Explains the singleton cults of SJWs and MGTOWs.
“No one should be married ever, that’s evil oppression!”
Explains the baby cult of crazy married people.
“No one should be single ever, they’re just depressed!”
Explains the singleton cults of SJWs and MGTOWs.
“No one should be married ever, that’s evil oppression!”
Explains the baby cult of crazy married people.
“No one should be single ever, they’re just depressed!”
Totally normal and biological. Evolution is amazing.
(Oxytocin also promotes patriotism, for those paying attention).
The low IQ Americans: MUH ANCESTORS
-died. Mostly died. STFU with the snowflaking outrage.
Although the human germline mutation rate is higher than that in any other well-studied species, the rate is not exceptional once the effective genome size and effective population size are taken into consideration. Human somatic mutation rates are substantially elevated above those in the germline, but this is also seen in other species.
What is exceptional about humans is the recent detachment from the challenges of the natural environment and the ability to modify phenotypic traits in ways that mitigate the fitness effects of mutations, e.g., precision and personalized medicine. This results in a relaxation of selection against mildly deleterious mutations, including those magnifying the mutation rate itself.
Actually, it’s anti-selection aka dysgenics. There is always a pressure in some direction, read Darwin?
You can’t have dystopia without dysgenics. That’s all a dystopia is.
The long-term consequence of such effects is an expected genetic deterioration in the baseline human condition,
By race and subrace.
potentially measurable on the timescale of a few generations in westernized societies,
Technically you only need one truly fuck-up generation (say Boomers) to install those social policies up to 3 (living memory). This is without external group effects i.e. invasion on a genetic level, rape. So it isn’t fair to say immigration caused this, it compounds it severely. The Boomers and their outsized ingroup-gene infanticide will go down in history as mass murderers, if there’s anyone left.
and because the brain is a particularly large mutational target, this is of particular concern. Ultimately, the price will have to be covered by further investment in various forms of medical intervention.
Medicine isn’t magic. It cannot do that. We already cannot afford the current population with the present and dwindling useful tax base, let alone Japan levels of old coots living to infinity and China levels of population size.
You can’t fuck your way out of this, r-types. You can’t immigrate it either, those new entries have a lower IQ, higher overall group fertility and represent a smaller usable tax base. Debt doesn’t exist to cover this medical cost, even digital money typing. You can’t even type your way out of it. Hyperinflation would occur first, long before actually. Try running the numbers, see if you’re as smart as me. The cost of quality food is the anchor point. Of all living expenses, that one actually keeps you alive?
Don’t become a doctor, kids. Medicine bubble, heard it here first.
Hell, NHS GPs are already quitting now. Retention will only get worse. The ones who stay have lower IQ and can’t find gainful employment anywhere else. This is how socialism degrades infrastructure, the first generation the NHS seemed fine but the second, it attracted parasites to become GPs for the money and by the third, the original talented ones (by private sector standards) had retired and died, leaving training downhill from there.
Other people have explained that before. That one isn’t me.
Resolving the uncertainties of the magnitude and timescale of these effects will require the establishment of stable, standardized, multigenerational measurement procedures for various human traits.
Measurement? We’re lower IQ than ingroup Victorian ancestors by reaction time.
No relevant barriers to entry? Say, for breeding? At least on state funding?
Shows what they think of the producers, dunnit?
Leave the leech alone! The parasites are fine!
Yeah wait a few generations, maybe a century and hope the metrics are correctly chosen to matter!
Long after the researchers are dead so you can’t kill them for being wrong.
This is Idiocracy, even academia is full of nitwits.
We used to have a breeding license, it’s called a marriage certificate.
Below a certain IQ, you can’t actually consent to get married or breed. Maybe study that first?
No, that would be both logical and responsible.
See, I don’t just sit here bitching. I have solutions but nobody listens.
nb Historians and real scientists say European, liars typically say Caucasian.
For example, among European populations in the year 1600 AD the average individual had around a 25-40 % chance of dying in infancy, a 50 % chance of dying during childhood (Volk and Atkinson 2008), and only around a 40 % chance of fully participating in reproduction (Rühli and Henneberg 2013). The average family size was close to five in 1600s England (Arkell & Whiteman, 1998) -given the high rates of pre- term, infant, and child mortality, the numbers ever conceived would likely have been considerably higher. These historical Western infant and child mortality statistics are similar to those observed in contemporary hunter-gatherer populations (Volk and Atkinson 2008)
I’ll list the maths since there’s always that one idiot who “disagrees”.
Of those born, low ball:
100 – 25% = 75
75 – 50% = 37.5
37.5 – 40% = 15
15 of 100 births eventually reproduced, at best.
Your ancestors in 1600 weren’t entitled to breed either. STFU, stupid sections of America.
Natural selection is important.
RITES OF PASSAGE. TOUGH ONES.
Assuming you aren’t tradlarping?
Bear in mind, that wasn’t sex-specific and those estimates are the population i.e. they have to breed with one another.*
Less conservative estimate:
100 – 40% = 60
60 – 50% = 30
30 – 40% = 12
12 of 100 births eventually reproduced, by academic estimate. The more realistic one.
Again, stop being so entitled. Considering the odds, five kids average is actually pretty low.
The entitled brats, appealing to a tradition that’s totally ignorant and imaginary, are the spiteful mutants. In any other time period, you’d probably be dead by now. Male infant mortality is higher than female overall for humans, which hasn’t been factored in.
And WWs 1 and 2 culled the bravest genes of that millennia selection by machine gun and sniper.
At least the bankers made mo- wait, they’ve already “run out” of fake money. Less than a century later.
What was it all for?
or 7.5/100 births eventually reproduced as a couple TOPS
down to, more reasonably
6% of MEN* (or women, maybe**) compared to the grandfather’s generation.
[Father 50% reproduction as male, Grandfather 100% comparison, since all grandfathers would have bred logically.]
or 6/100 births from the total population, coupled.
Assuming 50/50 male/female birth split and flat survival, which doesn’t exist.**
Since breeding requires TWO people, America.
3 generations tops, with a 6% male survival in 1600 Europe.
BE CAREFUL WHAT YOU WISH FOR.
This doesn’t further subdivide by health, wealth, religion or attractiveness.
If one surviving guy in that 100 births total was infertile or refused marriage, you can kinda see why it was a big deal.
This is why inheritance was always conditional on religion, approved choice of spouse and vitally, children.
If the Boomers wanna do some good, write into your will your kids get nothing unless actively Christian, married, with at least one child with a spouse you approve of. They won’t do it. They’ll complain about no grandkids though. That never gets old.
Social Epistasis Amplifies the Fitness Costs of Deleterious Mutations, Engendering Rapid Fitness Decline Among Modernized Populations
Deleterious mutations are typically understood exclusively in terms of their harmful effects on carrier organisms. But there are convincing reasons to think that such adverse effects are not confined to the individual level. We argue that in social species, interorganismal gene-gene interactions, which in previous literatures have been termed social epistasis, allow genomes carrying deleterious mutations to reduce via group-level pleiotropy the fitness of others, including noncarriers.
Personally I think that’s nature’s IQ test, but go on.
(If you can be talked out of your instincts, you don’t deserve to breed).
This fitness reduction occurs by way of degradation of group-level processes that optimize the reproductive ecology of a population for intergroup competition through, among other mechanisms, suppression of free-riding.
If you can be talked out of it by people who hate you…
Such damage to group regulatory processes suggests a hidden role for the accumulation of behavior-altering “spiteful” mutations in the dynamics of the demographic transition—these mutations may have contributed to the maladaptive outcomes of this process, such as widespread subreplacement fertility.
Hmm. Not really. Multi-factorial.
A structured population model is presented describing aspects of this social epistasis amplification model. This phenomenon is also considered as a potential explanation for the results of Calhoun’s mouse utopia experiments, which provide an opportunity to directly test a major prediction stemming from the model.
Discouraging breeding is spiteful mutant if the host does it themselves, particularly from their own inability (no mate) rather than true choice. Picture all the women running round babying tranny feels.
If not, could be eugenic if encouraging the unfit only to abstain OR environmental, as desire for a family drops for group survival temporarily based on crime level and as high trust society becomes low trust; although GDP is an important consideration, for men as provider, moreso than women.
There’s also a connection to solar cycles and crops/food availability. Nobody’s sure if white people can sense it. Needs a study. But birth rate is tracked quite well to solar cycle, if you look.
Is There a g Factor for Fitness?
Fitness Decline under Relaxed Selection in Captive Populations
Mini post. Kinda. Why is Benedict Cumberbatch so ugly?
No really. If we’re doing red pill observations, humour me.
I mentioned before about old world superstitions forgotten in recent years.
As recently as my parent’s generation, they considered ugly children the product of sin, that God was punishing their parents for their sin. You can still find this info around if you look but they rarely dive into it.
You could say it’s about STDs but back then people rarely travelled and slept around enough to frequently catch them. The modern microbiome of the slut is more taxed. So what?
Back to the school mocking. If a child had always married parents but became ugly in the teens, questions would be asked openly and they would get teased about whether one or both parents had ever cheated. This is where we get the term bastard. It isn’t actually about bastards, it’s about ugliness. The ugliness of parental deceit.
You can pretty much tell when there’s a birth defect in a baby, the eyes look dull if it’s mental. It’s a known indicator of fatal defects.
2015 Birth Defects in the Newborn Population: Race and Ethnicity
Overall birth defect prevalence was 29.2 per 1000 in a cohort of 1,048,252 live births, of which 51% were Caucasians.
Full white or mongrelised? Let’s assume pureblood despite America (mixed white, mostly). American whites are on average less attractive as white blended than single nation counterparts, even living in America. Models tend to come from homogeneous national areas, (i.e. subrace) a finding that is known to apply to white settlers in Brazil to this day, they send scouts. Specifically.
Compared with Caucasians, the risk of overall birth defects was lower in African–Americans (relative risk = 0.9, confidence interval 0.8–0.9) and Hispanics (relative risk = 0.9, confidence interval 0.8–0.9).
Failure to consider abortions for “no” reason or gender as defective. Selection bias. A lot of those already had abortions because they’re high abortion groups!
The risk of overall birth defects was similar in Caucasians and Asians. Relative to the Caucasians, African–Americans had a lower risk of cardiac, genitourinary, and craniofacial malformations but a higher risk of musculoskeletal malformations. Hispanics had a lower risk of genitourinary and gastrointestinal malformation. Asians had a higher risk of craniofacial and musculoskeletal malformations.
Didn’t control for proportion in the population, then non-whites are way ahead.
Craniofacial = ugly.
Musculoskeletal = ugly. Well, dumpy.
Unless you’re going to argue a big is beautiful for literal birth defects?
And “similar” isn’t same. It isn’t statistical. This is like IVF success studies again (see below).
Why did some old world men witness the birth? All babies look like those reddish potatoes, it can’t be a resemblance. You can tell a resemblance to one parent over another by middle childhood to puberty.
We’re told that it’s about adultery and it might be true if you suspect a man with certain features e.g. skin colour, an extra finger.
Yet, what can you tell at birth? Ugliness.
Whether or not the man in question remembers that reason.
Cinderella effect also applies to genetic but ugly kids (lookism, it’s aka). The parents reject them, even if one genetically caused their fug.
Take Cumberbatch, product of a union involving adultery.
Fugly. Nice voice, but his father is the looker. Mother is a looker too. The issue cannot be genetic.
Some superstitions have a basis in fact.
Why did old ladies peer into a pram to judge the ugliness of the babe?
To see if you’re a SINNER!
[inc Thou shalt not adulterate]
Picking on an ugly white guy wouldn’t be totally kosher. I have other evidence.
We’re looking for spiteful mutants.
Now the post gets huge.
To more data, ever more data, smother the liars in data:
“Please may I request the following information, records and documentation under the Freedom of Information Act:
Information in regard to people of mixed race parentage- often called ‘white and black Caribbean’, ‘white and black African’, ‘white and Asian’, ‘other mixed’- being at increased risk of being born with a birth defect, stillborn, or of suffering from fertility problems in their adult lives, which is related to their mixed race parentage
Information regarding NHS policy and practice on the advising of interracial couples, who are prospective parents, about the increased risk of their child being born with a birth defect, stillborn, or infertile in adult life, which would be connected to their, the child’s, mixed race parentage
Please may I also request statistical information and records which display the following:
The percentage of overall cases of babies born with a birth defect, which is attributable to each ethnic group
The percentage of overall cases of babies still born, which is attributable to each ethnic group
The percentage of overall cases of infertility, which is attributable to each ethnic group
The percentage of overall births, which is attributable to each ethnic group”
“In Tables 8 and 10, mixed race is included in a single category of Mixed, Chinese and any other ethnic group. This is because the numbers in these groups are sufficiently low to risk being disclosive, and follows agreed statistical guidelines.
a) being born with a birth defect – this information is shown in Table 10.
b) being still born – this information is not published. However, you could request a special extract (further details of how to do this are explained below).
c) we do not hold any information on infertility, and are therefore not able to answer your question about adults suffering from fertility problems, connected to their mixed race parentage.”
Do not hold information my lily-white arse.
“Page does not exist”.
“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
Mixed, Chinese and any other group, 44%;
For a majority, that’s incredibly low.
and those where ethnicity was
not stated, 49%).
For the Asian group, the most common cause was congenital anomalies (41%). A higher incidence of congenital anomalies in Asian populations is well-documented (Gray et al. 2009).”
“Low birthweight and prematurity are both measures of fetal development. Another measure is the baby’s size in relation to its gestational age. Babies whose birthweight lies below the tenth percentile for their gestational age are known as ‘small for gestational age’ (SGA).
Not all babies who are SGA have a pathological growth restriction; they may just be constitutionally small.
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.
Over one whole standard deviation below. According to the likes of Peterson, useless to a Western economy. The average Bangladeshi.
Recall regression to the mean. Also, friendliness correlates more to low IQ. Do not be fooled.
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
Black SGA: 9.2 and 12.3%.
Bangladeshi, Indian, Pakistani only SGA: 17%, 16.3%, 14.2%.
White SGA: 7.2%, 6.2%.
ALL SGA average: 8.2%.
Pre-term neonatal deaths
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
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
All others^1: 102.
That’s 11.4% from a tiny group of mixed.
Table 10 screen-capped, do your own charts.
Related studies, I do have a point about measurement error.
2009 Fertility by ethnic and religious groups in the UK, trends in a multi-cultural context
Asian tsunami in USA too
From one of the links, can’t find which. Calm down. Either they’re abstaining from having kids once here, infertile, the neonate dies or it’s retarded. Being here is actually a curse since they’re held to the standards and economy of a higher IQ nation. They’re voter birds here for a season or tax chattel and they’ll leave when it’s convenient to.
“How a patient’s ethnic background affects her chance of pregnancy, especially with IVF, is a fascinating yet poorly studied area of research. According to a 1995 national survey of family growth, non-Caucasian married women were more likely to experience infertility than Caucasian married women, yet these same non-Caucasian women were less likely to receive any type of infertility treatment—especially treatment with assisted reproductive technologies.
There is very little data in the literature examining ethnicity and its affect upon pregnancy rates with in vitro fertilization (IVF). Ethnic minorities compose a small percentage of patients in the nation’s IVF programs, making it relatively difficult to examine how they respond to various infertility treatments. In the few studies that have examined the affect of ethnicity on IVF pregnancy rates, differing outcomes have been found.
There have been only a few studies specifically comparing IVF success rates between African Americans and Caucasians. The results of two of these studies contradict each other, with one showing that African Americans had decreased pregnancy rates with IVF as compared to Caucasians, and the other finding no difference in pregnancy outcomes with IVF between these two ethnic groups.
Likewise, there are only a few studies directly comparing IVF pregnancy outcomes between Indians and Caucasians. One shows a trend towards decreased pregnancy rates in Indian women and finds that Indian women were significantly more likely to have their cycle cancelled as compared to Caucasian women. In comparison, another study found no significant difference in IVF pregnancy rates between Indians and Caucasians. A more recent study has shown that Asian ethnicity was an independent predictor of poor outcome with IVF. There have been no studies examining IVF pregnancy outcomes in Hispanics in comparison to any other ethnic groups.
We’ll see why.
When I was in training, I published the first study comparing IVF outcomes among multiple ethnic groups. It was a retrospective study utilizing a data set that was the result of the collaboration between three IVF centers in the Boston area: Boston IVF, Brigham and Women’s Hospital IVF Center, and Reproductive Science Center.
We retrospectively reviewed the cycles of 1,135 women undergoing IVF between 1994 and 1998. Only the first IVF cycle for each couple was reviewed. Ethnicity was self-reported. Women who categorized themselves as having a mixed ethnic background were excluded.
Seriously. Measurement bias much?
….In order to better understand how ethnicity affects IVF outcome, it will be necessary to study a larger number of minority patients. In these studies, it is important that all ethnicities be included. If racial differences do exist, IVF treatment protocols could be adjusted to improve the success rates for patients of all ethnic backgrounds. Therefore, further exploration in this area is necessary and very important.”
We did that.
“After adjusting for certain factors including the age of the patient at time of treatment, cause of female or male infertility, and type of treatment (ICSI vs IVF), the study found that White Irish, South Asian Indian, South Asian Bangladeshi, South Asian Pakistani, Black African, and Other Asian women had a significantly lower odds of a live birth than White British women. For example, the live birth rate for White British women was 26.4% compared to 17.2% for White Irish women and 17.4% for Black African women.
The study also found that some groups of women including South Asian Bangladeshi, Black African, Middle Eastern, have a significantly lower number of eggs collected than White British women.
Moreover, South Asian Indian, South Asian Bangladeshi, South Asian Pakistani, Black British, Black African, Black Caribbean and Middle Eastern women were at a higher risk of not reaching the embryo transfer stage.
The paper explores the possible reasons behind the variation and states that while genetic background could be a potential determinant of egg and sperm quality, variation in environmental exposures relating to lifestyle, dietary factors, socio-economic and cultural factors could be influencing egg and sperm quality, accessibility of fertility treatment and behaviour towards seeking medical care and consequently reproductive outcomes.
No, they were living in the same place. Muh Magic Dirt.
Genetics is the ONLY difference now.
You have NOTHING.
DNA causes germline DNA, really? Maybe?
Furthermore, the increased prevalence of polycystic ovary syndrome (PCOS) in South Asian women may have an impact on egg quality and lower implantation rates.
Shit tier WHR tipped us off on that one, see end.
Dr Kanna Jayaprakasan, Consultant subspecialist in Reproductive Medicine, Derby Fertility Unit, Royal Derby Hospital; Honorary Associate Professor in Gynaecology, University of Nottingham and senior author of the paper, said:
“The data suggests that ethnicity is a major independent factor determining the chances of IVF or ICSI treatment success.
“While the reason for this association is difficult to explain, the potential factors could be the observed differences in cause of infertility, ovarian response, fertilisation rates and implantation rates, which are all independent predictors of IVF success.
“The main strengths of the study are the use of the UK HFEA national database which includes a large number of women treated in all UK units. However, the numbers in some of the sub-ethnic minorities, such as Bangladeshi women, were low in the study.”
Professor Adam Balen, spokesperson for the Royal College of Obstetricians and Gynaecologists (RCOG) and Chair of the British Fertility Society (BFS) said:
“Infertility affects 10-15% of the population and more people are seeking fertility treatment.
“This interesting study looking at maternal ethnicity provides useful data based on a large number of women undergoing fertility treatment. The reasons behind the variation need to be looked at in more detail but in the future could potentially help improve success rates amongst all groups of women.”
“Black and South Asian women were found to have lower live birth rates compared with White women”
“Black and South Asian women seem to have the poorest outcome, which is not explained by the commonly known confounders. Future research needs to investigate the possible explanations for this difference and improve IVF outcome for all women.”
Almost like Anglo women evolved to breed in the Anglo climate?
The Ice Age killed the boyish ones.
“Variation in risk factors and outcomes was found in infants of White mothers by paternal race/ethnicity.”
I wonder which way.
Inbreeding or outbreeding depression?
“Status exchange hypothesizes that in a marriage market framework, minority men marry less-desired White women (e.g., of lower education) in exchange for higher social status. The second hypothesis, in-group preference, simply suggests that people prefer members from their own group, and thus, intermarriage is the less desirable scenario.”
Dudebros like “where’s da studies?”
I’m like “Have you even looked?”
“Together they found that mixed-race couples differed significantly with respect to their sociodemographic characteristics from the endogamous couples. After control for those variables, biracial infants were found to have worse birth outcomes than infants with 2 White parents but better than infants with 2 Black parents.6,8–12 (Henceforth, infant’s race/ethnicity will be referred to by the notation “maternal race/ethnicity–paternal race/ethnicity” [e.g., White–Black].)”
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.”
“…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.
2012 Biracial couples and adverse birth outcomes: a systematic review and meta-analyses.
“Biracial status of parents was associated with higher risk for adverse pregnancy outcomes than both White parents but lower than both Black parents, with maternal race having a greater influence than paternal race on pregnancy outcomes.”
Evolution is racist or instincts evolved for reasons? Pick ONE.
Your Third World surrogate plan may need retouching.
If it fails or dies or gets retarded, you still gotta pay up! What are the odds?
Why is it so hard to find studies about the most populous race on the planet?
What is associated with IQ and other development issues? Pre-term birth.
“Maternal age, education level, race and ethnicity, smoking during pregnancy, and parity were significant risk factors associated with PTB.”
It’s mentioned along with smoking.
“…The analysis of interactions between maternal characteristics and perinatal health behaviors showed that Asian women have the highest prevalence of PTB in the youngest age group (< 20 years; AOR, 1.40; 95% confidence interval (CI), 1.28-1.54).”
I want more studies about them. I’m not scared of reality.
That suggests a genetic predisposition to be present so young. I’d compare PTB to WHR, personally.
“Pacific Islander, American Indian, and African American women ≥40 years of age had a greater than two-fold increase in the prevalence of PTB compared with women in the 20-24 year age group.”
Their own women.
Pre-term study and IQ:
“RESULTS: Across all assessments, VP/VLBW individuals had significantly lower IQ scores than term-born controls, even when individuals with severe cognitive impairment (n = 69) were excluded. IQ scores were found to be more stable over time for VP/VLBW than term-born individuals, yet differences in stability disappeared when individuals with cognitive impairment were excluded. Adult IQ could be predicted with fair certainty (r > 0.50) from age 20 months onward for the whole VP/VLBW sample (n = 260) and from 6 years onward for term-born individuals (n = 229).
CONCLUSIONS: VP/VLBW individuals more often suffer from cognitive problems across childhood into adulthood and these problems are relatively stable from early childhood onward. VP/VLBW children’s risk for cognitive problems can be reliably diagnosed at the age of 20 months. These findings provide strong support for the timing of cognitive follow-up at age 2 years to plan special support services for children with cognitive problems.”
So it doesn’t cause but it is associated. Humans evolved long gestation for the brain.
Clear defect evidence in the genes- study it!
But surely, you say, genetic issues would be also hormonal (hormones regulate genes as well) and apply to men?
Yes. Yes it would.
“A total of 9079 patients were reviewed, of which 3956 patients had complete data. Of these, 839 (21.2%) were azoospermic. After adjusting for age, African-Canadians (odds ratio [OR] 1.70; 95% confidence interval [CI] 1.28-2.25) and Asians (1.34; 95% CI 1.11-1.62) were more likely to be azoospermic compared to Caucasians.”
Some of us form opinions AFTER reading.
White men are literally more fertile and most fertile with white women.
“Similarly, African Canadians (OR 1.75; 95% CI 1.33-2.29) were more likely to be oligospermic and Asians (OR 0.82; 95% CI 0.70-0.97) less likely to be oligospermic. Low volume was found in African-Canadian (OR 1.42; 95% CI 1.05-1.91), Asians (OR 1.23; 95% CI 1.01-1.51), and Indo-Canadians (OR 1.47; 95% CI 1.01-2.13). Furthermore, Asians (OR 0.73; 95% CI 0.57-0.93) and Hispanics (OR 0.58; 95% CI 034-0.99) were less likely to have asthenospermia. Asians (OR 0.73; 95% CI 0.57-0.94) and Indo-Canadians (OR 0.58; 95% CI 0.35-0.99) were less likely to have teratozospermia. No differences were seen for vitality. No differences were seen for FSH levels, however, Asians (p<0.01) and Indo-Canadians (p<0.01) were more likely to have lower testosterone.”
It’s always the damn Asians.
Magic Dirt won’t fix your shitty sperm.
Maybe if we spend more on the NHS! The evolution fairy may visit!
The lower sexual dimorphism of Asians makes them functionally partially infertile. This is why they marry so young (it isn’t traditionalism) and despite this, have a low birth count per person, and are the most populous race on Earth. They’re actually the most r-selected, Mother Nature holds them back from fertilization with mutations. Along with r-selection, more total fertility issues in the male/offspring (azoospermia, infant death), lower volume AND lower testosterone, it all fits!
Is that my fault? No. Stop blaming me for reading. I’m not, in fact, God.
Hey, we have our own group with shitty sperm. Theirs is just bigger and more characteristic of the whole.
“AR-CAG repeat length was longer in infertile men in Asian, Caucasian, and mixed races (SMD = 0.25, 95% CI: 0.08-0.43, P <0.01; SMD = 0.13, 95% CI: 0.02-0.25, P <0.05; SMD = 0.39, 95% CI: 0.15-0.63, P <0.01).
Notice p-value difference is so loose for white it doesn’t meet the medical standard? 0.05 is too high. Absurdly.
The overall study shows that increased AR-CAG repeat length was associated with male infertility. The subgroup study on races shows that increased AR-CAG repeat length was associated with male infertility in Asian, Caucasian, and mixed races. Increased AR-CAG repeat length was also associated with azoospermia. This meta-analysis supports that increased androgen receptor CAG length is capable of causing male infertility susceptibility.”
In the interest of intellectual honesty.
We literally have the studies. e.g. It’s metabolic.
“Sixty-four PCOS patients and 40 women served as the control group were studied. The two groups were subdivided according to the body mass index (BMI) into two obese and non-obese groups. Waist:hip ratio (WHR), plasma epinephrine level was estimated, sympathetic skin response (SSR); postural orthostatic tachycardia syndrome, heart rate variability (HRV), and valsalva ratio were measured in both groups.”
“Compared to the control group, obese PCOS patients demonstrated higher BMI and WHR, reduced palmar SSR latency and higher amplitude, altered HRV, higher plasma epinephrine level, and rapid pulse rate. Moreover, non-obese patients show reduced palmar SSR latency and higher amplitude, higher plasma epinephrine level, and higher pulse rate. BMI and WHR of the patients were positively correlated with plasma epinephrine level; while the HRV was negatively correlated WHR.”
“The BMI and WHR were significantly higher in the PCOS patients compared to the control group 36.63±4.23 kg/m2 vs. 34.14±3.39 kg/m2 (p=0.041) and 0.88±0.05 compared to 0.79±0.11 (p=0.001), respectively.”
“We demonstrated high plasma epinephrine level during lying and standing positions in PCOS patients. This could be of obesogenic origin as we noticed a positive correlation between plasma epinephrine level and both of BMI and WHR. PCOS patients of this study exhibited central abdominal obesity and the mechanisms by which central obesity drive an increase in sympathetic activity are not entirely clear. Yet, the fat cells have increased sensitivity to lipolytic agents and/or the factors inducing fat mobilization are turned on (16). This was further supported that adipocytes isolated from the visceral fat depot of women with PCOS had increased catecholamine-stimulated lipolysis (17).”
Nice boy hips. Don’t try for kids. (Goes for all races, Spartans forced girls to be lightly athletic to be ready for childbirth as a woman, that broadens hips beyond racial average).
And when the NHS totally fails, picture the fatal correction to reality when these women expect childbirth interventions. No waist? No taste.
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.
“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.”
Don’t marry the bimbo.
Should also look at spousal IQ disparity.
Presumably, bigger = higher % divorce.
In ‘The Bell Curve: Intelligence and Class Structure in American Life’, Herrnstein and Murray reported a negative relation between intelligence and divorce risks. This article analyses the relationship between intelligence and divorce risks for two different Dutch cohorts, for which data on their intelligence measured during their childhood, are available. A positive relation between intelligence and divorce risk is found for the Dutch fifty-year-olds born around 1940. Among this older cohort, divorced respondents have a higher mean intelligence score than respondents who stayed together with their spouses. However, a negative relation between intelligence and divorce risk is found for the Dutch thirty-year-olds born around 1958. Among this younger cohort, divorced respondents have a lower mean intelligence than respondents who stayed together. A possible explanation of the shift is that the democratisation of divorce over time has altered the nature of divorce from a highly selective to a more normal event.
Or r-types stopped marrying as much, from pressure. Therefore, fewer divorces.