36″ hip?
The fat ones I’ve seen were pufferfish.
“come puberty, the sex hormones start directing it differently.”
“Oestrogen, the hormone of female sexual characteristics, concentrates it on the buttocks and hips while the masculinising hormone testosterone encourages fat to form around the waist.’ At the same time testosterone encourages fat to be burnt off the buttocks while oestrogen takes it off the abdomen. These characteristically feminine fat stores are used in the last months of pregnancy and during breast-feeding. This is another reason why women who are seriously underweight often stop menstruating – they would not have the resources to support a pregnancy or a baby.”
“Women with a low ratio, Professor Singh says, tend to start ovulating younger, and those with a high ratio find it more difficult to become pregnant and tend to have children later. [not by choice]
Although a high waist-hip ratio most commonly goes with being overweight, it can also be found in women of normal weight who have high testosterone levels – a condition that is also associated with being hairy, infertile and having a ‘male’ body shape.”
Manly body, fertility problems. Study it. Avert tragedy.
“In a survey of 106 men aged 18 to 22, the favourite was a female of average weight with the classic hour-glass figure. Not only were such women rated as young, sexy and healthy, they were also seen as ideal for childbearing.”
Again, sexy is different from beautiful.
Porn is a lie.
“The young men regarded the underweight women – defined as women of 5ft 5in weighing less than 90lb – as ‘youthful’ but not particularly attractive, especially for childbearing.”
To prefer the obese over the mannish figured for motherhood is huge.
Youthful is code for making them feel like a pedophile.
“In Professor Singh’s other surveys, men of all ages agreed with these findings – thus bearing out her theory of the waist-hip ratio.”
Women dropped the corset to signal they weren’t just baby-making machines.
It’s hard to test low-WHR women in a world of obesity.
“These data indicate that BF% appears to be a strong cue for attractiveness and that the impact of WHR and BMI on attractiveness is dependent, in part, on BF%. The appearance of body fat may provide disruption in the visual cues of both shape and size of the female body, potentially impacting behavior.”
Speciation is determined by biological compatibility in sum. This includes many factors. On none I have seen do Asian-White hybrids succeed over their parental groups’ averages; even IQ gains, if true, would be worse for the individual’s own fertility rate.
The only other thing I could think of is a study on STD rates between couples.
https://www.ncbi.nlm.nih.gov/pubmed/2117964 http://sti.bmj.com/content/87/Suppl_2/ii14 http://www.expat.or.id/medical/stds.html
“The association between travel and STDs has been known for centuries”
What’s the Asian version of burn the coal? Pick the chopstick, get ripped? http://global-disease-burden.healthgrove.com/l/24974/Syphilis-in-Southeast-Asia Prevalance: “fairly common.”
The wages of sin. You can’t blame the white man. https://link.springer.com/article/10.1007/BF02438113 Syphilis present in Asian archaeological samples. http://www.scmp.com/news/asia/east-asia/article/2060294/young-women-among-sufferers-japan-records-huge-spike-syphilis
“Endemic syphilis” https://emedicine.medscape.com/article/1952297-overview http://sti.bmj.com/content/76/6/415
‘referred to as “the intraracial network effect,”’
Oh, that’s why they don’t study it.
“suggest that assortative mixing prevents the spread of STI to other subpopulations.”
“A number of studies in the literature, many of which did not measure biomedical markers of STI, suggest that mixing across subpopulations may contribute to spread of STI in the population, particularly across subpopulations.”
If you increase the microbe’s exposure to different parts of the human genome, it will evolve faster. Simple?
Age groups can be a larger factor, since the older immune system is weak and better for the microbe.
“In a recent study conducted in Seattle we found that most of the disease burden for gonococcal and chlamydial infections in both high prevalence and low prevalence subpopulations was attributable to mixing within the subpopulations”
I think we’ve found the reason white women mix out the least. Same reason we don’t like to eat meat raw – to avoid disease.
‘the proportion of infection attributable to indirect mixing, or so called “bridge populations,”
So it is attributable and naturally must inform sexual behaviour.
“While we found that sexual mixing between particular racial ethnic subpopulations increased the risk of STI significantly, the proportion of the population engaging in sexual mixing, and the numbers of sex partners reported by individuals engaging in sexual mixing across racial-ethnic subpopulations were too low for this increased risk to play a major part in disease burden.”
Hybrid vigour, guys!
The risk isn’t the major part, it’s fine! Water’s fine!
“The literature on racial-ethnic differentials in STI rates and the role of racial ethnic mixing on the spread of STI is emergent; many questions still remain unanswered.”
If miscegenation were unhealthy, we’d know, right?
37 is the age when maternal age starts to matter for women (depending on family history) if you look at the shift in gradient on the charts (barely any change before) but 40 is the huge risk age in both men and women, as in this study. “However, the increase in risk was much greater for couples composed of a woman aged ≥35 years and of a man aged ≥40 years.”
Is Human Reproduction not a prestigious enough journal?
The 37/40 thing: Age and the Risk of Miscarriage
It isn’t sufficiently studied in men but data on paternal age as a factor keeps coming out.
Looks like you can’t just blame the woman again. Takes two to make a baby. “a dramatic rise starting after age 37, with the steepest increase occurring after age 40.” “The man’s age matters too. Having a partner over the age of 40 significantly raises the chances of a miscarriage.” Nature doesn’t like old, mutant sperm either.
“Over half of miscarriages are caused by genetic abnormalities.” It isn’t a bad thing, really.
“On average, a woman in her early 20s will have chromosomal abnormalities in about 17% of her eggs” So that’s a really terrible metric considering humans are human. There is always risk.
It’s worse in men than women, so I’m hardly favouring women by opposing this reductionism.
“And as men age, chromosomal defects and point mutations–changes to a single nucleotide in their DNA–become increasingly common.”
Where minors are raped and studied, they tend not to do well either.
Memorize that chart.
A teenager is as bad (at-risk) as a woman with an additional two decades.
You’re still debating less than one percentage point of difference though. Are you autistic?
It’s an interesting variable but hardly everything.
An IVF study
Note: Again, 37 is the magic number.
“While IVF helps many couples overcome their fertility problems, it largely cannot overcome the age-related increase in genetic abnormalities. Without genetically normal sperm and eggs, a viable pregnancy is impossible.”
“Despite this problem, several studies involving couples discordant for age now paint a clear and consistent picture: older prospective fathers raise the risk of miscarriage by about 25-50%. One study found an a 60% increase in the odds of a miscarriage if the father was over 40. Another found a roughly 25% increase in the risk of miscarriage for fathers over the age of 35.”
I guess the Have it All guys can’t read.
As you can clearly see, getting a teenager up the duff would actually be worse.
All things considered.
There are plenty of studies on this but what’s the point?
They basically show the same thing.
No doubt they’ll try to cherry-pick something else to draw focus back onto Boo Women.
A little more then I’ll give up and hope men who value their health listen.
“Advancing paternal age has been shown to result in subfertility, adverse pregnancy outcomes (miscarriage, late foetal death, preterm delivery, low birth weight), birth defects (cleft lip and palate, congenital heart defects), achondroplasia, osteogenesis imperfect , Apert’s syndrome, schizophrenia, childhood cancer (brain cancer, retinoblastoma, acute lymphoblastic leukaemia) and adult cancer (breast, prostate and nervous system).3 Possible mechanisms for these problems include single gene mutations, autosomal dominant diseases, structural abnormalities in sperm chromosomes (e.g., reciprocal translocations) and multiple genetic / chromosomal defects. DNA damage in sperm of men aged 36 – 57 years was found to be 3 times that of men less than 35 years”
Good luck blaming females for that.
“The present study has demonstrated that the paternal age more than 35 years was an independent risk factor associated with spontaneous first trimester miscarriages. In order to eliminate the effect of maternal age, which is itself a known risk factor, we selected women between the age of 20 – 35 years, as this is considered to be ideal age for child bearing.”
Yes. 20-35 is the ideal range.
The reproductive system needs time to become stable, women take longer to physically mature (completed by the late twenties).
Paternal age is a factor in disease and infertility, independently.
“They recommend counselling of men more than 40 years of age when seeking pregnancy.”
I’m not gloating, my heart goes out to men who waited too long and have to raise, at best, a sickly child. They need to be warned of the risks of waiting just like women do.
“Kleinhaus K et al have studied various age groups and have found father’s age more than 40 years to be significantly associated with spontaneous miscarriage.13 Slama R has also studied age ranges and have found that risk of spontaneous miscarriage showed linear increase in the hazard of spontaneous miscarriage in male age between 20 and 45 years. They also observed that hazard ratio was highest with male age > 45 years compared with 18 – 24 years (HR = 1.87, 95% CI, 1.01 – 3.44).1 Others have used paternal age between 30 to more than 50 years.”
The male system matures before the female, (18, mid-20s). If we’re being nubile about social policy, the wife should be older slightly.
So the ideal female age for motherhood is 20-35, but as we see here, ideal male age for fatherhood is 18-24, up to 30 if we’re pushing it. You’d expect the male age to be earlier since they have more DNA damage over time and shorter lifespans combined with earlier physical maturation.
Freezing sperm doesn’t last by the way. They go off.
“Studies on paternal age and fertility suggest that male biological clock does exist. Similar to women, advancing paternal age results in negative effects on reproductive outcomes.”
“Klonoff-Cohen also found decreasing pregnancy rate with male age. Pregnancy rate was 53% for men less than or equal to 35 years, 35% for 36 – 40 years and 13% for men > 40 years.” Again, 35 seems to be the turning point for male infertility. Almost equal to the female 37 downturn but the male peak is earlier because the (greater) damage is cumulative (see next quote) and gamete production is ongoing.
Why do you oldies wanna marry young unless you’re admitting there’s a deleterious effect to counteract?
In future, more studies will look at differences in the under-35 men, between, say, 18-24, 25-29 and 30-35.
“We postulate from these studies that damage to sperm accumulates over a man’s lifetime. Sperm making cells continue to divide throughout the man’s life, increasing the chances of mutations. Impaired DNA replication and repair mechanisms and increased DNA fragmentation.
DNA damage could also result from reactive oxygen species formed by alcohol, nicotine and drug abuse.”
The wages of sin. “According to Aitken RJ’s study, male genital tract infection can result in DNA damage in male germ cells and therefore, increase the rates of miscarriage.”
Oh look, male chastity was logical.
“CONCLUSION Paternal age more than 35 years was found to be an independent risk factor in spontaneous first trimester miscarriages.”
They haven’t really studied younger in sufficient detail to claim that’s fine though, findings like those mentioned above show <30 is ideal in both sexes, to start.
“In this Opinion piece we argue that the tendency of sexually transmitted infections (STIs) to cause infertility is likely to reflect an evolutionary adaptation of the pathogens. We use an evolutionary perspective to understand how STI pathogens may benefit from reducing fertility in the host and what clues the mechanisms of pathogenesis can offer to the evolution of this ability. While we concentrate on human infections, we will also briefly discuss the broader context of STI-induced infertility in other species.
STIs are a common cause of human infertility worldwide…”
No, men can’t sow any wild oats.
No such thing.
“Reduced fertility and an increased risk of complications during and following pregnancy both contribute to reduced reproductive success in the host—and may benefit the sexually transmitted pathogen by destabilizing partnerships and increasing promiscuity.”
The microbes in your urethra are thinking for you.
Not even your dick.
This does explain gay culture. Wow, gay germ theory gets everywhere. This also explains their fetish for fluids and pozzing parties. At least they’re somewhat aware of it.
“Not only are highly promiscuous individuals exposed to a higher risk of acquiring STIs, but STIs may also actively generate hubs of transmission in a vicious circle of promiscuity and infertility: in traditional societies,”
It’s anti-natal and terrible for society.
You can’t leave behind a life of sin.
Also liberal fertility rates make a lot more sense right about now. It is a bug, and it is a feature!
“Writing in the journal Nature Communications, Bauch and his colleague Richard McElreath from the Max Planck Institute for Evolutionary Anthropology in Germany, describe how they built a computer model to explore how bacterial sexually transmitted infections such as chlamydia, gonorrhea and syphilis that can cause infertility, affected populations of different sizes. The authors considered both small hunter gatherer-like populations of around 30 individuals and large agricultural-like populations of up to 300 individuals, running 2,000 simulations for each that covered a period of 30,000 years.
In small polygynous communities, the researchers found that outbreaks of such STIs were short-lived, allowing the polygynous population to bounce back. With their offspring outnumbering those from monogamous individuals, polygyny remained the primary modus operandi.
[coughs in r-selection]
But when the team looked at the impact of STIs on larger polygynous societies, they found a very different effect. Instead of clearing quickly, diseases such as chlamydia and gonorrhea became endemic. As a result, the population plummeted and monogamists, who did not have multiple partners, became top dog.
[hums in Malthusian tones]
The team also found that while monogamists who didn’t ‘punish’ polygyny could gain a temporary foothold, it was monogamists that ‘punished’ polygyny – often at their own expense of resources – that were the most successful.
[religion is evolutionally fit]
[K-types FTW and for discrimination based on self-protection]
While the form of such punishments were not specified in the model, Bauch suggests fines or social ostracisation among the possible penalties.
[stop paying for their babies and STD treatments? FIRSTLY?]
[kinda like how prison was meant to keep you from breeding – a genetic death penalty – until you dummies invented welfare for their women and conjugal rights, making the whole thing useless]
The results, they say, reveal that STIs could have played a role in the development of socially imposed monogamy that coincided with the rise of large communities that revolved around agriculture.”
Well, he had to get published I suppose.
The social/cultural clearly comes after the rest. Like, the die-offs?
Pre-birth, failed by miscarriage. Many go this way.
Birth itself to infancy. Many went by malnutrition, starvation, abuse, maladaptive development or illness.
Reproduction. Nowadays, this tends to be how people go. Better written up as genetic suicide, when intentional.
Parental age (both genetic contributors) does affect risk, yes, but genetics research does NOT want to EVER acknowledge the varying benchmark of genetic quality to begin with. There are teenagers who miscarry for this reason or produce children with defects, the risk is always there with every conception that the conception event goes awry, it’s simple maths. The possibility is always there.
It really goes by family. If the people in your family could be first-time parents successfully in their 30s/40s, you’re fine, the overall genetic quality level is good.