Peştera Muierii woman is related to Europeans, but she is not a direct ancestor
Doesn’t have to be, a lot of bloodlines died.
Reduced diversity in Europe caused by Last Glaciation, not out-of-Africa bottleneck
Natural selection kills diversity. We know this.
Genetic load appears indifferent across 40,000 years of European history.
Postmodern habits like drugs, drinking, bad diet, sleeping around, can screw up your epigenetics over a few generations. We absorb viruses into our genome. Outbreeding depression does it in one. You can, in fact, fuck up tens of thousands of years of effort on part of your ancestors. If only we had a commandment about this.
Pet theory: planes are evil. Sink the boats.
Few complete human genomes from the European Early Upper Palaeolithic (EUP) have been sequenced. Using novel sampling and DNA extraction approaches, we sequenced the genome of a woman from “Peştera Muierii,” Romania who lived ∼34,000 years ago to 13.5× coverage. The genome shows similarities to modern-day Europeans, but she is not a direct ancestor. Although her cranium exhibits both modern human and Neanderthal features, the genome shows similar levels of Neanderthal admixture (∼3.1%) to most EUP humans but only half compared to the ∼40,000-year-old Peştera Oase 1. All EUP European hunter-gatherers display high genetic diversity, demonstrating that the severe loss of diversity occurred during and after the Last Glacial Maximum (LGM) rather than just during the out-of-Africa migration. The prevalence of genetic diseases is expected to increase with low diversity; however, pathogenic variant load was relatively constant from EUP to modern times, despite post-LGM hunter-gatherers having the lowest diversity ever observed among Europeans.
The Neanderthals were human. They were, at most, a race. Basic classification 101. It’s politically incorrect to admit this.
Welcome Global Cooling, it kills off redundant diversity. The people still living are the winners.
OOA is laughable at this point. Multi-Regional is correct. They don’t have to keep tweaking it to fit the data, replete with Black Swans that shouldn’t be there.
Assumption is incorrect, diseases become more serious, the higher the diversity. It’s akin to mixing random chemicals in a beaker. You’re more likely to blow your arm off, the more different the ingredients or elements. Well, mutations work the same way and most are disadvantageous i.e. they lower Darwinian fitness. A novel combination is dangerous. Inbreeding depression takes centuries in a super-restricted, incestuous environment; meanwhile, outbreeding depression occurs in one generation between any two genomes of sufficient distance. Odds are, if a kid has some super-rare obscure disease, barely recorded, they’re mixed race. The more mixed, the more health problems, including mental health. Taboos are based on health outcomes. They demonstrate low fitness for any one environment and ‘fail to thrive’ in either parental environment as a result. It dooms them to never belong and fit in, a core human need as a social species. Every group has a runt to its litter, but that shouldn’t be encouraged as the norm, it’s cruel. Happily, this means such mutants and feeble specimens were almost unheard of throughout our history, so we have nothing to feel guilty about. It’s literally the parent’s fault they made an experimental kid. Nobody forced you to play God.
This is why Africans in Africa are healthier than the mongrels in America. It isn’t just diet. Also why full-blooded Africans generally hate them. They are equally disgusted by the degeneration as any other race, it’s human aversion to disease.
Similarly, White Americans have extremely high white DNA but also suffer poorer health compared to their homelands. Why? Admixture of subrace. The same applies to a lesser-degree within a race, of sufficient genetic distance. It’s unlikely to be fatal, but breeding with a person with high mutations (r-type) will ruin the bloodline of the person whose is low. It’s only fine if they’re both low, which is unlikely when so distant in ancestry as to cross countries (and emigration is r-select). Consider the children of supermodels. Regression to the mean, except mutations only build. So you get a bland, dull looking child, nothing special. Breeding two racehorses is fine, breeding it with a donkey makes a mule, however good the racehorse genes of one parent. That’s the evil of genetic regression. Beware it. A racehorse with a regular horse may be fine but is likely to be uninspiring by the racing parental standard. This also applies to plants and flowers. Excess distance causes fertility dysfunction and is collectively called the process of speciation. Enough of the odd couples die off genetically while others, more natural, succeed and replace them using natural selection (by omission) to win zero sum. It works on a mathematical level. It’s basic game theory. Live or die.
EVOLUTION HAS NO CONTINUOUS SPEED. IT IS AN ONGOING PROCESS AND OPERATES FASTER SOME TIMES THAN OTHERS. I repeat, evolution is non-uniform as a biological driving force to live. I’ve never seen a shred of proof for it being the same everywhere, at all times and in all peoples. That smacks of absurd equalism and doesn’t account for the violence of history, both natural disasters and wars. There is much to the contrary, like this. Bloodlines die out, in part, all the damn time. All the bloody time! Yet certain people who claim to be high IQ like to pretend it has a constant speed like ‘c’, it is a positive claim and I’d like evidence. It doesn’t have to make sense to you, to be demonstrably true.
How many of Edison’s many children survived? Surprisingly few. That’s in a century. Writ large, same pattern. The birth rate doesn’t matter, longevity of genes does. Do not conflate them. Dilution is also a partial death. It’s like genetic atrophy. When children disappoint their parents, whose fault is that?
I find it funny supposed Christians mock evolution, only to insist on muh birth rates. If you believe in Revelations, it won’t matter, because winning is Darwinian. It isn’t about cross-comparisons to other groups, more r-select (read: arrogant while times are good) and their over-populating to over-consume and eventual, frequent famine (hello China), but quality within. Genetics are moreso about what you DON’T have than what you do. i.e. You can’t steal IQ, China, keep funding genetic engineering though. You tried. R-types can only run an ‘Empire’ of inferior quality by oppressing their own kind and even then, it fractures and implodes due to their sadism (low group loyalty > no in-group empathy). They are collectivists who hate freedoms and rights. Introduce more k-select competition and they’re easily brought to heel, like the French. Beaten (and saved) by a nation of shop-keepers. There’s a difference between conspicuous consumption and responsible innovation. R-types can’t tell until it’s all failing and none of their people running the machines (high corruption, nepotism) were smart enough to invent them (low child investment), so cannot fix it. Corrupt societies deserve to suffer and die. Evolution is social as much as genetic. = epigenome
TLDR: With debt bubbles as with population bubbles. It’s the same bubble. Malthus wins.
While K-types look foolish during good times, they lose the least (high child investment pays off) when times get tough and due to high group loyalty, fare better against challenges by more r-groups. Ks have the steadier gene = winning. You don’t buy a Ferrari on credit to compete with your neighbour, you wait for his to get repossessed.
See: Skyscraper Index. Recently: Asian.
This low load of mutations and high fertility into the modern era, suggests Neanderthals were the same race, and they’re trying to report the finding without admitting this. Curse the editors.
nb I wonder whether the RNA trial mutants will be having fertility problems with their own, or only with the rest of us. Speciation is epigenetic.
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.
Results: The analysis included approximately 1.6 million live births and 1749 stillbirths. In the unadjusted model, compared with two white parents, black/black and black/white couples had a significantly higher risk of fetal death. When all demographic, social, biological, genetic, congenital, and procedural risk factors except gestational age and birth weight were included, the odds ratios (OR) were all still significant.Black/black couples had the highest level of risk (OR 2.11, CI 1.77-2.51), followed by black mother/white father couples (OR 2.01, CI 1.16-3.48), and white mother/black father couples (OR 1.84, CI 1.33-2.54). Virtually all of the higher risk of fetal death was explainable by higher rates of low birth weight and prematurity.
Conclusions: Mixed race black and white couples face higher odds of prematurity and low birth weight, which appear to contribute to the substantially higher demonstrated risk for stillbirth. There are likely additional unmeasured factors that influence birth outcomes for mixed race couples.
53,293 deliveries occurred during the time period, of which 329 resulted in a stillbirth (6.2 per 1,000 births). Compared to White women, non-White ethnicity was associated with a doubling of the odds of stillbirth (aOR for Black women 2.15, 95% CI 1.56-2.97; and for South Asian women 2.33, 95% CI 1.42-3.83).
Obese women had a trend towards higher odds of stillbirth compared to women of recommended BMI (aOR 1.38, 95% CI 0.98-1.96), though this was not significant (p 0.07). < aka no excuse there
Both higher parity (≥2 compared to para 1) and hypertension were associated with a higher odds of stillbirth (parity ≥2 aOR 1.65, 95% CI 1.13-2.39; hypertension aOR 1.84, 95% CI 1.22-2.78) but there was no evidence that area deprivation or maternal age were independently associated with stillbirth in this population. < aka no excuse there either
There was some evidence of effect modification between ethnicity and obesity (p value for interaction 0.06), with obesity a particularly strong risk factor for stillbirth in South Asian women (aOR 4.64, 95% CI 1.84-11.70).
“There was a high prevalence of stillbirth in this multi-ethnic urban population. The increased risk of stillbirth observed in non-White women remains after adjusting for other factors.
Our finding of possible effect modification between ethnicity and obesity suggests that further research should be conducted in order to improve understanding of the interplay between ethnicity, obesity and stillbirth.”
but you just said obesity was non-sig?
And the only reason to do so has now gone.
“How is it that minority infants are still unhealthy if their parents are smoking less than White parents? This is probably due to genetics and environment as well. A Dutch study compared the various rates of smoking among different ethnicities/races, “Since maternal smoking during pregnancy is quite equally distributed among the ethnic populations, it does not contribute much to the observed differences in birthweight.”(34) That study compared native Dutch people and immigrants…..”
“….As one can see, the amount of stillbirths was higher for the interracial couples. This was especially true of White father/Black mother relationships, but the White mother/Black father rates were still far worse than the rates of stillbirth for White couples. The outcomes for mulatto infants was at the detriment of the surveyed White population.(10)
What are the specifics to this horrible process? For this, we have to understand that having mixed genetic ancestry through mtDNA and yDNA perpetuates this happening. Let’s look at one of the best studies that has been published on this subject: “Divergent Patterns of Mitochondrial and Nuclear Ancestry Are Associated with the Risk for Preterm Birth.” This study investigated the unusually high rates of preterm birth among African Americans: “Haplogroup-defining polymorphisms are not merely markers of ancestry, and have consequences for mitochondrial function, including the regulation of mitochondrial gene expression.”(20)
Some might be surprised to know that many African Americans have large amounts of European ancestry. The European ancestry that African Americans have was distributed from White males when slavery was still legal.(20) To put it another way, having ancestry from vastly different ancestors contributes to these genetic predispositions. It is necessary to demonstrate this with a principal component analysis. The turquoise dots below represent the African population. As one can see, the African American population is represented by a long cline between European American (CEU) and African (YRI) samples. (24)
The majority of mitochondrial haplogroups (mtDNA) that African Americans have are African, since these come from African women originally, “… individuals with L, U6, or U5b1 haplogroup mtDNA and primarily African nuclear ancestry were defined as having low levels of divergent ancestry, whereas individuals with non-African haplogroups and high degrees of African nuclear ancestry had high levels of divergent ancestry.”(20) These researchers looked at any potential confounding variables that would skew results for the African American population. They examined a number socioeconomic variables such as years of school taken, income, etc. According to the researchers, “There was no detected statistical association between divergent ancestry and any of these factors.” (21)”
“But White people aren’t marrying out as much as other ethnic groups. Therefore, in the rare instance that a White person has a non-White partner, it is unlikely that these interracial couples are being treated in a less-preferable way by their families:
“…Whites are somewhat less willing to marry and bear children interracially than to date interracially. These attitudes and behaviors are related to warmth toward racial outgroups, political conservatism, age, gender, education, and region. Third, White women are likely to approve of interracial relationships for others but not themselves, while White men express more willingness to engage in such relationships personally, particularly with Asians.
However, neither White men nor White women are very likely to actually engage in interracial relationships. Thus, positive global attitudes toward interracial relationships do not translate into high rates of actual interracial cohabitation or marriage despite the fact that most White Americans (especially White females) aren’t interested in being in a relationship with a non-White person.” (5)
In fact, different races/ethnicities do not experience the same amount of stress while they are in an interracial relationship. And this spans across different age groups, “The negative effects of interracial dating hold similarly for boys and girls and among White and Black youth. Interracial dating less negatively effects the depressive symptomatology of Hispanics, though, and actually appears to ‘protect’ Asian youth from depressive symptoms.”(9) Additionally, White women seem to get extremely stressed from being in a relationship between either Hispanic or Black males. Blacks in those relationships aren’t affected by stress in those relationships:”
“…Furthermore, non-Hispanic whites with non-Hispanic black spouses also fare worse than their interracially married peers with Hispanic spouses. In contrast, the self-reported health of married non-Hispanic blacks shows no significant difference between the interracially and the endogamously married.”(10)”
“Where this stress is coming from is another important aspect to consider: Even if there was a trend of neglect for interracial families/pregnancies, it would only be because of the natural inclination to find these relationships unacceptable, “Bias against interracial romance is correlated with self-reported feelings of disgust”. (12)This phenomenon can be observed via brain scans. There is an intense neural mechanism that is triggered when a person observes interracial couples,“Interracial couples elicit a neural disgust response among observers — as indicated by increased insula activation.”(12)In this case, this psychological disgust could be considered an extension of ethnic nepotism or association; if people are disgusted by these relationships it would imply that being involved with an individual of an out-group is not beneficial to the in-group. Because the effects of race mixing create unhealtheir children, this natural disgust is moral. And as I have shown above, the most distinctive evidence proves this.”
At a neurological level, they’re viewed as animals, as sub-human, and even babies perceive race and avoid the out-group.
“That indicates that viewing images of interracial couples evokes disgust at a neural level,” Skinner said.
Participants were quicker to associate interracial couples with non-human animals and same-race couples with humans. That suggests that interracial couples are more likely to be dehumanized than same-race couples, the researchers write, and previous studies have shown that people tend to exhibit more antisocial behavior and are more likely to use aggression and even violence toward dehumanized targets.”
Nobody is jealous. Are we also jealous of the dirty toilets used in the study? Anyone can trade down. It isn’t hard. Black women trading down to omega white men is still a trade down. Race-mixers are always omegas.
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.”
The KA woman’s face did not fit the neoclassical facial canons. Compared with NAW women, 24 of the 26 facial measurements in KA women were significantly different. Only 9 of the 26 facial measurements were significantly different when the attractive KA women were compared with the NAW women. [surgery??] Nine of the 17 nonsignificant facial measurements were very similar to those of the NAW women; many of these facial features centered around the midface.
Although the average KA woman’s facial anthropometric measurements were very different from those of the NAW woman, attractive KA women reflected many of the facial features of NAW women. These findings support the need for ethnically sensitive facial canons and further research into transcultural aesthetics.
Facial beauty arises from symmetric, balanced, and harmonious proportions. Reestablishment of facial harmony requires restoration of proportional facial structures and elimination of disproportionate relationships. The optimal relationships between facial structures are used to assess the face during aesthetic and reconstructive consultations.
Although facial analysis and proportions are well discussed in whites1-3 and African Americans,4-7 only a limited number of studies exist for Asians,8-11 and none exist for Asian Americans. Aesthetic surgery on Asian American patients relying on white norms may result in dissonant facial proportions. Furthermore, many Asian Americans seek to maintain their ethnicity through cosmetic procedures. The challenge for surgeons is to maintain appropriate ethnic facial features and correct only the features that are disproportionate to the rest of the face.
As illustrated by the work of artists and anatomists of the 17th to the 19th centuries, the concept of beauty and “normal” facial proportions has changed with time. [nope?] Furthermore, as the population becomes more heterogeneous, new facial proportions have emerged from interracial mixing. It is now apparent that what has been considered beautiful and acceptable as the norm for one culture may be different for another. Inherently, the notion of a single aesthetic standard and beauty is grossly inadequate and naïve. What is required is a new model of aesthetic standards and beauty that is unique to different ethnic groups to better fit their facial skeletal and skin profile and culture.
[diluting a standard is no standard? ego stroking won’t affect beauty!]
This study assesses the differences in facial proportions between Korean American (KA) women and North American white (NAW) women, and it also describes aesthetic facial features in the typical KA woman. The quantitative determinations will be useful in preoperative and postoperative facial assessment for cosmetic and reconstructive purposes.
[there it is]
Clearly I’m imagining this, right?
“There are inherent problems associated with applying outdated artists’ impressions of beauty to modern facial analysis and surgery. The subjects used in formulating the neoclassical paradigm were exclusively white.”
“cardiometabolic clinical correlates related to total testosterone (TT), free testosterone (fT), androstenedione (ASD), dehydroepiandrosterone-sulfate (DHEAS), estrone (E1), estradiol (E2), and sex hormone-binding globulin (SHBG).
Results: Waist circumference and BMI (β-coefficient: -0.03; 95% CI: -0.04; 0.03) were inversely related to SHBG, and BMI was positively related to TT (β-coefficient: 0.005; 95% CI: 0.001; 0.009), fT, E1, and E2. Smoking was positively related to TT (β-coefficient: 0.04; 95% CI: 0.01; 0.06), ASD, and fT. Systolic blood pressure (TT: β-coefficient: 0.002; 95% CI: 0.001; 0.003), hypertension (TT: β-coefficient: 0.05; 95% CI: 0.003; 0.11), low-density lipoprotein (LDL) cholesterol (TT: β-coefficient: 0.02; 95% CI: 0.01; 0.05), and total cholesterol (TT: β-coefficient: -0.03; 95% CI: 0.01; 0.05) were positively related to TT and ASD. Finally, type 2 diabetes mellitus (T2DM), and metabolic syndrome (MetS) were positively related to fT, but inversely related to SHBG.
Conclusions: Our population-based study, with sex hormone concentrations measured by liquid chromatography tandem mass spectrometry, revealed associations between clinical correlates including waist circumference, smoking, cohabitation, systolic blood pressure, cholesterol, and MetS with sex hormones. Thus, sex hormones and SHBG may play a role in the cardiovascular risk profile of women.”
Both obesity and anxiety symptomatology were separately associated with the same sex hormone alteration in premenopausal women: higher total testosterone level (0.97 ± 0.50 in obese vs. 0.86 ± 0.49 nmol/L in normal-weight women, p = 0.026 and 1.04 ± 0.59 in women with vs. 0.88 ± 0.49 nmol/L in women without anxiety symptomatology, p = 0.023). However, women with anxiety symptomatology had non-significantly higher estradiol levels than women without anxiety symptomatology (548.0 ± 507.6 vs. 426.2 ± 474.0 pmol/L), whereas obesity was associated with lower estradiol levels compared with those in normal-weight group (332.7 ± 386.5 vs. 470.8 ± 616.0 pmol/L). Women with anxiety symptomatology had also significantly higher testosterone and estradiol composition (p = 0.006). No associations of sex hormone levels and BMI with anxiety symptomatology in postmenopausal women were found.
Conclusions: Although both obesity and anxiety symptomatology were separately associated with higher testosterone level, there was an opposite impact of anxiety and obesity on estradiol levels in premenopausal women. We did not find an evidence that the sex hormone alterations related to obesity are playing a significant role in anxiety symptomatology in premenopausal women. This could be the explanation why we did not find an association between obesity and anxiety. In postmenopausal women, other mechanisms seem to work than in the premenopausal group.
Regional fat distribution (RFD) has been associated with metabolic derangements in populations with obesity. For example, upper body fat patterning is associated with higher levels of free testosterone (FT) and lower levels of sex-hormone binding globulin (SHBG). We sought to determine the extent to which this relationship was true in a healthy (i.e., non-obese) female population and whether RFD influenced androgen responses to resistance exercise. This study examined the effects of RFD on total testosterone (TT), FT, and SHBG responses to an acute resistance exercise test (ARET) among 47 women (22+/-3 years; 165+/-6 cm; 62+/-8 kg; 25+/-5%BF; 23+/-3 BMI). RFD was characterized by 3 separate indices: waist-to-hip ratio (WHR), ratio of upper arm fat to mid-thigh fat assessed with magnetic resonance imaging (MRI ratio), and ratio of subscapular to triceps ratio (SB/TRi ratio). Skinfolds were measured for the triceps, chest, subscapular, mid-axillary, suprailaic, abdomen, and thigh regions. The ARET consisted of 6 sets of 10 RM squats separated by 2-min rest periods. Blood was obtained pre- and post- ARET. TT, FT, and SHBG concentrations were determined by radioimmunoassay. Subjects were divided into tertiles from the indices of RFD, and statistical analyses were performed by an ANOVA with repeated measures (RFD and exercise as main effects). Significant (p < or = .05) increases following the AHRET were observed for TT (approximately 25%), FT (approximately 25%), and SHBG (4%). With multiple regression analysis, anthropometric measures significantly predicted pre- concentrations of FT, post-concentrations of TT, and pre-concentrations of SHBG. The SB/TRi and MRI ratios but not the WHR, were discriminant for hormonal concentrations among the tertiles. In young, healthy women, resistance exercise can induce transient increases in testosterone, and anthropometric markers of adiposity correlate with testosterone concentrations.
So exercise will boost a woman’s natural T. If they already have high T….
If their BMI is higher for their size, they already have high T comparatively. If they already have it racially… probably not good.
Compared to the decline in E2 concentrations, androgen concentrations declined minimally over the MT. T (β 9.180, p < 0.0001) and E1 (β 11.365, p < 0.0001) were higher in Whites than in AAs, while elevations in DHEAS (β 28.80, p = 0.061) and A4 (β 0.2556, p = 0.052) were borderline. Log-transformed E2 was similar between Whites and AAs (β 0.0764, p = 0.272). Body mass index (BMI) was not significantly associated with concentrations of androgens or E1 over time.
so black and white is off the hook
This report suggests that the declines in E2 during the 4 years before and after the FMP are accompanied by minimal changes in DHEAS, A4, T, and E1. There are modest differences between Whites and AAs and minimal differences by BMI.
During a median follow up of 6.3 years, 45 patients relapsed. Testosterone levels significantly increased across BMI categories (p = 0.001). Both circulating testosterone and BMI were positively associated with disease free survival (p = 0.005 and p = 0.021, respectively). A significant interaction was found between testosterone and BMI (p = 0.006). For normal-weight women, testosterone concentration around median (0.403 ng/mL) or third quartile (0.532 ng/mL) showed a high significant HR of relapse (5.52; 95% CI:1.65–18.49 and 4.55; 95% CI:1.09–18.98, respectively). Overweight patients showed increased HR at increasing testosterone levels, reaching a significant high HR (4.68; 95% CI:1.39–15.70) for testosterone values of 0.782 ng/mL (95th percentile). For obese patients HR decreased (not significantly) at increased testosterone concentrations, explaining the interaction between testosterone levels and BMI categories.
In ER-positive postmenopausal breast cancer patients, high testosterone levels are associated with worse prognosis in normal-weight and overweight women, whereas in obese seems to be associated with a better outcome. Although the results require further validation, they suggest that assessment of circulating testosterone and BMI could help to identify postmenopausal ER-positive patients at higher risk of relapse and potentially open new therapeutic strategies.
High T isn’t good, even in normal weight women. Water is wet.
“The findings of this study suggest high plasma levels of testosterone could play a role in the pathogenesis of type 2 diabetes among women,” Jon Jarløv Rasmussen, MD, PhD, a specialist registrar and postdoctoral researcher in the department of endocrinology at Rigshospitalet in Copenhagen, Denmark, told Healio. “The incidence of type 2 diabetes was rather low in the study, but the results implicate that screening for type 2 diabetes among women with higher plasma levels of testosterone may be beneficial, even among women who are young and without established comorbidities, such as polycystic ovary syndrome.”
In a retrospective study, Rasmussen and colleagues analyzed data from 8,876 healthy women (mean age, 38.5 years) who provided blood samples to measure plasma testosterone, dehydroepiandrosterone-sulfate (DHEAS), dihydrotestosterone (DHT) and sex hormone-binding globulin (SHBG) between January 2007 and December 2015. Researchers analyzed androgens using tandem liquid-chromatography mass spectrometry. Researchers used Poisson regression models to calculate incidence rate ratios for developing type 2 diabetes during a median follow-up of 8.1 years, stratified by androgen quartiles.
‘Normal weight’ women can get Type 2. Since Asians have higher T from higher BMI (against the white norm), they’ll be more likely to get it. This also explains the gestational diabetes common in Asian women, especially if the baby is mixed.
Nationwide, as many as 1 in 4 people who have diabetes don’t know they have it. But for Asian Americans, that number is much higher—1 in 2, the highest of all ethnic/racial groups. Why aren’t more getting diagnosed?
Weebs do not mention this. If your apparent rationale for avoiding fat white women is avoiding the Diabeetus genes, Asian is then categorically the worst racial group to mix with.
1 in 2, flip a coin, rice cooker.
I bet it’s higher in the women due to sweet tooth, so likely worse.
But people of Asian descent have less muscle and more fat than other groups and often develop diabetes at a younger age and lower weight. That extra body fat tends to be in the belly (visceral fat). This isn’t the “inch you can pinch,” the fat stored just under the skin. Visceral fat is out of sight, wrapped around organs deep in the body. You can’t tell how much visceral fat someone has by looking at them.
I didn’t call them skinny-fat to be mean, they really are!
Visceral fat is also sometimes known as “active” fat because it drives certain processes in the body that can increase the risk for heart disease, stroke, and other serious health conditions. Everybody has some visceral fat, but having too much is a major risk factor for developing type 2 diabetes.
….But BMI doesn’t catch Asian Americans in the normal weight range (18.5 to 24.9) who may very well have too much visceral fat and be at risk for type 2 diabetes. Researchers are now suggesting that people of Asian heritage get tested if their BMI is 23 or greater. Type 2 diabetes can be prevented or delayed, but only if people know they’re at risk and can take action!
They need a totally different (lower) testing standard, but they’re just like us, guys! Nay, SUPERIOR!
The same volume food in a smaller body, this isn’t hard to figure out. They’re not white women, eating like us makes them FAT.
Pregnant South Asian women carry a higher risk for developing gestational diabetes, a condition that’s dangerous for both mother and child. Between 2 and 10 percent of all pregnancies each year are complicated by gestational diabetes
2-10% in which demographic? Sounds like all? I bet it’s higher in certain ones, isn’t it?
Under risk factors is basically – be non-white
Being of Hispanic, Native American, African-American, Asian-American or Pacific Islander descent.
Women who have had gestational diabetes have a 20 to 50 percent chance of developing diabetes in the 5 to 10 years following pregnancy.
Our data indicate that although the historical or clinical risk factors for GDM are valid in Asians, using risk factors alone to select such patients for testing for GDM is inadequate. Many Asian women who develop GDM have no risk factors at all.
When Natural Selection hates you so much… maybe give it up?
r-types have higher numbers of issues like this, that would be fatal under natural law
They don’t ‘choose’ to stop at 1-2 kids, it isn’t ‘culture’, it’s fear (see below).
To avoid overlooking significant numbers of women with GDM, one may lower the specificity of the criteria, but this requires that the majority of patients be tested.
wow, that bad
Logistically, it is much simpler to conduct universal screening for all Asian women in Western countries, rather than to apply selective testing in order to spare a small percentage of women from being tested. Therefore, our findings strongly support recommendations for universal screening for GDM in pregnant women of Asian origin in Western countries. However, in places where the incidence of GDM is low, such as in some developing countries, the selection of patients for testing by the risk factors may be reasonable.
Introduction:Asian women have a higher prevalence of gestational diabetes mellitus than women of other races/ethnicities. We aimed to compare the prevalence of gestational diabetes among Asian American women to other racial/ethnic groups and explore whether the higher occurrence of the disorder among Asian women can be explained by acculturation.
Clearly I am making this all up to feel better, right guys?
Among the 5,562 women studied, the weighted prevalence of gestational diabetes was 15.5% among Asian American women, followed by 9.0% among non-Hispanic black women, 10.7% among Hispanic women, and 7.9% among non-Hispanic white women.
15.5% v. 7.9%
Diabetes at DOUBLE the rate of whites!
but they’re just like us
2.44x the risk
and that’s controlled, independently
Compared with non-Hispanic white women, Asian women had 2.44 (95% confidence interval [CI], 1.81–3.29; P < .001) times the odds of having gestational diabetes, independent of maternal age, education, marital status, income, prenatal care adequacy, prepregnancy BMI, and physical activity. Acculturation was negatively associated with having gestational diabetes (odds ratio [OR] = 0.93; 95% CI, 0.86–0.99) and explained 15.9% (95% CI, 11.38%–25.08%; P < .001) of the association between Asian race and the condition.
About 85% genetic. Great odds.
We found that Asian race was an independent risk factor for gestational diabetes, and higher acculturation may play a protective role against it in Asian American women.
What is already known about this topic?
Asian women have a higher prevalence of gestational diabetes mellitus than women of other races. However, little data exist on why prevalence is highest among Asian women.
I sense genetics.
If they’re having unnatural babies (too large for their race, mixed) supported by modern medicine, they’d be more likely to die anyway, right? Medicine can only do so much. Weaker genes die a la Darwin.
The biggest r-select factor would be risk of death while breeding, that would be the surest thing. The genes trying to extinct themselves.
Does this data exist? Also for the neonates?
YOU BET IT DOES.
Let’s see the weebs explain away these studies. They’ll probably just ignore me… again.
Pregnancy related mortality can be defined as death of the mother during pregnancy, delivery, or within one year postpartum. While 700 pregnancy-related deaths occur each year, 2/3 of these deaths are considered to be preventable.
Modern medicine, dysgenic again.
Overall pregnancy related mortality in the United States occurs at an average rate of 17.2 deaths per 100,000 live births. However, that number jumps to 43.5/100,000 for non-Hispanic Black women and decreases to 12.7/100,000 for non-Hispanic white women and 11/100,000 for Hispanic women.
No data listed for Asian, odd?
For mothers of all backgrounds, leading causes of death include cardiovascular conditions, hemorrhage, and infection. However, for non-Hispanic Black women, leading causes of death include cardiovascular conditions in addition to cardiomyopathy, pre-eclampsia, and eclampsia (hypertensive disorders).
Non-Hispanic Black women are also significantly more likely to have a severe maternal morbidity (SMM) event at the time of delivery. For every maternal death there are 70 cases of SMM events that are considered “near misses.” These events can have long-term or short-term consequences to a woman’s health. Over the past 20 years, cases of SMM have increased by over 200%, while cases disproportionately affect Black women. One study found Black women experienced SMM at a rate 2.1 times greater than that of white women.
To better understand and address these disparities, researchers suggest providers increase screening for social determinants of health. Levels of stress, trauma, food insecurity, neighborhood violence, and access to prenatal care are all factors that may contribute to the disparities and warrant further investigation.
Although most maternal deaths result from cardiovascular and hypertensive disorders, researchers found Asian/Pacific Island women exhibit the highest prevalence of gestational diabetes, which can increase pregnancy complications, at 14.8%.
One study presented in the session focused on behavioral interventions and protective factors among women with gestational diabetes. A Kaiser Permanente analysis of women in northern California found Black women have a lower prevalence of gestational diabetes when compared with Asian Indian, Filipina, Southeast Asian and Chinese women. White women had the lowest rates of the disease overall.
Screening for postpartum diabetes is recommended to all women within 4 to 12 weeks postpartum. However, rates of screening vary among women with different racial and ethnic backgrounds, suggesting tailored strategies to reduce risk and improve healthcare behaviors may be effective.
Racial medicine, openly.
An additional study explored how racial and ethnic disparities impact severe neonatal morbidities, specifically among very preterm children (born <32 weeks of gestation). Preterm birth has been associated with several health conditions developing later in life, including diabetes.
Presenter Teresa Janevic, PhD, defined race as “linked to phenotype and /or ancestry that indexes one’s location on the US social hierarchy of socially constructed groupings (i.e., races) that has been based primarily on skin color.”
genes aren’t social
Africans in Africa also have the same ‘risk’ as one in America. No magic dirt.
In contrast, Janevic defined ethnicity as “tied to race and used both to distinguish diverse populations and to establish personal or group identity, usually based on shared culture or beliefs.”
Culture? Belief? Believe your way out of diabetes. I’ll wait.
In a population-based retrospective cohort analysis using hospital discharge data linked with vital statistics at birth and death records, researchers determined Black infants were at the highest risk of dying within less than 28 days after discharge, or suffering neonatal morbidities in the time between birth and discharge. Black infants were followed by Hispanic infants, while white and Asian infants had similar low risks.
We’ll see about that.
Of the 39 New York City hospitals included in the study, researchers found a 6-fold difference in risk of combined mortality and morbidity outcomes. “Black infants were at twice the risk of being at a hospital that has risk-adjusted high rates of combined mortality and morbidity,” Janevic noted, while Hispanic infants had a 1.5 increased risk to receive care from one of these hospitals. “Hospital quality where women of color deliver likely contributes to these disparities,” she concluded.
Like schools, it depends on the IQ of the people working there.
Another investigation detailed how environmental factors and population level exposures impact disparities in preterm birth and infant mortality. “Non-Hispanic Black infants compared with non-Hispanic white infants have twice the risk of death in the first year,” explained presenter Heather Burris, MD. “This is particularly striking because Black infants just make up 15% of all births in the United States but are counting for 29% of all deaths.”
Among causes of infant death, preterm birth and low birth weight related death, along with pregnancy complications, account for the highest racial and ethnic disparities between non-Hispanic Black and white infants. Black infants are also significantly more likely to be born preterm than white infants.
an r-factor unless twins
Researchers note genetics and education level have very little impact in accounting for disparities in preterm birth. Although women with higher education tend to have lower preterm birth rates, Black women who graduated from college have a higher risk of preterm birth than white women who dropped out of high school.
I’m so glad white people already survived multiple genetic purges in our history.
Through analyzing delivery data and creating models based on air pollution severity in Philadelphia, Pennsylvania, investigators discovered air pollution is associated with spontaneous preterm birth. Data also show Black Americans experience consistently higher exposure to air pollutants, measured in fine particulate matter (PM)2.5.
An additional analysis between preterm birth and nationwide neighborhood deprivation index (encompassing income below the poverty level, vacant homes, education levels, among other factors) found that Black women experience neighborhood deprivation exposure at almost 2 standard deviations (SDs) higher than white women in Philadelphia.
Overall, Black women are 4 times more likely to live in a neighborhood with high violent crime and high air pollution than white women. “When we look at preterm birthweights, we can see that it is women living in these high-high neighborhoods that have the highest risk of preterm birth,” Burris said. However, these associations were consistent regardless of race.
They gestate for less time than whites, this is known. Africans in Africa do it.
Now we’ve established some things. An r-study in Asian women.
Increased Perinatal Morbidity and Mortality Among Asian American and Pacific Islander Women in the United States
Background: Asian American/Pacific Islanders (AAPIs) are the fastest-growing racial group in the United States.
America is now owned by Asia, demographically.
Despite a higher socioeconomic status, AAPI women experience higher rates of maternal morbidity and mortality.
can’t pay your way out of r-genes
if controlled for SES, aka $, their data would be even worse
Methods: Using the National Inpatient Sample, we performed a retrospective cohort analysis of women who were hospitalized for delivery from 2002 to 2013. The primary outcome variable was inpatient mortality rate, and the presence of severe maternal morbidities was estimated using the Bateman Comorbidity Index, a validated tool for predicting obstetric morbidity.
Results: AAPI women presenting for delivery between 2003 and 2012 were older, more likely to reside in a zip code in the top quartile of annual income, be privately insured than Caucasian women,
where’s Asian privilege?
and less likely to have a higher Bateman Comorbidity Index. However, AAPI women had a higher likelihood of postpartum hemorrhage (3.4% vs 2.7%, P < .001), uterine atony, severe perineal lacerations, and severe maternal morbidities. Procedures such as transfusion, hysterectomy,
So they could have one kid and die, have one kid and have that die, OR have one kid and then their organs all removed – so no more kids?
Yes clearly our biological superiors, right weebs? Totally not rationalising a fetish, are we?
I wonder why one child was law? They don’t have a culture of many kids because they’re too r-select to survive without modern medicine. Wake up. They pretend 1-2 is a choice and that’s why they mock and envy large white families (3+ standard) like the Amish. They envy us that ability. They would die.
and mechanical ventilation were also more common in AAPI women.
Calling it – Mother Nature is anti-Asian.
Furthermore, AAPI women had a higher mortality rate that persisted despite adjustment for an apparently higher income and comorbidities (odds ratio 1.72, 95% confidence interval: 1.14-2.59, P = .01).
Conclusions: Despite having a higher socioeconomic status, AAPI women had higher rates of maternal mortality during hospitalization for delivery. This increase persisted even after adjustment for factors known to affect peripartum outcomes. Further investigation is needed to better clarify the causes of racial differences in maternal morbidity and mortality.
Results: A total of 360,370 women with postpartum hemorrhage from 2012 to 2014 were included in this analysis. Risk for severe morbidity was significantly higher among non-Hispanic black women (26.6%) than non-Hispanic white, Hispanic, or Asian or Pacific Islander women (20.7%, 22.5%, and 21.4%, respectively, P < .01).
The white is 20%, Asian is 21%.
And these are the fattest white people, like, ever.
White and Asian bolded-
For non-Hispanic black compared with non-Hispanic white, Hispanic, and Asian or Pacific Islander women risk was higher for disseminated intravascular coagulation (8.4% vs 7.1%, 6.8%, and 6.8%, respectively, P < .01) and transfusion (19.4% vs 13.9%, 16.1%, and 15.8%, respectively, P < .01). Black women were also more likely than non-Hispanic white women to undergo hysterectomy (2.4% vs 1.9%, P < .01), although Asian or Pacific Islander women were at highest risk (2.9%). Adjusting for comorbidity, black women remained at higher risk for severe morbidity (P < .01). Risk for death for non-Hispanic black women was significantly higher than for nonblack women (121.8 per 100,000 deliveries, 95% confidence interval, 94.7-156.8 vs 24.1 per 100,000 deliveries, 95% confidence interval, 19.2-30.2, respectively, P < .01).
The weebs either did 1. no research (typical gammas) or 2. they’re delusional.
Almost double the risk of hysterectomy, roughly.An additional 52% risk over white women, minimum, in just this study.
What’s the point of being married to them, at that point? Their baby machine is broken.
Non-Hispanic black (black) and non-Hispanic American Indian/Alaska Native (AI/AN) women experienced higher PRMRs (40.8 and 29.7, respectively) than all other racial/ethnic populations (white PRMR was 12.7, Asian/ Pacific Islander PRMR was 13.5 and Hispanic PRMR was 11.5). This was 3.2 and 2.3 times higher than the PRMR for white women – and the gap widened among older age groups.
Notably, we found that, when aggregated, the top cause of death among Asian Americans is cancer. However, when disaggregated, there is wide variation in the leading cause of death. For instance, for Asian Indians, nearly twice as many men die of heart disease (31 percent), compared to cancer (18 percent). In contrast, for Koreans, the opposite is true — the death rate for cancer (34 percent) is much higher than the death rate for heart disease (19 percent).
Remember the breast cancer and Asian BMI/testosterone stuff?
Research led by the University of Birmingham has found that increased levels of hormones including testosterone could cause a brain condition that can lead to blindness in women.
We are all jealous of your waifu, yes.
Idiopathic Intracranial Hypertension—also known as IIH—is caused by high pressure in the brain with consequences from blindness to incapacitating daily long-term headaches. IIH was originally identified over 100 years ago yet the cause of the condition has remained unknown although there has been much speculation about why more than 95 per cent of total incidence is in women with obesity.
And Asians, they’re 1/2 obese in America!
They then compared the results with the levels observed in women with obesity of the same age and body mass index (BMI), as well as a cohort of women with polycystic ovary syndrome (PCOS).
PCOS is far more common in Asians. Look it up.
Most notable were the high levels of the androgen ‘testosterone’ found in the blood in IIH women. Crucially, levels of androgens were uniquely increased in the brain fluid (CSF) of women with IIH. When the researchers, analysed human choroidal plexus tissue, which is the site in the brain where CSF is produced, they confirmed that androgens could increase the rate of CSF secretion, a potential driver for increased brain pressure.
Results: We found that the South Asian women presented at a younger age for the management of sub-fertility. An extended stimulation phase and Caucasian ethnicity showed an inverse correlation with the number of oocytes retrieved in the PCOS subgroup. Caucasian ethnicity was associated with a higher fertilization rate however increase in body mass index (BMI) and the laboratory technique of IVF appeared to have a negative impact on fertilization rates in the PCOS subgroup. Commencing down regulation on day 1 of the cycles was negatively associated with fertilization rates in the tubal group. In terms of clinical pregnancy rates, the Caucasian PCOS had a 2.5 times (95% CI: 1.25-5) higher chance of an ongoing clinical pregnancy as compared with their Asian counterpart. Also, a unit increase in the basal FSH concentration reduced the odds of pregnancy by 18.6% (95% CI: 1.8-32.6%) in the PCOS group.
Conclusions: The Asian PCOS have a greater sensitivity to gonadotropin stimulation with lower fertilization and ongoing clinical pregnancy rates as compared with their Caucasian counterparts.
The ethnicity of women undergoing fertility treatments like IVF can affect the rate of successful live births, according to new research. After adjusting for certain factors including age of patient at time of treatment, cause of female or male infertility, and type of treatment, 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.
White women, still winning. Thank God for the Ice Age.
Overall, studies have shown higher testosterone levels in women and lower levels in men are related to incident diabetes. The major risk factors contributing to diabetes are biochemical, environmental, sedentary lifestyle, socioeconomic status and genetic factors. All of them together or independently are responsible for the development of the DM.  Besides, certain studies show Impaired Glucose Tolerance (IGT) is more common in females than males independent of age. 
We found a high prevalence of GDM among the Asian population. Asian women with common risk factors especially among those with history of previous GDM, congenital anomalies or macrosomia should receive additional attention from physician as high-risk cases for GDM in pregnancy.
Body mass index (BMI) was a very strong negative predictor of body attractiveness ratings, similar to previous findings. Zero-order associations between women’s mean hormone concentrations and mean attractiveness ratings were not significant; however, after controlling for BMI, attractiveness ratings were independently and positively associated with both estradiol and testosterone concentrations. Discussion focuses on the implications of these findings for whether attractiveness assessment mechanisms are specialized for the detection of cues of differential fecundity in young women’s bodies.
High T = ugly!
Did I mention water is wet? Can they seriously accuse of cherry picking? I’m not even looking hard.
Previously covered WHR, use search bar. Asians lose. Even black women do better.
Asians have way more T as a race than Europeans, get over it. Historically, we considered them savages, less civilized, for that reason. How is this surprising? Do you think we colonised India for fun? It’s obvious in the broad manjaws, duh. Marquardt covered this. Anyone can do a replication study, but I suggest you include the women too, so it isn’t just a sexual effect but race.
From a blog “East Asians were found to have the highest average total plasma testosterone (5,673 ρg/mL) followed by Africans (5,442 ρg/mL) and then Europeans (4,992 ρg/mL). Given that the sample size for Africans is smaller (N < 10,000), their relative position may change with more data. Nonetheless, the claim that East Asians have the least testosterone is not supported by scientific data. “
Yeah, fake redpills who think T = manly, good thing. It’s just a hormone.
“There is no way of accurately determining free testosterone. Even if there was, this would also be irrelevant since bio-availability is prime. Since race realists use total serum testosterone, why is this an issue?”
true, it’s just applying the same standard
Culturally, gang rape is more normal in Asia than Africa. This is why. You don’t get African Taharrush, really. Asia has Eve Teasing and the like. Trust me, you don’t want this.
“Mass sexual assault is the collective sexual assault of women, and sometimes children, in public by groups of unrelated men. Typically acting under the protective cover of large gatherings, victims have reported being groped, stripped, beaten, bitten, penetrated and raped.”
As for the contention that there are no studies indicating a 10% difference between East Asians and Europeans, I did find one age controlled study where the Chinese sample had 8.8% more total T, 11.4% more bio-available T and 12% more free T than the European sample. The Japanese sample had 10.5%, 5.1% and 6.7% more than Europeans respectively [Wu et al. 1995]. Wonder if race realists discuss this study, or perhaps they are too busy in celebratory dance around the Korean/Swede campfire?
They’re not really redpill. I believe data even if I dislike it. Asians have high T as a race. Get over it.
High T can also dovetail with lower national IQs e.g. India, so…. why want this? Low IQ nations have more crime.
Additionally, this recent study shows HK Chinese having some 3% more bio-available T than US Europeans.
Lol, he’s right. But T isn’t a good thing. It’s just a hormone, in men or women.
Being a race realists seems to be a length engagement with delusion, fantasy and ‘scientific’ homo-erotica.
Not here, son. I believe the T-data. Penis size generally correlates to racial height (in white men), not really T. Forum bros are wrong again. Penis stuff is sexual selection, aka chosen by women.
There was a similar increase in the positive effect of penis size on attractiveness with a more masculine body shape (i.e., greater shoulder-to-hip ratio). Surprisingly, larger penis size and greater height had almost equivalent positive effects on male attractiveness. Our results support the hypothesis that female mate choice could have driven the evolution of larger penises in humans. More broadly, our results show that precopulatory sexual selection can play a role in the evolution of genital traits.
It was concluded that all penile measurements are interrelated to each other; the height and weight also the other body measurements that are related to the penile measurements in less than 50%. It seems that the penile measurements are polygenic traits and are under multifactorial influences.
There are racial differences in associations of hormone levels with age and BMI in late reproductive age women. Further study is needed to replicate these findings and to determine the relationships of these hormonal associations with menopausal symptoms
Obesity is an important factor in hormone dynamics independent of age, race and smoking in mid-life women, although the mechanisms remain unclear.
From “A Study of the Correlation of Some Sex Hormone with Obesity in Women with Secondary Infertility” (google it)
Infertility is the inability to conceive a child for more than one year. The present study indicates
that the obesity associated with infertility. The aim of the study to determine follicle stimulating
hormone, luteinizing hormone, testosterone hormone and prolactin levels. and cholesterol and
triglyceride concentration in 2nd inferetid women. This study was carried out at kamal al-samaarai
hospital the data were collected from 95 secondary infertilial women were age between 16-45 years old and grouped them in to obese (n = 46) and non obese(n = 49). There was no significant difference between the two groups (p <0.05).Body mass index in Infertile obese women is slightly higher than non obese Infertile women which is statistically significant (P<0.001). However LH,
TSH, cholesterol and triglyceride concentration in obese infertile women is significantly higher than
non obese infertile women (p >0.05).The BMI was correlated positively with triglyceride in obese
group while BMI was positive correlation highly significant with cholesterol in non obese group.
Regression analysis revealed obese to be strongly associated with observed infertility. The elevated
prolactin values in secondary infertile women clearly shows that there is a mechanism operating at
the anterior pituitary level which shows an abnormal distribution of FSH and LH which may further
explain the abnormal delay ovum maturation. This study also indicates obese associated with
infertile more than non obese women.
TLDR Asians carry more fat than whites (in America, at least).
Well yeah, the junk food and spices diet is hell on the hormones too. They evolved for multiple famines (especially the Chinese and Indians) so they tend to weight-gain like that, too. Fat deposition isn’t the same between race (black thighs/’ass’) so why would accumulation patterns and proclivity to gain work like that either?
Results: A convenient sample of 1626 adults with BMIs ≤35 was evaluated. Independent percentage body fat predictor variables in multiple regression models included 1/BMI, sex, age, and ethnic group (R values from 0.74 to 0.92 and SEEs from 2.8 to 5.4% fat). The prediction formulas were then used to prepare provisional healthy percentage body fat ranges based on published BMI limits for underweight (<18.5), overweight (≥25), and obesity (≥30).
Conclusion: This proposed approach and initial findings provide the groundwork and stimulus for establishing international healthy body fat ranges.
But they’re not the same. Bio-logically.
The Asian ‘gym girls’ also trying to pass off the manjaw as ‘gains’ by matching on the stomach and thighs, I’ve seen white lawyer types do the same. Do NOT fall for it, men. If the jaw is square and broad as a child and pre-teen, RUN.
The small, squat (squarish) skeleton and pedomorphic features of the Asian race (historically, accurately called Mongoloid if you can search for it in anthropology) already pre-dispose their young people (teens) to lower BMI anyway, so the ‘losing weight’ excuse is bullshit, they’re building muscle to match the jaw and trap some sucker with their high T and bad temper. This lower BMI is not a consequence of health (dietary or genetic) so compared to the unhealthiest white people EVER (sorry America) they still have higher BMIs. HOW.
White women have a naturally high BMI (taller, curves) so it’s actually worse than it looks. The effect is maintained in every age group, how can one fuck up age 20? Any 20yo complaining about their metabolism needs a slap. The fat Asian hypothesis also holds true within the race, compared the Asian men to women matching age.
IF ONLY THE MANOSPHERE ACTUALLY READ THE DATA.
Every other claim about Asians it’s like  yet when I go to look…. they lied.
I expected the one claim the weebs consistently made about Asians in America (being thin) must be true but … no.
18.5 is a terrible BMI cut-off because it includes anorexics, smokers, druggies and petite women all in one. Women look wildly different at low and too-low body fats, which also varies by race. At the same BMI, Asians look more husky because the skeleton is squared-off. They’re also likelier to lay down fat than muscle.
The Asians are larger than white women pre-menopause, what EXCUSE is there?
The only time whites actually have slightly higher BMIs (ever so slightly) is in the elderly range (60-79, at which point yeah you’re excused, you can go).
I’m seeing through the model minority propaganda and there’s nothing to it. Rule #1 of moving to America – DON’T GET FAT. YOU HAD ONE JOB.
“In contrast, models for Asians predicted a different percentage body fat from that predicted for African Americans and whites. “
That’s code for ‘they evolved so much for famine that we had to invent new maths to count it’.
“For example, Deurenberg et al (35) found that American blacks had a 1.3-unit lower and Polynesians a 4.5-unit higher BMI than whites with the same body fatness (35). Even within the white cohort, the investigators observed small differences between Americans and Europeans.”
Asian placement is denser. Squat Mongoloid skeleton, anthropologically. If you disagree, it’s cope.
Americans are mixed white, generally, that’s why. German/French hybrids and other nonsense. You lose adaptive advantage from your subrace too.
They studied one of the thinnest types of Asians (japs) so I guarantee you others would be worse.
“The underlying causes of ethnic variation in relations between BMI and percentage body fat are likely due to small between-center body fat measurement differences and biological between-group differences (35).”
“The evaluation of Asians was confined to Japan and that of African Americans to the United States. Therefore, the underlying causes of observed ethnic differences in terms of measurement, environmental, and genetic factors are difficult to ascertain. Nevertheless, it appears evident that a single set of universal percentage body fat ranges cannot be easily developed without considerable additional analysis of this problem. Our equations and associated tables provide several ethnic-specific ranges as working guidelines. Because African Americans and whites differed only slightly in percentage body fat (by 1–2%) after BMI was first controlled for, we presented a combined equation (Equation 5) and table (Table 4) based on 4C percentage body fat for these 2 groups.”
That’s right, our fat deposition is more alike blacks than Asians. That’s how different the races are.
Background: Asians who have a healthy body mass index (BMI) range have been observed to have higher levels of obesity and risk of cardiovascular disease than whites, which suggests that the relation between BMI and adiposity may be different for Asians.
Objective: The primary aim of this study was to investigate the influence of childhood and adolescent exposure to a westernized environment on the relation between BMI and percentage body fat in young Asian American women.
So no, this isn’t their age. No cope here son.
Design: Secondary data from 129 Asian women, aged 20–25 y, with variable lengths of residence in the United States and 327 white women of comparable ages who had participated in the Latina and Asian Bone Health Study (1999–2000) and the Berkeley Bone Health Study (1998–2000), respectively, were analyzed by using multiple linear regression with percentage body fat as the outcome variable and place of birth, ethnicity, length of US residency, and BMI as predictor variables.
Results: Asians who lived in the United States <12 y showed the same relation between BMI and percentage body fat as did whites. In contrast, Asians who had lived in the United States ≥12 y had higher percentage body fat than did whites for BMIs (in kg/m2) <20.5 and lower percentage body fat for BMIs in the overweight and obese range.
Responding to the same stimuli wildly differently > genetic!
They’re more likely skinny-fat, aka fatal fat.
Whites evolved to eat Roman grains like processed wheat.
Conclusions: Our findings suggest that childhood environments may influence the relation between BMI and adiposity. Research is warranted on the role that childhood environments play in the accumulation and distribution of body fat and hence metabolic disease risk later in life.
There’s still a huge difference in the same environment.
Asians with more years in the United States had higher mean percentage body fat than did whites at low BMIs and lower mean percentage body fat at high BMIs with the regression lines intersecting at BMI ≈20.5 and body fat of 26.5%.
Again, Magic Dirt isn’t real. Enjoy your BBW Ting Tong for your golden years.
We are supremely jealous.
Asian-immigrant adults who were living in North America were observed to have higher adiposity levels
at the same BMI level than did whites (6). However, most of the Asian-immigrant adults studied were raised outside of North America. To our knowledge, our study was among the first studies to observe a difference in how BMI relates to percentage body fat between Asian Americans who had spent more years of childhood in the United States compared with Asian Americans who were minimally exposed to the United States during childhood and adolescence.
Lesson for weebs – do NOT move the Thai bride to America.
Stay in Asia or do NOT bother. She WILL get fat. You have been warned.
American-born Asians had a higher percentage of mothers with college degrees (59% of mothers compared with 37% of mothers in foreign-born Asians and 32% of mothers in whites).
Fat SJWs, great catch!
in our study, which suggested that obesity rates in our sample of Asians were likely lower than in the general population.
They admit it.
Is the general observation that, at the same BMI level, Asians have higher total body fat and visceral fat and higher risk of cardiovascular disease risk than do whites applicable to Asians in general,
or is this observation applicable only to Asians living in Asian societies? If the latter, does the environment during early life influence how body fat accumulates and distributes and, therefore, affects the relation between BMI and body fat? How strong a predictor of child growth and body composition is socioeconomic background and, in particular, the mother’s education? Are our findings also applicable to men?
We concluded that the early life environment may influence the relation between BMI and adiposity in later life. In particular, we speculated that Asian women substantially exposed to the American environment early in life exhibited different patterns of accumulation of body fat than did Asian women raised in Asia;
non-sig, see above
these differences may be partially attributable to environmental and lifestyle factors that affected diet and physical activity. For example, compared with Asian children raised in the United States, children who live in Asia tend to spend more time studying, whether in school or at home, and less time doing sports and engaging in recreational activities (25). In the past, diets of Asians raised in Asia also tended to be different, with a lower consumption of breakfast cereals, dairy products, and processed meats, than diets of Asians raised in the United States (26).
Yes, they do try to eat white. Silly Asians, didn’t evolve for dairy.
So your grandkids will definitely be fat, even if she isn’t by some fluke? Great, very likely to pass on your genome.
What a waste of time and resources.
However, with the rapid changes that have been taking place in Asian economies and the globalization of the food supply, we expect to see further changes in the diets of children in Asia (27) and, consequently, in body composition.
The understanding of how childhood environments influence the relation between BMI and percentage body fat has implications for the use of BMI as a screening indicator for obesity and obesity-related conditions. In addition, research to understand the influence of environmental factors on the accumulation and distribution of total body fat and metabolically active visceral fat during critical life stages will add insight into the use of clinically relevant screening tools for chronic disease risk.
Plan on growing old together, spending a loooong time with fatass.
South Asians are susceptible to insulin resistance even without obesity. We examined the characteristics of body fat content, distribution and function in South Asian men and their relationships to insulin resistance compared to Caucasians.
so no, you can’t tell by ‘looking at her’, your norms are informed by white women
Research Design and Methods
Twenty-nine South Asian and 18 Caucasian non-diabetic men (age 27±3 and 27±3 years, respectively) underwent euglycemic-hyperinsulinemic clamp for insulin sensitivity, underwater weighing for total body fat, MRI of entire abdomen for intraperitoneal (IP) and subcutaneous abdominal (SA) fat and biopsy of SA fat for adipocyte size.
Compared to Caucasians, in spite of similar BMI, South Asians had higher total body fat (22±6 and 15±4% of body weight; p-value<0.0001), higher SA fat (3.5±1.9 and 2.2±1.3 kg, respectively; p-value = 0.004), but no differences in IP fat (1.0±0.5 and 1.0±0.7 kg, respectively; p-value = 0.4). SA adipocyte cell size was significantly higher in South Asians (3491±1393 and 1648±864 µm2; p-value = 0.0001) and was inversely correlated with both glucose disposal rate (r-value = −0.57; p-value = 0.0008) and plasma adiponectin concentrations (r-value = −0.71; p-value<0.0001). Adipocyte size differences persisted even when SA was matched between South Asians and Caucasians.
Marry those genes, go ahead.
Insulin resistance in young South Asian men can be observed even without increase in IP fat mass and is related to large SA adipocytes size. Hence ethnic excess in insulin resistance in South Asians appears to be related more to excess truncal fat and dysfunctional adipose tissue than to excess visceral fat.
in the men
harsh to call a racial adaptation to famine ‘dysfunctional’
There are four main blood types: O, A, B, and AB and two Th factors, positive or negative. Most people are either A positive or O positive and the fewest are AB negative. Because blood types are genetic, they are inherited from the parents, blood types have different racial and ethnic differences. The majority of people in the world and across various ethnicities have Rh+ blood type. Subsaharan African populations have a 97-99% Rh+ factor. East Asian communities have 93-97% Rh+ blood. Rh factor is a big determinant in both fertility and pregnancy. If you’re Rh-negative, you will need to take certain precautions during your pregnancy because an Rh positive fetus can conceivably be affected
wait so does Nature abort hybrid babies?
if the RH negative mother has previously been exposed to Rh positve blood and creates antibodies that cross the placenta and attack the fetus’ RH positive blood.
It isn’t our fault Asians need IVF more and more often fail at it, it’s literally in their blood. What are they implying otherwise, a curse?
Unfortunately, many Asian couples face challenge trying to conceive naturally or using fertility treatment. The decline in natural fertility and the lower success of IUI and IVF in Asian women is documented in The US, UK, China, Japan, Korea and other Asian countries.
Fertility in Asian countries has declined to the population replacement rate 2.1 or lower. Many factors contribute to decline in natural fertility in Asian women;
Not our fault. Not our problem. Nature tends to curb the over-population of r-types by introducing more threats to thin the herd.
It happens to Asians who never lived in the West, stop blaming whites.
Repost on the Asian female infertility problem:
When compared to Caucasian women, Asian women undergoing IVF significantly produce less eggs at all Anti-Mullerian hormone (AMH) levels, even in women with high AMH. AMH is the most accurate marker for ovarian reserve.
Gynecologic and medical disorders that impairs fertility: PCOS, endometriosis and Systemic lupus (SLE) are more common in Asian women.
Vaginismus : may interfere with regular intercourse in some Asian women.
Environmental Factors: Asian women has more exposure to methyl Mercury and vitamin D deficiency.
Culture : surveys of Asian women and men indicate that they are less likely to consent to be contacted for fertility research, are fatalistic about failure to conceive, less informed about fertility issues, only 36 percent knew that chances of getting pregnant declined with age, and are less likely to suspect a male factor.
Asian women are commonly late at seeking care for infertility and overestimate the chance for getting pregnant.
Look at the national IQs, hardly surprising.
Genetics : Many genes are likely involved. FMR1 is a gene on X chromosome responsible for Fragile X syndrome and its variants. High repeats at this gene may reduce ovarian reserve.
It’s literally genetic. R-selection doesn’t keep those repeats low in the populace.
Did pesky white women interfere with their genes?
Yeah we tinkered with the Ts, the Gs, the As, all of it!
Fertility Treatment Outcomes in Asian Couples
Pregnancy and delivery rates are lower in Asian women following ovarian stimulation and IUI compared to white women
IVF: when compared to white women in the US, 31 per cent of the Asian women gave birth successfully compared to 48 per cent of the white women. Asian women were also less likely to become pregnant; 43 percent against 59 per cent even after control for many fertility factors. Endometrial lining was thinner in Asian women compared to Caucasian women.
Shit, is white supremacy real but only for women? We did need to weather the Ice Age.
I think endometrial lining has a connection to T-levels, it gets thinner with higher T, if memory serves.
I didn’t find enough conclusive data on white men v Asian when I linked sperm quality studies. A little but not as clear. There are fewer studies like that on men in general.
Asian women should be aware that fertility treatment may be less successful and seek care of a reproductive endocrinologist and fertility specialist as early as possible.
In addition there are other factors that require attention in Asian women during fertility treatment especially the higher prevalence of chronic hepatitis B infection.
After conception, asian women at are a higher risk for gestational diabetes.
That’s why anglos, who have a lot of Rh-neg, have so many historic geniuses.
Blood type by race/ethnicity:
O-positive is the most common blood type. Blood types vary by ethnic group. More Hispanic people, for example, have O blood type, while Asian people are more likely to be type B. In 2014, Oklahoma Blood Institute saw this ethnic diversity and blood types in its donors.
The O stats for whites are shockingly different.
Limited by who donated, wish I could find broader data.
Some patients require a closer blood match than that provided by ABO positive/negative blood typing. For example, the risk of a reaction to transfused blood can sometimes be reduced if a patient receives blood that is from a donor with the same ethnicity. That’s why African-American donors may be the best hope for patients with sickle cell disease, 98 percent of whom are of African-American descent.
A comparison between eight individual samples demonstrated that the Asian male one has an extremely large number of ACE2-expressing cells in the lung. This study provides a biological background for the epidemic investigation of the 2019-nCov infection disease, and could be informative for future anti-ACE2 therapeutic strategy development.
We may dub it The Elliot gene.
…..We also noticed that the only Asian donor (male) has a much higher ACE2-expressing cell ratio than white and African American donors (2.50% vs. 0.47% of all cells). This might explain the observation that the new Coronavirus pandemic and previous SARS-Cov pandemic are concentrated in the Asian area….
Almost like the Chinese wanted to wipe out most of their own race IF there were a war.
“Yet many languages also have words that English speakers might think of as “basic” emotions — love, hate, anger, fear, sadness, happiness. Early theories, influenced by Charles Darwin and pegged to shared biological structures in humans, suggest there are certain universal emotions that serve as the source material for all others, as primary colors might be blended to create many new shades.
Universalism is bullshit. All shades. Not All ___ is a derailment, attempt to enable, dismiss or deflect or simple result of a category error.
But just as later work has suggested that different cultures do not always categorize color in the same ways,
Different rods/cones plus evolution.
there’s a growing understanding that even those supposedly “primary” emotions may hold their own meanings and nuances in different cultures that aren’t directly translatable.“
Apply Occam to this. People are not cogs, Rousseau!
Language is also genetic. Really. This is known.
Preview of what they’ll “discover” next, trying to get ahead of the net?
Humanity, as we WEIRD individualists think of it, is also non-uniform throughout the species. Diversity aka variation exists, a scale of 0-100, if you will. Basically? Some races are crueler than others, simply put. Others less sadistic, even to their own people, animals, children, elderly etc. Science is catching up. We are not, as we’ll be told, dehumanising THEM, they dehumanise themselves, they hurt one another, what better treatment can WE expect?
Civilization is a combination of simple factors and conditions inc. IQ (organism and national), honesty (low cultural corruption*), genetic individualism, K-select breeding and rearing and finally, low sadism (antisociality in the population, little pathology, especially sexual sadism). When “high trust” is required historically (the current PC code for this) the West succeeds because of its low racial sadism (and resultant bias towards justice) and tendency to punish/cull predators (civil unrest) instead of reward with money, rape victims, goats, whatever. High culture is produced by ALL these factors, you can’t make exceptions for your own hedonism.
It looks like collectivism but it isn’t – it doesn’t hide personal responsibility or agency behind Muh Group Card (like the men who marry in China and are allowed to cheat, two-faced “duty”) or the need for virtue as The Other Guy’s Problem. It isn’t cruel or cowardly in secret, it’s openly FAIR.Cruelty is the key sign of an inferior mind.
The SJWs don’t name me for that reason. The science is coming out.
m-m-m-muh appeal to authority?
*So neither China nor Russia will run jack shit. They cannot innovate in a vacuum. The kitten-crushers of Japan and China make shitty parents and military generals. Honour culture isn’t a parade, it’s bravery. It’s sacrifice.
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.”