and their r-select offspring, too, if they have them. Quantity over quality doesn’t work in the long run, see, so don’t worry about immigrants that much. Low fitness cannot win, long-term.
Mother Nature culls bachelors.
Slight repost for SEO. Nature, this year.
Impact of genetic risk score on the association between male childlessness and cardiovascular disease and mortality
Men need purpose of family or wither away. Believe no copes.
Childless men are reported to have a higher risk of cardiovascular disease (CVD) and mortality. Information on inherited genetic risk for CVD has improved the predictive models. Presuming that childlessness is a proxy of infertility we aimed to investigate if childless men inherit more often genetic traits for CVD and if combining genetic and parenthood information improves predictive models for CVD morbidity and mortality. Data was sourced from a large prospective population-based cohort where genetic risk score (GRS) was calculated using two sets of either 27 (GRS 27) or 50 (GRS 50) single nucleotide polymorphisms (SNPs) previously found to be associated with CVD. Part of the participants (n = 2572 men) were randomly assigned to a sub-cohort with focus on CVD which served as an exploratory cohort. The obtained statistically significant results were tested in the remaining (confirmatory) part of the cohort (n = 9548 men). GRS distribution did not differ between childless men and fathers (p-values for interaction between 0.29 and 0.76). However, when using fathers with low GRS as reference high GRS was a strong predictor for CVD mortality, the HR (95% CI) increasing from 1.92 (1.10–3.36) for GRS 50 and 1.54 (0.87–2.75) for GRS 27 in fathers to 3.12 (1.39–7.04) for GRS50 and 3.73 (1.75–7.99) for GRS27 in childless men. The confirmatory analysis showed similar trend. Algorithms including paternal information and GRS were more predictive for CVD mortality at 5 and 10 years follow-ups when compared to algorithms including GRS only (AUC 0.88 (95% CI 0.84–0.92) and 0.86 (95% CI 0.84–0.90), and, AUC 0.81 (95% CI 0.75–0.87) and 0.78 (95% CI 0.73–0.82), respectively). Combining information on parental status and GRS for CVD may improve the predictive power of risk algorithms in middle-aged men. Childless men and those with severe infertility problem may be an important target group for prevention of CVD.
The Wall literally kills men. It’s undeniable. The MGTOW types are an anti-natal death cult as much as SJWs, except spinsters live longer, actually.
There is no accounting for this but genetics, as we see in the premature mortality of children if they do have them.
Risk of childhood mortality in family members of men with poor semen quality
Men who wait until post–Wall to have kids, tend to have dead kids. It isn’t just paternal age, it’s poor genetic quality or fitness.
Stop lying to men about this, they don’t have immortal sperm. No such thing. Don’t tell them to leave it too late while you hock them playa e-books.
So the kids they do manage to have will die early, this is also seen among the mixed with rare genetic conditions.
What is known already: Semen quality is an established predictor of men’s somatic health. We can gain a better understanding of possible genetic or environmental determinants of the infertility phenotype by exploring familial aggregation of childhood mortality in relatives of men with poor semen quality.
Get rekt, you’re already dead. So are your r-type kids.
This is why r-types evolved to have children as early as humanly possible, and as often. The high quality K strategy is genetically barred from them, no wonder they hate happy families, it’s like fat women hating thin ones. The kids don’t live long enough to act like a K, long-term. This is why fake Ks make me laugh and largely don’t concern me. You can’t cheat your own inferior genetic quality. Go ahead, have expensive medical bills for likely retarded or mentally ill kids, that will die before you get grandkids. See if I care.
The Lord works in mysterious ways. Or maybe you aren’t listening to Him.
The sins of the father…..
“You say, ‘God stores away a man’s iniquity for his sons.’
Let God repay him so that he may know it.
“Prepare for his sons a place of slaughter
Because of the iniquity of their fathers.
They must not arise and take possession of the earth
And fill the face of the world with cities.”
Sounds like early mortality to me!
There are many studies on weak sperm and premature mortality in men, I’m surprised really. Nature has the gold standard one because I know they’ll try to cherrypick around it.
They never discuss real redpills like this, do they?
If something cut a childless woman’s lifespan in HALF, you’d be sure they’d talk about it.
Men are, at best, dying of a broken heart in the mid-30s, early-40s because they have no family, and you hear crickets from the con artists who don’t really care about men, only wish to profiteer from them.
It directly contradicts their pure copium that ALL men have magical sexy singleton 30s (as K-type high fitness men might exclusively*), despite going outside, touching some grass and seeing how many let themselves go into grotesque swamp monsters. It isn’t just the women. Speaking to some Americans, I attributed a full decade or two onto their claimed age. I don’t think they were lying. The GMO carbs and booze age them like shit. The diabeetus fairy sprinkles them with powdered sugar.
*but Ks don’t sleep around, so it’s redundant to be hot. Rs want to be Ks so badly but slut genes lose.
CVD is the leading cause of morbidity and mortality in the US as well as in the European Union to a cost of hundreds of billion €, and responsible for 400,000 annual US deaths and 1.8 million EU deaths11,12,13. Therefore, improving CVD risk prediction and prevention is an important public health goal and is embedded in the Action Plan for the Prevention and Control of Non-Communicable Diseases in the WHO European Region for the time period 2016 to 202514.
This risk was most pronounced in childless men with high genetic risk scores having up to more than three times increased risk of CVD mortality, as compared to fathers with low GRS. Furthermore, we showed that adding information on paternal status to the GRS-based risk algorithm increases the predictive power for CVD mortality during 5- and 10-years follow-up.
Previously, by using data from a prospective cohort of 22,000 men with long follow-up from the same urban population, we were able to show that childlessness can be regarded as an independent risk marker for CVD along with other well-known risk factors2, an association previously reported by other authors4,26,27,28. In the current study we used a similar cohort from the same region of southern Sweden which provided genetic data and was specifically designed to study CVD risk. We were able to show the same effect of paternal status on CVD mortality estimates as previously published2. To the best of our knowledge this is the first study which evaluates the impact of established genetic risk scores for CVD on the association between parental status and the risk of CAD and CVD mortality.
Family size can be directly linked to the male fertility status29 and therefore male infertility is most likely overrepresented among childless men. Similarly, increased mortality and morbidity risk have been associated with impaired semen quality2 suggesting biological factors related to fertility to also play an important role for the risk of adverse health events in those men—association already established for women30.
The hypothesis of shared genetic traits for CVD and male infertility is based on the model proposed by Skakkebaek et al.18. It suggests a common mechanism, involving a combination of prenatal life exposures and adverse genetic factors to affect the future health of male fetuses making them more prone to develop subfertility as well as various diseases in adult life and to have shorter life span16,17,18,19. The mechanism suggests a primary testicular dysfunction including low testosterone—hypogonadism—as a possible mediator for the aforementioned risks31,32. Since up to 15% of the genome is directly involved in the physiology of reproduction16, disruption of non-reproductive, including metabolic, pathways likely impacts reproductive function and vice versa. However, the lack of interaction between parental status and inherited genetic risk for CVD reported by us suggests independent mechanisms when using childlessness as proxy for infertility.
Our study has several strengths but also some limitations. Comprehensive information from Swedish national registries allows for precise information on date and cause of death, emigration, disease diagnosis and represents men from all socioeconomic backgrounds. The meticulous data collection at baseline provides an opportunity to adjust for a large number of well-known risk factors for CVD. Furthermore, the genetic scores used in the analysis were previously verified as a risk factor using data from more than 55,000 individuals15, thus making it a reliable factor in risk estimation.
The robustness of our findings is underlined by confirmation of the findings based on MDC-CVC sub-cohort in the analysis of data from the remaining MDC subjects. In the latter analysis some additional GRS 27 subgroups showed statistically significantly increased CAD HRs, probably due to larger sample size.
therefore the risk of our cohort to reflect voluntary childlessness is low.
TLDR: Genetic r.
Solution? Simple. Compel hot people to breed like military service and ban the ugly.