A debate has arisen regarding the validity of racial/ethnic categories for biomedical and genetic research. Some claim ‘no biological basis for race’ while others advocate a ‘race-neutral’ approach, using genetic clustering rather than self-identified ethnicity for human genetic categorization. We provide an epidemiologic perspective on the issue of human categorization in biomedical and genetic research that strongly supports the continued use of self-identified race and ethnicity.
“Instead, we looked at DNA from modern humans belonging to African populations and searched for unusual regions in the genome.” And they were older than modern. Imagine my shock. “What we do know is that the sequences of those forms, even the Neanderthals, are not that different from modern humans,” he said. -BECAUSE THEY THE SAME SPECIES. Sorry, broke into spontaneous ebonics because of the topic. “They have certain characteristics that make them different from modern DNA.” No shit?
Could be better or worse depending on the variant. They refuse to clone Neanderthals because no company could own them (human rights are based on demonstration of human IQ) and they’d be the smartest human on the planet. It would show us all up. I want it to happen. Neanderthals were more civilized than us, we learnt funerary rites from them. Please clone the African ancestors too, see what happens.
“Then we asked ourselves what does the general pattern of variation look like in the DNA that we sequenced in those African populations, and we started to look at regions that looked unusual,” Hammer said. “We discovered three different genetic regions fit the criteria for being archaic DNA still present in the genomes of sub–Saharan Africans. Interestingly, this signature was strongest in populations from central Africa.” I’ll fly high on this one and say no comment.
“We are talking about something that happened between 20,000 and 60,000 years ago – not that long ago in the scheme of things,” Hammer said. “If interbreeding occurs, it’s going to bring in a whole chromosome, and over time, recombination events will chop the chromosome down to smaller pieces. And those pieces will now be found as short, unusual fragments. By looking at how long they are we can get an estimate of how far back the interbreeding event happened.” Outbreeding depression…. it isn’t inter-breeding, it’s out-breeding…. “We think there were probably thousands of interbreeding events,” Hammer said. “It happened relatively extensively and regularly.”
He can’t be saying, they were literally fucking monkeys? No. …No? No. Are they technically humans they were screwing or not? At best, they mixed races. At worst, bestiality. I read a conspiracy that human anatomy is so weird because we’re the result of primates mating with hogs. That’s why pig hearts and such work on us. It was surprisingly detailed and I couldn’t think of anything to counter it.* I am also scared now.
I’m making the odd low/no effort post when I can be asked.
No one has typed out an explanation of this, to my knowledge. Sure there are linguistic essays but… still.
Here’s the logical explanation of certain things. Ending with collaborating science.
Adultery is a sin because it’s a pollution of bloodlines, that’s why it’s called that but the sexual action or compulsion is already covered under the coveting commandment. Fornication between two singles, while a sin, is not polluting the bloodlines of the marital couple. It doesn’t defile the marital bed, as the Bible puts it (Hebrews 13:4). It’s “and” adulterers, they’re discrete categories. The adultery involving one married party may produce a child with defects (especially with the effect of STDs from sleeping around, which they’d bring back to the marital bed, onto their own children – and might kill them), or the child maritally or the one “extra-maritally” may eventually marry their own part-sibling and then produce defect. All the sexual prohibitions are henceforth founded in an avoidance of bloodline corruption.
They’re not being ‘lame’ and killing your ‘buzz’ man, it’s babymaking. Don’t make broken babies!
The sterile view of reproduction is like a Marxist’s view of labour – delusional.
re Deut 23:2 and the mistranslation in later editions: Legitimacy is based on bloodlines more than marital status but under the parent-approved marriage model the former suitability led to the latter ceremony. They’d have veto power on funding the wedding and allowance of inheriting anything should the child try to brattishly insist on an adulterous match. Banishment (disowning) is the parental right should the child “dishonour” (commandment) their parent’s standards. A bastard didn’t refer to unmarried parents back then but moreso what we’d call politely a hybrid, Darwin a mongrel. Later editions mistranslated the concept of ‘bastard’ for ((reasons)). Logically, unmarried parents could feasibly marry at any point in the next 18 years and 9 months, the insult cannot be based on something so easily remedied. Instead it’s “in the blood”, it’s about the “seed”, it’s genetic. It’s the existence of the kid itself which is the affront, the offense to the holy, and that’s why ‘bastard’ is levied at the child – not the parents! They brought shame on their pre-existing family (bloodline) by virtue of their dishonourable existence, of a blemish. The OT often condemns men who mate with ‘foreign women’, the archetype of demonic seductress. That’s why usually understanding God (who forgives individuals) forbade the child to enter the church, holy ground, sacred temples, unto the 10th generation, because it was a perversion of his creation and divine, famous plan for separation of peoples; its existence was Satanic, a testament to playing God. Its existence was an insult to God, directly, it was an ABOMINATION.
Now we have the medical stats to back this up from the individualist perspective, from mental problems to organ death from child cancer, nobody mentions it…? Why? Why not? Who’s behind that cultural ignorance? https://www.kingjamesbibleonline.org/Bible-Verses-About-Race-Mixing/
The sins of the father onto the child i.e. you produce an unnatural thing, it suffers unnaturally.
So bad marital discernment (selection) relates to the reprobate mind. Selection is the ONE job of men looking for a wife. The Bible gives plenty of advice on men seeking a wife, what to look for.
Cast not ye pearls among swine, neither spill your seed, it’s very simple conceptually. Don’t waste a breeding opportunity with a bad match or selfishness. You want societal shame back? Start with masculine self-control (Lev 22:4) because you’ll be healthier for it. This isn’t just spiritually good but physically too. Like don’t stick your dick in crazy. At least a woman’s period isn’t alive for all the stigma, there’s nothing to kill. God designed women to self-clean the baby oven, there’s no shame in it. Poor analogy to the modern Onans. You have a specific story about sexual continence, sexual hygiene, call it whatever, it’s being a man. https://www.openbible.info/topics/spilling_your_seed https://biblereasons.com/evil-women-and-bad-wives/
If you marry badly, that doesn’t absolve you of responsibility for her sins. You’re the man, you’re responsible, be she some Polish whore (they’re mostly marrying Arabs and Japs) or an ABG/LBFM thot (mostly autists).
Prov 22:14 The mouth of an adulterous woman is a deep pit; a man who is under the LORD’s wrath falls into it.
I’m picturing the conceited weebs who start lecturing the rest of us (projection in ego defense of their error) on how white people in the West should become more Asian. You eat the bugs first, bug boy. Such cucking is, as you can see, Biblically predicted as God’s wrath upon the reprobate mind. Insecurity breeds insecurity, misery loves company, fuck-ups want you to copy them.
If everyone fails, the sexual Marxists reason, then nobody fails!
They want no holy (wholesome, pure) group to be able to compare poorly to.
why be envious of people you claim to be doing better than? Why talk about the West at all after you left? Why are you obsessing over it, if it’s inferior culturally? Racial deserters should STFU and stay in their jungle. We don’t want to hear from you, stay gone. There’s a rise in snarky gammas online giving weeb “commentary” that sounds like CCP propaganda. It’s anti-white, sod off. Why should we care what you think? You ran away from the problems, drop them. It’s like a Boomer who retired to France complaining about UK immigration. No Susan. You don’t get to.
Stats show up their forum anecdotes as fantasies. They wanted mixed bloodlines, right, they’ll be happy with the black grandkids I presume (since mixed dates other mixed, statistically).
In Deut 7:3 even the unequal yoking between the races is forbidden, before the prospect of children is mentioned. https://www.biblegateway.com/passage/?search=Deuteronomy%207&version=KJV
Cultures are intended to be sovereign. Interconnection is weakness.
7:4 says how mixed marriages are insults because of cultural cucking i.e. your child will adopt foreign ways.
Learn to tell your kids no, Boomer. JUST SAY NO.
Otherwise, unchecked, they “invent new forms of evil” like the conceited weebs that are becoming the new Fedora Boy.
insolent, arrogant, boastful….
It’s like the Gap Year story that never ends.
And we’re all expected to listen to it.
One word: why?
Do evil, fine, don’t be boastful though. I shouldn’t be socially expected to listen to some woman’s sob story about how she married a Muslim either. Tough tits, bitch. You knew they was a snake. You signed up for shit. It’s like the thots joining Islamic State, I no longer feel loyal to you either. I owe you nothing.
Our results confirm that there are ethnic and racial differences in the incidence of childhood leukaemia. These differences indicate that some genetic and/or environmental/cultural factors are involved in aetiology of childhood leukaemia.
American diet means you should compare to European whites for accuracy. Twinkies are thots, not food groups.
The highest risk of ALL was observed for children with a combination of Hispanic ethnicity and White race compared with non-Hispanic whites (OR=1.27, 95% CI 1.12 to 1.44).
Deny the lies of the spiteful mutants, anti-natalists aren’t so toxic to the zero sum of Darwinian competition. To actively encourage our genocide is evil.
Funny that the cuckservatives slagging off the Boomers want a free pass to act just like them despite decades of data now. That didn’t exist for them. You’re living in the experiment.
And yes, the Boomers should’ve been disowned by their parents for marrying wrong or too often.
They’ll deport, sorry “return” tortoises for their own good – but not humans.
A new study of Chinese-Caucasian, Filipino-Caucasian, Japanese-Caucasian and Vietnamese-Caucasian individuals concludes that biracial Asian Americans are twice as likely as monoracial Asian Americans to be diagnosed with a psychological disorder.
Zane and his co-investigator, UC Davis psychology graduate student Lauren Berger, found that 34 percent of biracial individuals in a national survey had been diagnosed with a psychological disorder, such as anxiety, depression or substance abuse, versus 17 percent of monoracial individuals. The higher rate held up even after the researchers controlled for differences between the groups in age, gender and life stress, among other factors.
1/3. Over a THIRD of them are literally mentally diseased at the intensity to diagnose.
The study included information from 125 biracial Asian Americans from across the U.S., including 55 Filipino-Caucasians, 33 Chinese-Caucasians, 23 Japanese-Caucasians and 14 Vietnamese-Caucasians.
Stop listening to spiteful mutants.
Nobody’s jealous, they’re clinically evil. Shun the reprobate mind.
nb. The edgy anti-natal rhetoric worked on the Boomers first, ask the dead half of Gen X. However, there’s more than one way to skin a cat and clearly more than one way to commit genetic suicide.
The womb is a very sophisticated form of printer. It prints people. That’s why women hate being conflated for one, it’s an appliance. Don’t defile the womb of your people, that’s treason. Do not corrupt the seed.
Plato’s natural slaves, do not follow. Degenerates are compulsive liars e.g.
High levels of infection in these groups are found in most sub-Saharan African and South-East Asian countries. There is a high rate of concurrent infection for HIV and other well known STDs in patients. Rates as high as 70% of HIV infection are found in African patients with STD, whereas the rates are reaching 15–20% in patients with STD in Thailand [9,10].
Ting Tong has HIV. 1 in 5, roll the die to die. Is it really cheaper to live there with pozz med bills?
If you wanna larp as a gay guy, at least do fun things with your prostate.
Over the course the study, Hahm unmasked some myths common about Asian Americans. She said, “There’s a perception that Asian Americans in particular aren’t practicing sexually risky behaviors. But we found that Asian American young women are at risk of high STDs. For instance, Asian American women had a higher prevalence of STDs than White women in both 1995 (10.4% vs. 7.7) and 2001 (13.5% vs. 8.3%). The incidence of STDs (not diagnosed with STDs in 1995, but developed STIs in 2001) among Asian American women was also higher than that of White women.” Moreover, the power dynamic between genders became immediately clear. Asian American women were four times more likely to have a STD than their male counterparts. “This was shocking,” said Hahm, “It was so much higher than the males.” Accounting for the gender disparity, Hahm suggested that…“Asian and Pacific Islander women also have broader interracial dating patterns than Asian American men. This might explain why these women are exposed to higher rates of STDs.”
when you mix, expect an itch
I think these findings definitely go against some prior conceptions about Asian Americans and sexually transmitted diseases. The 4:1 ratio of STDs among Asian American women to men is astounding. To see what this means, I looked up some global data of STD rates around the world, broken down by gender. In East Asia, and on every other continent, women have slightly higher STD rates than men, however nothing comes remotely close to the 4:1 ratio among Asian Americans.
It’s unclear what the study means by “power dynamic,” whether it means sexual power/demand, or power within the culture. One can speculate on a wide variety of reasons for why the STD rates are the way they are. I’ll refrain from doing so, but nevertheless I thought it was noteworthy to bring up, as a point of discussion. How does this strike you?
it means they culturally celebrate and enable whores – like the childbearing geisha
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.”
“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.
https://www.photius.com/rankings/national_iq_scores_country_ranks.html Bangladesh 82
Over one whole standard deviation below. According to the likes of Peterson, useless to a Western economy. The average Bangladeshi. India 82
Recall regression to the mean. Also, friendliness correlates more to low IQ. Do not be fooled. Pakistan 84
Jamaica 71, where we’re picking up new NHS nurses.
Enjoy that decline.
Tables 8 and 10 mentioned in FOI request not listed, have to know it’s there.
Under Downloadable Tables:
“Table 8: Live births, neonatal and infant mortality by ethnic group and gestational age at birth, 2012 birth cohort, England and Wales
Table 10: Infant mortality by ONS cause groups and broad ethnic group, 2012 birth cohort, England and Wales”
For future reference, write your FOI requests as “concern for services provided to BAME women” and “progressive need for up-to-date medical guidance for mixed race couples and the biracial in family planning”.
You have to download the excel, click to tables 8 and 10, then read the footnote of superscript 1 to know to scroll right.
Table 8: All others^1 7.1% under 37wks 9.2% SGA
Black SGA: 9.2 and 12.3%.
Bangladeshi, Indian, Pakistani only SGA: 17%, 16.3%, 14.2%.
White SGA: 7.2%, 6.2%.
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.
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.”
“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?
“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.”
“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?
“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.
“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.”
“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.”
Historically they didn’t exist until recently, in the archaeological record. Recent colonialism also mingled some Euro DNA into Indians to make obvious castes but this isn’t about that, it’s about East Asians specifically and WAY before that.
They’re Mongoloid-Negroid half-breeds.
Literally. They’re the first mixed race.
I’m not kidding. Just East Asians and like I said before, the morphological similarities bear this out.
Stronger jaws, larger head overall in size and lower national IQs, huge lips.
Okay, you argue, but how do we know they actually interbred? And this wasn’t some labeling error or mistake?? Wouldn’t there be modern Africans who look Asian too? Interbreeding goes both ways, after all.
Yes, there would. Again, plenty of morphological similarities.
That’s an African girl.
Tell me there was no inter-breeding.
Asian, just to throw you off. Note the nose.
Large mouth, pronounced raised brow, pronounced nostrils, broad jaw.
The Asian one, large mouth, pronounced nostrils, raised brow, broad jaw.
I saw it before but didn’t realize we had genetic proof.
The broad flat nose with flared nostrils with characteristic dip between the eyes plus forehead bulge ALL pinged to me as African.
The profile is very African, mathematically. In profile many of the blacker ones have a very curved forehead in profile.
To test the hypotheses of modern human origin in East Asia,
because it isn’t ancient, archaeologically
we sampled 12,127 male individuals from 163 populations and typed for three Y chromosome biallelic markers (YAP, M89, and M130). All the individuals carried a mutation at one of the three sites. These three mutations (YAP+, M89T, and M130T) coalesce to another mutation (M168T), which originated in Africa about 35,000 to 89,000 years ago. Therefore, the data do not support even a minimal in situ hominid contribution in the origin of anatomically modern humans in East Asia.
A lot of weebs are gonna be pissed.
And to study the men… so that’s an African man chromosome in your waifu, she been blacked centuries ago!
To test the hypotheses of modern human origin in East Asia, we sampled 12,127 male individuals from 163 populations and typed for three Y chromosome biallelic markers (YAP, M89, and M130). All the individuals carried a mutation at one of the three sites. These three mutations (YAP, M89T, and M130T) coalesce to another mutation (M168T), which originated in Africa about 35,000 to 89,000 years ago.
An international study has found that the Chinese people originated not from “Peking Man” in northern China, but from early humans in East Africa who moved through South Asia to China some 100,000 years ago,
Based on DNA analyses of 100,000 samples gathered from around the world, a number of human families evolved in East Africa some 150,000 years ago, said Li Hui (李輝), a member of Jin’s team.
About 100,000 years ago, some of those humans began to leave Africa, with some people moving to China via South and Southeast Asia, Li said.
According to the newspaper article, it has been proven that the “65 branches of the Chinese race” share similar DNA mutations with the peoples of East and Southeast Asia.
This all explains very well why Aboriginal Australians look SO black.
Their ancestors evolved on the African continent and were the first modern humans to arrive in Asia, the work confirming they have occupied Australia continuously since that time, perhaps 70,000 years.
“Australians are truly one of the world’s great human populations and a very ancient one at that, with deep connections to the Australian continent and broader Asian region. About this now there can be no dispute.
“The study also confirms controversial claims that the ancestors of all living Eurasians interbred with the Neandertals,
Both Europeans and Asians, we’re distinct races by genetic distance studies.
Eurasian, like Caucasian, is a category error.
Asians also bred with Neanderthals, we knew this.
while past Asians/Oceanians also mated with the mysterious ancient humans from Denisova cave in Siberia. This is clear and independent validation of DNA work on both these extinct humans, confirming their deep connections to Australians and other indigenous people in our region.”
Wow so they’re like the most mixed race, like the race OF mixes.
The Han Chinese are the largest ethnic group in the world, and their origins, development, and expansion are complex. Many genetic studies have shown that Han Chinese can be divided into two distinct groups: northern Han Chinese and southern Han Chinese. The genetic history of the southern Han Chinese has been well studied. However, the genetic history of the northern Han Chinese is still obscure. In order to gain insight into the genetic history of the northern Han Chinese, 89 human remains were sampled from the Hengbei site which is located in the Central Plain and dates back to a key transitional period during the rise of the Han Chinese (approximately 3,000 years ago). We used 64 authentic mtDNA data obtained in this study, 27 Y chromosome SNP data profiles from previously studied Hengbei samples, and genetic datasets of the current Chinese populations and two ancient northern Chinese populations to analyze the relationship between the ancient people of Hengbei and present-day northern Han Chinese. We used a wide range of population genetic analyses, including principal component analyses, shared mtDNA haplotype analyses, and geographic mapping of maternal genetic distances. The results show that the ancient people of Hengbei bore a strong genetic resemblance to present-day northern Han Chinese and were genetically distinct from other present-day Chinese populations and two ancient populations. These findings suggest that the genetic structure of northern Han Chinese was already shaped 3,000 years ago in the Central Plain area.
So it’s applicable.
And some Chinese are so mixed they’re distinct from their own ancestors.
Despite the fact that the continuity of morphology of fossil specimens of modern humans found in China has repeatedly challenged the Out-of-Africa hypothesis, Chinese populations are underrepresented in genetic studies. Genetic profiles of 28 populations sampled in China supported the distinction between southern and northern populations, while the latter are biphyletic. Linguistic boundaries are often transgressed across language families studied, reflecting substantial gene flow between populations. Nevertheless, genetic evidence does not support an independent origin of Homo sapiens in China. The phylogeny also suggested that it is more likely that ancestors of the populations currently residing in East Asia entered from Southeast Asia.
East Asia is one of the few regions in the world where a relatively large number of human fossils have been unearthed–a discovery that has been taken as evidence for an independent local origin of modern humans outside of Africa. However, genetic studies conducted in the past ten years, especially using Y chromosomes, have provided unequivocal evidence for an African origin of East Asian populations. The genetic signatures present in diverse East Asian populations mark the footsteps of prehistoric migrations that occurred tens of thousands of years ago.
The timing and nature of the arrival and the subsequent expansion of modern humans into eastern Asia remains controversial. Using Y-chromosome biallelic markers, we investigated the ancient human-migration patterns in eastern Asia. Our data indicate that southern populations in eastern Asia are much more polymorphic than northern populations, which have only a subset of the southern haplotypes. This pattern indicates that the first settlement of modern humans in eastern Asia occurred in mainland Southeast Asia during the last Ice Age, coinciding with the absence of human fossils in eastern Asia, 50,000-100,000 years ago. After the initial peopling, a great northward migration extended into northern China and Siberia.
Global distribution of Y-chromosome haplogroup C reveals the prehistoric migration routes of African exodus and early settlement in East Asia.
The regional distribution of an ancient Y-chromosome haplogroup C-M130 (Hg C) in Asia provides an ideal tool of dissecting prehistoric migration events. We identified 465 Hg C individuals out of 4284 males from 140 East and Southeast Asian populations. We genotyped these Hg C individuals using 12 Y-chromosome biallelic markers and 8 commonly used Y-short tandem repeats (Y-STRs), and performed phylogeographic analysis in combination with the published data. The results show that most of the Hg C subhaplogroups have distinct geographical distribution and have undergone long-time isolation, although Hg C individuals are distributed widely across Eurasia. Furthermore, a general south-to-north and east-to-west cline of Y-STR diversity is observed with the highest diversity in Southeast Asia. The phylogeographic distribution pattern of Hg C supports a single coastal ‘Out-of-Africa’ route by way of the Indian subcontinent, which eventually led to the early settlement of modern humans in mainland Southeast Asia. The northward expansion of Hg C in East Asia started approximately 40 thousand of years ago (KYA) along the coastline of mainland China and reached Siberia approximately 15 KYA and finally made its way to the Americas.
That’s how your so-called Natives were made, so …technically, blacks were there first?
Genetic evidence of an East Asian origin and paleolithic northward migration of Y-chromosome haplogroup N.
The Y-chromosome haplogroup N-M231 (Hg N) is distributed widely in eastern and central Asia, Siberia, as well as in eastern and northern Europe. Previous studies suggested a counterclockwise prehistoric migration of Hg N from eastern Asia to eastern and northern Europe. However, the root of this Y chromosome lineage and its detailed dispersal pattern across eastern Asia are still unclear. We analyzed haplogroup profiles and phylogeographic patterns of 1,570 Hg N individuals from 20,826 males in 359 populations across Eurasia. We first genotyped 6,371 males from 169 populations in China and Cambodia, and generated data of 360 Hg N individuals, and then combined published data on 1,210 Hg N individuals from Japanese, Southeast Asian, Siberian, European and Central Asian populations. The results showed that the sub-haplogroups of Hg N have a distinct geographical distribution. The highest Y-STR diversity of the ancestral Hg N sub-haplogroups was observed in the southern part of mainland East Asia, and further phylogeographic analyses supports an origin of Hg N in southern China. Combined with previous data, we propose that the early northward dispersal of Hg N started from southern China about 21 thousand years ago (kya), expanding into northern China 12-18 kya, and reaching further north to Siberia about 12-14 kya before a population expansion and westward migration into Central Asia and eastern/northern Europe around 8.0-10.0 kya. This northward migration of Hg N likewise coincides with retreating ice sheets after the Last Glacial Maximum (22-18 kya) in mainland East Asia.
Very very mixed.
So China relates to East Asia discussions.
They moved up and into Europe, like they’re trying to do now. To be pushed back, again.
At least we didn’t have the African result like they do.
The human genetic history of East Asia: weaving a complex tapestry.
East Asia encompasses a wide variety of environments, peoples, cultures and languages. Although this review focuses on East Asia, no geographic region can be considered in isolation in terms of human population history, and migrations to and from East Asia have had a major impact. Here, we review the following topics: the initial colonization of East Asia, the direction of migrations between southeast Asia and northern Asia, the genetic relationships of East Asian hunter-gatherers and the genetic impact of various social practices on East Asian populations. By necessity we focus on insights derived from mitochondrial DNA and/or Y-chromosome data; ongoing and future studies of genome-wide SNP or multi-locus re-sequencing data, combined with the use of simulation, model-based methods to infer demographic parameters, will undoubtedly provide additional insights into the population history of East Asia.
South Asia–comprising India, Pakistan, countries in the sub-Himalayan region and Myanmar–was one of the first geographical regions to have been peopled by modern humans. This region has served as a major route of dispersal to other geographical regions, including southeast Asia. The Indian society comprises tribal, ranked caste, and other populations that are largely endogamous. As a result of evolutionary antiquity and endogamy, populations of India show high genetic differentiation and extensive structuring.
aka outbreeding depression
Linguistic differences of populations provide the best explanation of genetic differences observed in this region of the world.
No, they don’t.
Within India, consistent with social history, extant populations inhabiting northern regions show closer affinities with Indo-European speaking populations of central Asia that those inhabiting southern regions. Extant southern Indian populations may have been derived from early colonizers arriving from Africa along the southern exit route. The higher-ranked caste populations, who were the torch-bearers of Hindu rituals, show closer affinities with central Asian, Indo-European speaking, populations.
Indo-European only refers to a language, stop.
Still not European, let alone isolated Anglo. Stop.
East Asia is widely concerned as one of the important places for the dispersal and evolution of the Anatomically Modern Human (AMH). How the diverse ethnic groups in East Asia originated and diversified is also widely focused by different disciplines of Anthropology. The adoption of genetic data had provided new clues for reconstructing the genetic history of East Asian populations. Genetic studies supported the hypothesis that the AMHs originated from Africa’s Homo sapiens at about 200 kilo years ago (kya) and then migrated out of Africa at ~100 kya, followed by expansions into the whole East Asia since their arrival in Southern East Asia at 5~6 kya along the coastal route.
Early Homo Sapiens might have genetic contribution to the non-African AMHs. Early settlement, cultural assimilation, population migration and genetic exchanges are crucial in the origination and evolution of East Asia populations. Previous studies made detailed analysis for the genetic history of East Asian populations, which largely resolved the longstanding divergence between archaeology and history. However, this needs further verification by whole-genome sequencing and ancient DNA studies. Here we briefly reviewed the progresses of genetic studies in exploring the population origin, dispersal and diversification in East Asia, which improved understanding of the evolution of East Asian populations. We also prospected the future of genetic studies in revealing the prehistory of East Asians.
The main unequivocal conclusion after three decades of phylogeographic mtDNA studies is the African origin of all extant modern humans.
This is a study about Asians. No.
Title: Carriers of mitochondrial DNA macrohaplogroup L3 basal lineages migrated back to Africa from Asia around 70,000 years ago.
Stay in your lane.
In addition, a southern coastal route has been argued for to explain the Eurasian colonization of these African pioneers.
new term for rapist, exotic
Based on the age of macrohaplogroup L3, from which all maternal Eurasian and the majority of African lineages originated,
doesn’t make sense, if ALL humans are from them, ALL humans would have that…
the out-of-Africa event has been dated around 60-70 kya. On the opposite side, we have proposed a northern route through Central Asia across the Levant for that expansion and, consistent with the fossil record, we have dated it around 125 kya. To help bridge differences between the molecular and fossil record ages, in this article we assess the possibility that mtDNA macrohaplogroup L3 matured in Eurasia and returned to Africa as basal L3 lineages around 70 kya.
So you’re comparing Asian fossils to African DNA, nothing to do with Europeans.
The coalescence ages of all Eurasian (M,N) and African (L3 ) lineages, both around 71 kya, are not significantly different.
Different enough to call different.
The oldest M and N Eurasian clades are found in southeastern Asia instead near of Africa as expected by the southern route hypothesis. The split of the Y-chromosome composite DE haplogroup is very similar to the age of mtDNA L3. An Eurasian origin and back migration to Africa has been proposed for the African Y-chromosome haplogroupE. Inside Africa, frequency distributions of maternal L3 and paternal E lineages are positively correlated. This correlation is not fully explained by geographic or ethnic affinities. This correlation rather seems to be the result of a joint and global replacement of the old autochthonous male and female African lineages by the new Eurasian incomers.
See pictures above.
The reservation “Americans”, genetic Asians were also well known for gang rape up until the 19th century, even of little girls.
These results are congruent with a model proposing an out-of-Africa migration into Asia, following a northern route, of early anatomically modern humans carrying pre-L3 mtDNA lineages around 125 kya, subsequent diversification of pre-L3 into the basal lineages of L3, a return to Africa of Eurasian fully modern humans around 70 kya carrying the basal L3 lineages and the subsequent diversification of Eurasian-remaining L3 lineages into the M and N lineages in the outside-of-Africa context, and a second Eurasian global expansion by 60 kya, most probably, out of southeast Asia. Climatic conditions and the presence of Neanderthals and other hominins might have played significant roles in these human movements. Moreover, recent studies based on ancient DNA and whole-genome sequencing are also compatible with this hypothesis.
So more using the Eur- of Eurasian without a shred of proof to include white people.
People with dark skin at those altitudes die of Vit D deficiency. Even in England, the NHS warn about this, let alone Sweden with even FEWER rays. How did their cranial morphology magically evolve, then?
Africans have zero Neanderthal DNA so pretty easy to test for. They have it? Not black.
There is plenty of proof of African-Asian mixing, however.
This explains their lower IQs in many nations, larger overall heads and stronger jaws.
HUGE lips, too.
Naturally the page tries to lie about white people as all magic albinos BUT the Asian part has this:
And morphology considerations:
Of the three crania Upper Cave 101, the “old man”, has been studied in more detail primarily due to its better preservation and clearly adult status. In comparison to modern East Asians the cranial vault is extremely long and low, with a receding frontal squama and marked angulation in the occipital region. The forehead is broad and the supercilliary region well developed. The nasal bones are pinched, with a high bridge, and the nose must have been more prominent than is common amongst living East Asians. The orbits are relatively low and rectangular, which is a common feature in terminal Pleistocene and Neolithic crania from many parts of the world. The lower border of the nasal aperture is gutted, which is customary amongst East Asians, Australian Aborigines and sub-Saharan Africans.
East Asians are just mongrels. They simply didn’t exist as we know them today and the modern Indian is typically a halfbreed with a Brit a century or two ago. This caused their ‘caste’ system.
All analysis of “Early Humans” in China, agree that the Mongoloid type Humans currently inhabiting the area, did not start to appear until quite recently.
But here the devil is in the definitions; we know that modern Chinese (Mongols) are a Mulatto/Mixed Race of Mongol featured Blacks like the San, their Albinos, the Albinos of Central Asians (who later became Europeans), and Blacks like the Jomon in Japan. But understanding just when these admixtures took place requires we know exactly what was meant by “Primitive Mongoloid” or “Evolving Mongoloid” and how is that different from Eskimo? (Not saying that Eskimo are primitive).
Any admixture was usually rape.
As was shown with the Peking man nonsense, many Albino and Mulatto Chinese are loath to admit that they derive from Africans. But the fact is that the Chinese, Japanese, Koreans, and South Asians, have all been scientifically proven to be Africans. Albeit, as is true in many places i.e. the Americas, the Middle East, etc. They are a mixture of Albino people and the original Native Blacks.
I don’t believe albino is a race, it’s a mutant and they’re often sterile.
But Asians do have substantial African morphology, you can see it in their face.
This phenomenon can occur in two ways. One way is by the “swamping” of locally adapted genes in a wild population by straying from, for example, a hatchery population. In this case, adaptive gene complexes in wild populations are simply being displaced by the immigration of genes that are adapted to the hatchery environment or to some other locality. For example, selection in one population might produce a large body size, whereas in another population small body size might be more advantageous. Gene flow between these populations may lead to individuals with intermediate body sizes, which may not be adaptive in either population. A second way outbreeding depression can occur is by the breakdown of biochemical or physiological compatibilities between genes in the different populations. Within local, isolated populations, alleles are selected for their positive, overall effects on the local genetic background.
Due to nonadditive gene action, the same genes may have rather different average effects in different genetic backgrounds—hence, the potential evolution of locally coadapted gene complexes. Offspring between parents from two different populations may have phenotypes that are not good for any environment. It is important to keep in mind that these two mechanisms of outbreeding depression can be operating at the same time. However, determining which mechanism is more important in a particular population is very difficult.
beige people, blandifying selection traits
In other words, genetic structure, aka, genetic correlation structure is more than additional ethnic genetic interest—it can be function, hence loss of that structure results in loss of function resulting in outbreeding depression.
Evidence for outbreeding depression is much less extensive than evidence for inbreeding depression, but outbreeding depression is nevertheless a general genetic phenomenon. One problem in studying outbreeding depression is the number of generations that may occur before outbreeding depression reveals itself. The effects of outbreeding enhancement due to the masking of deleterious alleles and outbreeding depression due to hybrid breakdown may cancel each other in the first generation after crossing individuals from two populations. So the effects of outbreeding depression may not be apparent for a few generations.
They just know that inbreeding is more of a problem than outbreeding—and that’s why they’re “justified” in imposing outbreeding on populations with government force and technologically amplified panmixia.
This paper demonstrates that, in an analysis of Icelandic couples born between 1800 and 1965, there is a “significant positive association” between kinship and fertility; maximal reproductive success was observed for couples with kinship relatedness at the level of third or fourth cousins.
The authors conclude that these differences in reproductive success (i.e. fitness*) have a “biological basis” – that is, a genetic basis.
Strikingly, however, our results show that couples related at the degree of third to fourth cousins exhibited the greatest reproductive success.
In order to maximize fitness, therefore, one doesn’t have to move that far from the endogamous extreme. Just a few rungs upward on the kinship distance ladder produces benefits superior to that of both extremes. It’s totally irresponsible and mendacious to use the fitness costs of obvious incest to argue for reckless hybridization (**) with the most genetically distant organisms with which individuals are cross-fertile.
“It could be argued that in human populations there is a point of balance between the disadvantages associated with inbreeding versus those with outbreeding,” said Alan Bittles, director of the Center for Human Genetics at Edith Cowan University in Western Australia.
Therefore, not only is it unlikely – as has been asserted on this blog previously – that any putative “hybrid vigor” can compensate for lost parental kinship, but it’s also highly unlikely that “hybrid vigor” exists to any significant extent for most human populations past the “second cousin” level. Defining fitness in the proper biological sense, the recent deCODE findings suggest that increased hybridity past an optimal point may in fact reduce reproductive fitness above and beyond the real losses in genetic interests due to foregone parental kinship.
From the Udry study discussed by J. Richards in a previous blog post, to the lack of any evidence of enhanced reproductive success of mixed couples and their offspring, to these latest deCODE findings that reproductive success may be maximized by closer kinship, it would seem that when in doubt, one should err on the side of increased endogamy (to the level of “third cousins” only, of course).
When even deCODE – which decided to sift through James Watson’s ancestry and make public their dubious findings because of a politically correct distaste at what they perceived as Watson’s (presumably “racist”) comments on African intelligence levels – publishes findings that show a biologically based enhanced fitness for mating at high levels of kinship relatedness, then one must wonder how any scientifically objective individual could possibly still peddle the idea that cross-racial mating is somehow a biologically preferable choice.
An important point: it’s really not so important that high kinship actually enhances reproductive fitness, or the mechanisms whereby that occurs. More important is the lack of evidence for the contrary view: that increasing levels of exogamy leads to “hybrid vigor” and enhanced fitness. The findings from this study constitute yet more evidence that “hybrid vigor” is not an important force – if it is one at all – for humans.
It doesn’t exist in humans, we’re not racehorses.
Prized, rare (or unique) traits like genius, maybe, but that’s kin-related, subrace max.
In the absence of such “hybrid vigor,” parental kinship takes “center stage.” The possibility that endogamy may actually raise fitness per se, as suggested by deCODE, is just “icing on the cake,” hammering home the point that mating “between the lines” of genetically distant groups is not required for enhanced fitness.
*Reproductive success and the maintenance/expansion of distinctive genetic information are the reasonable measures of biological fitness, not whether “Tiger Woods smells better on the golf course,” or any other inane commentaries that spew forth from the addled “minds” of certain hysterical proponents of objectively maladaptive inter-racial couplings.
An example of maladaptive inter-racial hybridization is found here. Again, that’s not even considering reproductive fitness or parental kinship, but merely negative health consequences of introducing one race’s genes into another race’s genome.
**Responsible researchers and conservationists are beginning to understand the consequences of reckless hybridization and outbreeding depression. Some quotes, and my comments:
the available data suggest that risks of outbreeding, particularly in the second generation, are on par with the risks of inbreeding.
If there’s no advantage for hybridization in the long run, then what’s the point? Note that this paper is talking about decisions to “intentionally hybridize” animals – we are not concerned with parental kinship when considering animals, only the relative “quality” of the resultant phenotypes. Even with that, hybridization is questionable. However, we are humans, and as such, have concerns above and beyond these considerations – such as kinship issues. So, everything said about hybridization in animals holds true for humans, but, for humans, the underlying cost of hybridization – foregone parental kinship – is something additional that concerns us in dealing with mating choices.
Meanwhile, managers can minimize the risks of both inbreeding and outbreeding by using intentional hybridization only for populations clearly suffering from inbreeding depression…
Yes. This is the conservative approach. While Ashkenazi Jews can be said to “clearly suffer” from “inbreeding depression” the same cannot be said of European ethnic groups, or Europeans as a whole (or, for that matter, Africans, Asians, etc.).
The low IQs of Eastern Europeans are inbreeding depression.
Again – and this cannot be stressed enough – that’s not even considering parental kinship (or genetic interests in general). The Ashkenazim may have preservationist considerations that may lead them to reject hybridization independent of whatever “benefits” genetic mixing may bring, and the cost/benefit ratio may very well favor that rejection. However, given that Europeans are not “clearly suffering” from “inbreeding depression” there is no reason to follow Ziv’s advice and destroy our genetic interests for non-existent “benefits” to “solve” a non-existent “problem.”
Destroy yourself now because you might, at some point, destroy yourself!
….maximizing the genetic and adaptive similarity between populations…
In other words, if, for some reason, hybridization is decided upon, one should pick for the hybridization a population as genetically similar to the original population as possible. One does not pick the most genetically distant populations possible!
…and testing the effects of hybridization for at least two generations whenever possible.
to ensure fertility, not the liger issue
Yes – instead of promoting widespread human panmixia based upon how Tiger Woods might smell on the golf course. Of course, one may look at highly admixed populations throughout the world and use those for “testing the effects.” Even leaving kinship concerns out of the picture, the results with respect to positive traits have not been encouraging.
While the data on outbreeding depression are dwarfed by those on inbreeding depression, the few studies that exist suggest that concerns over outbreeding should be taken seriously, as the effects can in some cases be as damaging as severe inbreeding.
Yes, taken seriously, instead of making juvenile comments about which male celebrity may be better able to “induce orgasm” in which female celebrity. Again, given the costs for humans of foregone kinship, where are the “benefits?”
As a start, managers should strive to do no harm.
What should we think of those who, seemingly, wish to maximize harm?
That is, we should intentionally hybridize populations only when there is hard evidence that a population is suffering from inbreeding depression.
Speculation about how Tiger Woods might smell after a round of golf does not constitute said “hard evidence.” There is no “hard evidence” that European populations (or Africans, Asians, etc.) are “suffering” from inbreeding depression. Other small populations may be “suffering;” in that case, let those groups decide to balance the costs and benefits of hybridization – and a “pro” choice hardly means choosing the most distant groups possible as mates.
…low levels of gene flow are predicted to have disastrous effects on populations vulnerable to outbreeding (Edmands & Timmerman 2003).
As a final postscript, readers may be interested in an alternative viewpoint with respect to the function of sexual reproduction – which stresses species and chromosomal stability over “increased genetic diversity.”
By diversity they mean the healthy range.
Unhealthy is culled by natural selection.
“Well, South Asians are the product of mixing between several Caucasoid and Asiatic people, and problems with their racial classification notwithstanding, the fact remains that European Caucasoids and East Asians clearly belong to different races. In a classic example offered by Arthur Jensen, different bands of a rainbow blend into each other, yet this does not mean that a rainbow doesn’t contain different color bands that are easily distinguished from each other, except at the boundaries. ” marriage post (so not really gene heavy)
Genetic distance studies. Forensic skull analysis. Actually, you can clearly see group and case boundaries.
“blending pictures of Caucasians and Asians to form a hypothetical Eurasian composite”
not how miscegenation works
The authors wrote:
The disadvantage of computer-generated mixed-race composites is that they may not precisely capture the appearance of mixed-race individuals.
Damn right! However, the major problem is not one of precision but of accuracy. Caucasoid/Mongoloid hybrids generally look more Mongoloid than Caucasoid because: 1) Mongoloids have retained more ancestral traits such as robust cheekbones, robust mandibles, and various primitive (ancestral) indices of facial flatness [American Journal of Physical Anthropology 111:105-134; year 2000]; 2) some trait variation is due to dominant and epistatic genes; and 3) the genes associated with primitive features likely comprise of an excess of dominant genes with respect to the newer mutations behind the more-recently-originating facial features disproportionately found among Caucasoids.
One quibble: Broad cheekbones are robust but not attractive.
They’re flat. Very very flat.
“However, in contrast to the first two experiments, the hypothetical Eurasian composite was not rated as more attractive than the Caucasian composite, a result that has been previously reported in a different study.”
When you didn’t skew your method enough to be PC.
“Therefore, the individuals that went into the average female Caucasian likely disproportionately included ugly, obese white women (possibly of mostly Irish ancestry). In this case, the blending appears to have improved the attractiveness rating from ugly to unattractive.”
Yeah, that’s a fair test.
Figures 5 and 6 below show the pictures used in the third experiment. One reason behind the attractiveness of the actual Eurasian composites (EurasianAV) in Figures 5 and 6 is the narrower face due to less prominent cheekbones, narrower than even the Caucasian! The Eurasian facial breadth should be in between the European (narrow) and the Asian (broad).
They do that on purpose to rig the finding.
Supposed Cauc75 looks Celtic, ancient Briton type.
Fuck-all to do with even Eastern Europe!
Their upper fake average is noticably more white than the actual lower pic average.
Again, fellow Brits have more good looking people by volume than other European countries.
So-called Cauc75 looks like my relatives, so I know it’s full of shit to call that a mix.
Genetic isolation from the invasions of European landmass preserved our features.
That’s why so many models are from our isles over Denmark/France/Germany/Poland etc, same reason applies to Asians with Japanese models, more sought after (by genes) and have a higher volume of Lookers than Asia mainland.
They also rig what data they release, omitting profile data.
Notice that Gillian Rhodes has not addressed the attractiveness of facial profile (side view). I’d be damned if Caucasians consider facial flattening resulting from Mongoloid admixture as more attractive than the attractive Caucasoid norm. Additionally, how can the following traits resulting from Mongoloid admixture among Caucasians be considered more attractive than the norm among Caucasians: reduced height, less muscularity in males, slanted eyes, flatter buttocks, smaller breasts in females, relatively shorter limbs, relatively longer trunk, and a smaller penis?
How dare you know statistics.
How DARE you.
Flatter faces in whites are considered by neonate doctors a sign of genetic disease. If they spot it in a newborn white, they do other tests for specific things, most of which are linked to retardation of the mind too.
Nasal bridge low, flat midface, short nose – Eurasian traits.
Williams Syndrome nose:
Our gut reaction as white people against mongrelization (in this case, Eurasian mixing) is an aversion to severe genetic disorder.
It could be a coincidence or not, who knows? What does it matter, since an aversion is there?
And has every right to be.
As for the eyes….
Look up downies, harsh but true.
Similar eye shape, tilt angle and placement on face to the Asians without monolids too.
So… there’s that.
Whites don’t find flat faces or stretched, narrowed eyes attractive.
even in fellow whites like Cumberbatch (for the eyes).
Technically, it isn’t about race but avoiding deformed offspring (or deformed looking, who’ll meet the same sexual selection ‘success’).
The authors controlled for age, sex, verbal IQ, grade point average, family structure (living with one or both parents), and family education
On the other hand, there exist several examples in the animal literature where matings between more genetically distant individuals within the same species/different races result in offspring that are less healthy than the parents, on average, [30-37] and this cannot be blamed upon struggle with identity formation. There also exist examples of hybrid vigor, but nothing remotely close to hybrid vigor is seen in Udry’s data.
Udry’s data are compatible with the likelihood of race mixing improving one or more parental traits in some mixed-race offspring, who may be better off than both parents on multiple counts, provided that a greater number of mixed-race offspring are overall worse off than both parents. The former possibility is surely not implausible given that the tremendous racial and species diversity out there implies that nature does not rule out equally-well functioning/better functioning novel genetic correlation structures, which could be brought about by race mixing, though the chances of improvement would typically be slim if more distant races are involved.
the parents improve their own DNA at the expense of the child
It is seen in Table 2 that those identifying as mixed race have worse health than even populations known to be highly admixed (American black, Native American, Hispanic). This could be accounted for if one assumes that first-generation hybrids who have the worst health/behavior problems would disproportionately not be very successful in reproducing, i.e., the healthier mixed offspring could, within a few generations, set up a mixed-race population that is healthier, on average, compared to the first-generation hybrids, but for this mixed-race population to approach or exceed the overall health of the original single-race populations, it would take many generations of [naturally] weeding out the unhealthy and settling toward a novel population-typical genetic correlation structure that corresponds to good health (more on this and on hybrid vigor in a subsequent post).
Nature’s laughing at all of us, really. That time never exists.
This also assumes the mixed race want kids – no or fewer than average, from what I read and talking to them.
Zero or below replacement level, and lower numbers for kids they actually have.
To conclude, it is irresponsible for any scientific organization to pretend that race mixing has no adverse health effects and it is obviously inappropriate to portray race mixing as desirable or virtuous.
30. Aspi J: Inbreeding and outbreeding depression in male courtship song characters in Drosophila montana. Heredity 2000, 84 (Pt 3):273-282.
31. Edmands S, Feaman HV, Harrison JS, Timmerman CC: Genetic consequences of many generations of hybridization between divergent copepod populations. J Hered 2005, 96:114-123.
32. Garnier-Gere PH, Naciri-Graven Y, Bougrier S, Magoulas A, Heral M, Kotoulas G, Hawkins A, Gerard A: Influences of triploidy, parentage and genetic diversity on growth of the Pacific oyster Crassostrea gigas reared in contrasting natural environments. Mol Ecol 2002, 11:1499-1514.
33. Miller LM, Close T, Kapuscinski AR: Lower fitness of hatchery and hybrid rainbow trout compared to naturalized populations in Lake Superior tributaries. Mol Ecol 2004, 13:3379-3388.
34. Neff BD: Stabilizing selection on genomic divergence in a wild fish population. Proc Natl Acad Sci U S A 2004, 101:2381-2385.
35. Peer K, Taborsky M: Outbreeding depression, but no inbreeding depression in haplodiploid Ambrosia beetles with regular sibling mating. Evolution Int J Org Evolution 2005, 59:317-323.
36. Thornhill R, Moller AP: Developmental stability, disease and medicine. Biol Rev Camb Philos Soc 1997, 72:497-548.
37. Livshits G, Kobyliansky E: Lerner’s concept of developmental homeostasis and the problem of heterozygosity level in natural populations. Heredity 1985, 55 (Pt 3):341-353.
Charles Darwin on race mixing; more here (don’t take this very seriously):
These latter facts remind us of the statements, so frequently made by travellers in all parts of the world, on the degraded state and savage disposition of crossed races of man. That many excellent and kind-hearted mulattos have existed no one will dispute; and a more mild and gentle set of men could hardly be found than the inhabitants of the island of Chilce, who consist of Indians commingled with Spaniards in various proportions. On the other hand, many years ago, long before I had thought of the present subject, I was struck with the fact that, in South America, men of complicated descent between Negroes, Indians, and Spaniards, seldom had, whatever the cause might be, a good expression.(1) Livingstone,- and a more unimpeachable authority cannot be quoted,- after speaking of a half-caste man on the Zambesi, described by the Portuguese as a rare monster of inhumanity, remarks, “It is unaccountable why half-castes, such as he, are so much more cruel than the Portuguese, but such is undoubtedly the case.”An inhabitant remarked to Livingstone, “God made white men, and God made black men, but the Devil made half-castes.”(2) When two races, both low in the scale, are crossed the progeny seems to be eminently bad.
thou shalt not adulterate
Thus the noble-hearted Humboldt, who felt no prejudice against the inferior races, speaks in strong terms of the bad and savage disposition of Zambos, or half-castes between Indians and Negroes; and this conclusion has been arrived at by various observers.(3) From these facts we may perhaps infer that the degraded state of so many half-castes is in part due to reversion to a primitive and savage condition, induced by the act of crossing, even if mainly due to the unfavourable moral conditions under which they are generally reared.
nurture has been debunked (adoption studies)
 Journal of Researches, 1845, p. 71.
 Expedition to the Zambesi, 1865, pp. 25, 150.
 Dr. P. Broca, on ‘Hybridity in the Genus Homo,’ Eng. translat., 1864, p. 39.
Past research has consistently found that men with shorter and wider faces are more aggressive, more prejudiced, more likely to deceive others, more dominant, and more driven to succeed compared to men with longer and narrower faces.
Low trust, sluttier, violent, compulsive lying – r-types in a nutshell.
This is even true for non-humanprimates, and among women this link is found for dominance, but not aggression. Furthermore, other people pick up on these facial cues, perceiving wide-faced men and women as more masculine, dominant and threatening.
R-selected women, more aggressive as sole protectors of their spawn.
It all FITS.
Why would all these personality traits be related to this seemingly random facial feature, also known as facial width-to-height ratio (FWHR)? Because they are all thought to be influenced, at least partly, by exposure to the masculinizing effects of testosterone. Although data are mixed as to the exact timing of this exposure (in utero, at puberty or in adulthood), more testosterone generally means higher behavioral masculinity, dominance, aggression and also a higher facial width-to-height ratio.
Examples of measurement of the FWHR in faces with relatively low and high FWHRs.
FROM GENIOLE ET AL., 2015, PLOS ONE
Find the more attractive woman, I fucking dare you.
Also applies to retro women:
A long face is more attractive in women (read: feminine).
As history shows, feminine women like Vivien Leigh can have low testosterone but a fiiiiine sex life.
[despite gaslighting from a gay bitch of a husband]
Feminine face = better WHR measures, so best of both worlds, actually!
Wide hips – higher sex drive, partnered or not.
Long face in women is not horse face.
Except SJP but she isn’t white so… who cares?
Now, a set of two new Canadian studies find that FHWR is also linked to several aspects of people’s sexual psychology (sex drive, casual sex and infidelity), also known to be influenced by testosterone.
Water is wet, go on.
In the first study, 145 heterosexual Canadian students (52% female, 82% White, mean age = 22) currently in romantic relationships answered questions regarding their sex drive (like how often they experience sexual desire or how often they masturbate). They then had their face photos taken by the researchers (under identical distance, lighting, and backdrop conditions for all participants), and those photos were later carefully measured by two raters for width, height and some other facial features like cheekbone prominence.
Note: libido doesn’t equal promiscuity in women, which warrants separate study so hot does not equal slut. Discernment among the most attractive women in studies prove this (the sluttiest women are average or slightly above to hook more attractive mates). Yet it does explain partially why men would find certain women better options sexually if not marriage material (sexy over beauty). There’s a mutual exclusive at play here between availability (broad, manjaw) and beauty (dimorphic female, narrow face and soft jaw).
Because their average genes want to survive with anyone v no one.
And naturally propaganda and rhetoric factor below awareness.
This must change based on r/K cycling, what percentage of men find mannish women ‘hot’ rather than meh or repulsive (probably charts onto the man’s wing leaning too).
Could she be a porn star and how good (you imagine) at it? That’s sexy in our gross pornified culture and a 10 for Hotness.
Could she be portrayed as an ancient goddess in a sculpture? That’s beauty and a 10.
Beautiful, but by modern standards (which are dumb and/or anti-white, generally) – not hot.
sorry about the meme but you get the point
There’s a distinct look, defined or softer.
Like popular celebrities
Beautiful face + voluptuous body = Ideal.
By comparison, note how the limbs look thin? Odd side effect.
Shows natural fat % (so limbs must be less to be within range) but not obesity (female fat deposition, see WHR posts).
Rarely…. a woman is both.
Fuck you, Monica. Fuck you and your flawlessness.
The analyses confirmed the researchers’ hypothesis: Wider-faced men and women reported higher sex drive than their counterparts with narrower faces. This link remained even when other facial features were statistically controlled for.
A second sample of 314 students (57% female, 91% White, 93% heterosexual, mean age = 20) from a different Canadian university confirmed these findings regarding sex drive. This second study also asked participants about their desire for, attitudes towards and experiences with casual hookups and their expectations of future infidelity to a partner. The men with higher facial width-to-height ratios reported greater openness to hookups and a higher likelihood they’d be unfaithful to a partner compared to their narrow-faced peers. A link between FWHR and propensity for casual sex or infidelity was not found for the women in this sample.
but libido finding is solid
Together with prior research on this facial feature, this study suggests that the facial width-to-height ratio, and our ability to perceive and interpret it, may be part of an evolved system that emerged long ago in our evolutionary past in order to help us figure out who may be dangerous vs. safe, trustworthy and faithful vs. likely to deceive or cheat on us, or more likely to stick around and raise babies vs. “hit it and quit it.”
Maybe r-oriented men don’t care if the woman is available to other men because, in times of r, any port in a storm, right?
R-selected men = low investment, might as well be low EFFORT.
Sorry but…. true, right?
Whites on average have the narrowest faces plus highest trust societies.
Japs are the closest non-whites. Says it all.
This is the first study to ever link FWHR to an aspect of human sexual psychology, so the findings need to be replicated in other samples and more diverse samples, including teens and older adults, non-whites, nonheterosexual and trans populations and using additional measures of sexual psychology before we can accept them.
Those studies can’t be published, you’ll kill them.
They’re in a drawer somewhere. PC people, you play yourself.
We should also remember that even if there is some positive correlation between FWHR and these personality and sexual traits, that this correlation is far from perfect. Not every person with a wide, short face is likely to be violent, cheat, hook up or crave sex several times a day. Being aware of our perceptual biases is an important first step in correcting our automatic tendency to stereotype someone based on the shape of their face.
Why did Marilyn make her face look broader with hair?
Assuming 100% of them were “Christian”, your cultural, political and genetic futures are still dead.
CHINO is multicultural Christianity, and it’s bullshit. An Italian Christian is not an English Christian is not a Syrian Christian is not a Jamaican Christian is not a Chink Christian. That’s multiculturalism via the back door.
I am shook. Women don’t wanna be lumbered with the baby of a man who doesn’t care enough to be a husband and father?* They aren’t attracted to feckless manchilds?
“That’s because the decline in fertility has been far greater among minorities than among non-Hispanic whites”
NOT. A. BUG.
Chart for the lazy people:
Look at the actual data before whining.
That’s called a selection pressure, children.
Men won’t marry? Women won’t breed.
Who wins? [women, their relatives breed]
“But the “white” fertility figure is a bit misleading, as it includes most Hispanics, who have historically had much higher birth rates than non-Hispanic whites. Looking at all Hispanics together, these women are missing nearly 19% of the babies that would have been born from 2008-2016, or about 2.2 million births, as their age-adjusted fertility rates have fallen from 2.85 births per woman to just 2.1, and continue to decline. Meanwhile, non-Hispanic fertility has only declined from 1.95 births per woman to 1.72, yielding about 2.3 million missing births. Solidly half of the missing kids over the last decade would have been born to Hispanic mothers, despite the fact that Hispanics only make up about a quarter of fertility-age women.
Thus, in racial or ethnic terms, America’s “Baby Bust” is kinda, sorta, a little bit racist”
Telling them to be breeding sows isn’t?
Hey, what exactly are they claiming these women should do?
Get back in the maternity ward? Pump out future Dem voters?
*If you really “care” (virtue signal) about Western birth rates, Chicken Littles of the internet, ask MGTOW why they’re complaining about the birth rate but not marrying. You don’t get to complain if you’re causing the ‘problem’.
[GDP will go up in a generation with fewer lower IQ drains on its system.]
Other data article:
For the lazy:
“That is, most long-run change in fertility can be accounted for by changes in the marital composition of society.”
“Marital status is a key determinant of whether or not women have as many kids as they want.”
HALF OR MORE.
Meanwhile, student loans must be written off if you care about IQ.
“It’s possible that debt may also reduce fertility, independently of marriage. Some studies do show that student debt has a strong effect on delaying fertility. The economic rationale is simple: having and raising children costs money, and student debt gobbles up a share of income right off the top of the budget. Crucially, even income-based repayment doesn’t fix this, as it resets with higher incomes: a debtor can’t earn their way out. As income rises, so do debt payments. At some high threshold, of course, the debtor can exceed the required payments and can advance the date of final repayment, but the point is that student loans, no matter how they are structured, divert money that might have gone towards planning for a child. It’s even possible that student loans delay marriage because they cause debtors to change their childbearing anticipations: maybe debtors realize they won’t be able to afford a child for a long time, and so they postpone marriage until they are (financially) ready for a child.”
Men can’t afford to marry, have kids unless loans are much lower.
Loan control would be a conservative policy, boosting high IQ fertility.
More babies being born are born to high IQ, educated parents.
Again, actual data.
“Finances, and student debt, specifically, aren’t the only reason for delayed marriage. Most unmarried people who want to get married say either that they are too young and unready for marriage, or else they haven’t found the right person. It may be that part of the problem is the decline in “marriageable men.” At the metro area level, the imbalance in sex ratios can sometimes be enormous.”
“The simple fact of the matter is that marital status is a key determinant of whether or not women have as many kids as they want.”
Women want to have kids, it’s the mens’ fault.
“Combined, it turns out that a combination of marital status, age, and fertility ideals is a pretty good predictor of individual-level fertility. In other words, marital status serves as a circuit-breaker on fertility aims: married people get close to achieving their aims, while never-married people generally don’t.”
“But one vital driver of birth rates is marriage. And as long as the average age of first marriage rises and the number of prime childbearing years the average woman spends married falls, we can expect to see fertility linger at low levels. Therefore, any policy supporting childbirth—however generous it may be—that does not also somehow impact marriage trends is unlikely to boost long-term fertility.”