“It might sound strange, but its true, this remedy has been passed around the feminist community since the 70’s, appearing in many grassroots publications, some of which are cited here. There are also numerous reports of women using it successfully from this era, I’ve heard many stories, but never saw any kind of documentation, which isn’t surprising in a time, where a woman’s right to choose an abortion and have access to safe legal abortion services was just being won.”
Great for ye olde days of gang rape though. Useful if the Red Army comes around town. Abortion does make sense where continuing would kill the mother so there is an ethical grey area e.g. ectopic. I acknowledge that. We also must know what kills a baby so all mothers know to AVOID it. This is why keeping women ignorant leaves them vulnerable to such evil. Parts of nature hate us. Wiccans are imbeciles.
This is why I don’t supplement liposomal Vitamin C, as I suggested for OLDER people.
“The scientists who conducted the research, Samborskaia and Ferdman came to the conclusion that high doses of Ascorbic Acid appeared to increase estrogen levels which contributed to the interruption of an otherwise normal pregnancy. 20 women who approached doctors requesting an abortion participated in the study. Research was conducted by ob/gyn L.I. Ivanyuta. The women ranged from 20 to 40 years of age. The article does not say if a positive pregnancy test was obtained from the participating women. We also don’t know how much ascorbic acid the women were given. They did however measure estrogen levels before and after treatment with ascorbic acid, finding that estrogen levels were higher after taking the ascorbic acid. Of the 20 women, 16 began menstrual type bleeding within 1 to 3 days from administration of ascorbic acid.”
It makes giving kids lemonade real sinister. Mountain Dew, Sunny D, the works.
“Vitamin C works to produce an unfavorable climate within the uterus so that the egg does not implant, or if implantation has already occurred, Vitamin C can weaken the fertilized ovum’s grip on the uterine wall. Possibly by stimulating estrogen, and interfering with progesterone. This also makes it useful as an emergency contraceptive, when taken before implantation occurs on the 6th day following ovulation. The hormone, progesterone is essential for pregnancy, its function is to prepare a nourishing bed for the fertilized egg, if there is not enough progesterone the uterus becomes less supportive to the egg. Which is desirable when the goal is to end pregnancy.”
Progesterone means pro-gestation. Anything that reduces that and/or increases oestrogen causes miscarriage, including xenoestrogens. BPA also causes genetic defects inc. Downs, and can cause abnormal egg development in a female fetus, which can go on to experience many miscarriages (modern rates?) and Downs children themselves.
Also NO parsley. Yes, it kill babies. Viva Italia some other time. Can be used to induce labour, ironically.
History will view the use of xenos as pure evil*. I think endometriosis is caused by it, like a poisoning. Explains the miscarriage common to it. Most common cause of infertility in women. Pure progesterone creams hard to come by, easier to patent a toxic variety close enough. Even pure creams can include preservatives that are oestrogenic! Vegan love of vit C may cause vegan menopause, imho. Xenos also cause premature puberty in girls as young as ONE, especially seen in high-estro skin products used by American blacks and not found in African ones. Xenos (including hops in beer**) also cause a small penis and breast development in boys/men. This shit should be BANNED forever in all skincare vehicles (10x more potent, bypassing liver filter). The amount required (parts per billion) is rarely tested for but maintains estrogenic effect at this level. Parabens were disused in some products due to this. Others like SLS and phthalates also. It isn’t hype, it’s killing men/women hormonally and babies silently. A silent killer in shampoo, lotion, food etc. No wonder American rates of miscarriage are so high. Test ALL skin products for endocrine disruption, especially those that break down into it (XENOS), in rats. Xenos can bio-accumulate for decades in the body (heard of DDT?) and stay for decades too. I share this hoping people won’t abuse the info.
*file under Molech
**how Anglos have gotten softer and softer and softer… literally and morally.
Synthetic perfume is also a xeno. Sorry. I’m sad about it too. They’re aiming this at teen girls and boys, who get fat. And in the case of girls, look sexual. The boys look twinkish. I’m sure the traffickers love that.
They blame kids for being fat when they’re hormonally drugged from seemingly everywhere. They cannot lose weight! The environment is too polluted!
Phyto-estrogen can bind protectively and reduce the capacity of xeno to attach. This is limited. It’s less potent but still oestrogenic and thus reduces progesterone. Can detox from the body in a matter of days since it’s natural.
The UK is trying to push a chemical abortifacient over the counter. No minimum age limit, paedo paradise. How many rape gangs or child groomers will feed this to their prey, coercive or secretly? The capacity of even parents for reproductive abuse, secretly giving it to their children like a harmless preventative (when they might already be taking it themselves) is abhorrent. There are no proportionate laws criminalizing giving this to children. Mull over that.
““Pharmacists have the expertise to advise women on whether desogestrel is an appropriate and safe oral contraceptive pill for them to use and to give women the information they need, to make informed choices,” she said.” It isn’t only women who will buy it, fathers raping their daughters, rape gangs attacking girls en masse, controlling mothers drugging their daughters ‘just in case’…. pharmacists are not doctors and cannot order appropriate tests to maintain healthy hormone levels. You cannot make informed choices as a minor by definition.
“The MHRA’s decision to reclassify the desogestrel products follows a safety review by the Commission on Human Medicines (CHM) and a public consultation taking in views from patients, pharmacists and doctors.” Patients are idiots and so are pharmacists. They’ll opine when they’re damaged, but why didn’t you warn us?
“Edward Morris, the president of the Royal College of Obstetricians and Gynaecologists, said he was delighted that some contraceptive pills would be available in local pharmacies after the college’s years of campaigning against “unnecessary barriers” for women and girls.” Women and girls. No minimum age noted.
He said: “Even before the pandemic, too many women and girls were struggling to access basic women’s health services. The consequences of this include an increase in the number of unplanned pregnancies, which can result in poorer outcomes for women and their babies.” These people are child rape enablers. Apparently the TRUE evil (sarc) is holding child rapists accountable for the fruit of their loins. This is rape culture if the term ever applied.
Saving money on actual medical advice again, cost cutting: “She said: “The fragmented sexual and reproductive healthcare system is notoriously difficult for women to navigate, and successive cuts to public health budgets have made it harder for women to get the contraception they need. Reclassification may also reduce unnecessary pressures on GPs, who will not need to see patients for repeat prescriptions.” They need to monitor anything hormonal. When are steriods OTC? No? They have noted health benefits.
The Pill’s push to the unmarried will go down in history as true evil. Yes, it counts as abortion. They continue to lie about its basic mechanism. They already pushed the morning after form OTC. Long term use of any medication requires doctor supervision to ensure the organs aren’t being poisoned. Oestrogen dominance is rising amid well, everyone, and causes severe damage including obesity. Progesterone can mess with all other hormone levels. The idea of drugging just women/girls with this shit is misogyny. It’s purely misogynistic. You must hate them to endorse this. Are we selling testosterone and other supplements OTC at drug concentrations to anyone, whatever the age? This is tacitly enabling child rapists and pretending children can consent to be raped. It places blame squarely on the child. It enables the continual abuse of children under the guise of ‘responsibility’. There will now also be social pressure to conform among girls. It isn’t harmless. If you have to ban sugar lollipops at schools for being ‘bad for health’, this is nothing less than evil to push. A gyno on GB News, claiming to be a patriotic TV station here, had her go on about ‘painful periods’ – which is no excuse to drug the reproductive organs of a developing child. You also know the BPD parents will be forcing this onto their sons like tranny abuse of the drug class for ‘therapy’. Even if a girl has painful periods, painkillers already relieve that, as I well know. There are no longitudinal studies on the damage of chronic Pill use. I repeat, no long term studies. In adult starters, let alone minors. The Guardian even sub-links to an article about blood clots caused by the Pill.
Tracking Pill use is vital to monitor whether a woman is being abused, and whether SHE actually wants to take a medication, rather than being drugged. She must attend her own appointment and talk to a doctor, bearing in mind her medical history. This system of protection prevents coercion. They tried pushing this shit on me for no medical reason as a minor and virgin (obviously) so I know they do it. Thankfully I understood what longitudinal studies were and told them like three or four times on separate occasions, no I don’t want their drug pushing (I had a normal ovarian cyst*, the first time – making it completely random and insulting to suggest) and no amount of fear mongering or ‘you’ll be sorrys’ will make me anything less than really really sure. The longest I had to repeat this was about twenty to twenty five minutes. They don’t take no for an answer. They don’t even care if your family has an extensive history of damage reactions to hormones. They will still look you dead in the eye and gaslight you that it’s ‘really harmless’. Based upon??? They are actively PUSHING this shit onto women/girls. Painful periods require giving up sugar half a week before it starts, not this bullshit. But they want to save money and face on child abortions. It’s difficult to call a girl a liar if she’s literally pregnant. This is all about enabling child abusers and disempowering victims, who have no legal recourse against food adulteration and coercion when it’s available like a breath mint. No proof of crime, no time.
*one or two cysts happen naturally when you ovulate but they’re so accustomed to seeing women and girls drugged up to the eyeballs that they treated this like I needed meds. More like they wanted kickbacks.
Recommended this after a Clarey video, must be the discussion of hormones in the algo. I think this explains the contentment in singleness, newfound. The lone 50s comparison study is a cope, over-cited by the ‘redpill’ as confirmation bias, since marriage reduces female lifespan the study that controls for partner absence/presence is legitimate methodology and married women are generally miserable compared to single peers on many metrics. But female suicide is never like male. With the postmodern pressures of Supermum duty and the pressure to be active and masculine too, like a second husband, this dissatisfaction with modern marriage is understandable. Men get high on service, that spike in T, just look at the military. Women just get burned out. I believe MGTOW have higher oestrogen, they seem to have higher voices. Low pitch men tend to want marriage and especially monogamy, fidelity. There’s more mate guarding and sexual jealousy. They crave that union that releases oestrogen to balance their natural T. Women also replaced husbands with friend groups, the ‘support network’ men can’t really do. I have noted a trend in men only dating because they want therapy and think women could/should give them this – NO, go to a real therapist. Do not date to complain about your problems. She is not your mother, you’ll attract a personality disorder that way. Look at Harry and Meghan – LOOK AT THEM. Same goes for women dating for therapy sometimes but they rarely burden men with their emotional labour. That’s exhausting, why do you think shrinks are paid so much? The duality of the sexes must be recognised without shame. A sizeable chunk of the manosphere is actively misogynist polluting the discourse on healthy marriages out of spite for their fellow man (if I can’t have it, no one can!*) and tries to justify it by the mere existence of misandry – the same thing misandrists do… Feminine things and ladies’ priorities are not weak/silly/crazy/inferior/hysterical/stupid and if you think otherwise you just plain don’t like women. Try dating men, really. If you want a man mentally, just date one? Misandrists call men the same dismissive things and it isn’t cricket either. Nobody is biologically inferior or weak, God made both. Different is not crazy, that’s just silly. Biology isn’t a marker of immaturity, it’s healthy. They shame women about being women, about being men, about ‘trying to be’ men (whatever that means), about trying to be neither – no wonder women avoid them and mentally check out! They just plain don’t like women, it’s the common denominator. *Sabotage you see in SJWs saying get fat and tatted. You get ‘I shouldn’t have to pay for the meal’ when that’s what a date is. Otherwise you’re friends ‘hanging out’ and she’ll ‘flake’ accordingly**. Do you want to be the man or not? These guys want their cake and to eat it. If you’re the masculine provider, it shouldn’t be ‘equal’, that’s an SJW trope and look – they’re not happy.
XEs are messing everyone up but I feel it’s making some men feel entitled to caregiving – like a woman. They think like a woman, that’s why they mentally compete with women, it’s like they’re turning partially homosexual in gender – if not sexuality. Too much fluidity, which they blame on women and ‘society’ – if your hormones are screwy, that ain’t on me. Your insecurity isn’t society’s fault, fatphobia people try the same BS.
As an outsider – It’s like they’re (American MGTOW) holding (American) women to ransom on their fertility, as if they have gold-plated sperm, only to realise –bitterly– that sperm is cheap. It’s always cheap. It’s evobio. Don’t like it? Get a sex change, seriously. Women won’t chase you, at least never the feminine ones you psychologically want. Their physiology is at cross purposes. The sexes are not and should not be the same but they actually believe postmodern lies. It’s a huge bluff and they’re being called on it. What kind of idiot thinks women want to give birth? Women can get the oestrogen in many ways, like adopting a puppy. That’s why men get dogs. They’re broody. Women are being replaced with pets too. The Romans did this as they declined. They spoiled their dogs like children. Visitors were disgusted because patriarchs replacing their role of mastery (and duty) is existentially morbid and morally perverse.
Anti-marriage bigots mentioned above (they are, by definition) giving advice on marriage is like asking the ‘fatphobia’ people for diet advice.
nb Women need that marital romance for oestrogen, makes sense I guess. Men are replacing their T with porn and FPS video games. They literally only want a wife when those two supernormal stimuli are dropped. The Marxists control them for this reason. SJWs get scared when men give up porn because it takes back their power i.e. control of their hormones.
**Flake is a cope for men repeatedly abandoned by women expecting them to grow up. Women don’t have a group chat trying to ‘string them along’, they always repeat toxic behaviours usually after a certain time period and poof the woman disappears. What was he always doing just before she disappeared? They get weirdly defensive when you ask this question.
“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.
Here is a short list of psychiatric symptoms and traits associated with copper overload:
Hyperactivity, academic underachievement, learning disabilities, ADHD, autism, skin sensitivity to tags in shirts or rough fabrics, intolerance to estrogen and birth control pills, onset during puberty, pregnancy or menopause, white spots on fingernails, skin intolerance to cheap metals, emotional meltdowns and frequent anger, ringing in ears, sensitivity to food dyes and shellfish, high anxiety,depression, poor immune function, sleep problems, poor concentration and focus, low dopamine activity, and elevated activity of norepinephrine and adrenaline.
“I have anxiety” sure Dave
Other medical conditions associated with copper overload include acne, allergies, Candida overgrowth, hypothyroidism, anemia, hair loss, chronic fatigue and fibromyalgia, migraines and male infertility.
Fatigue, hair loss, MALE infertility.
It can do this to a female body, imagine what it does to the male?
I’d sue, if I were them. The consent was uninformed.
The reason that copper is linked with such a long and varied list of conditions is that it is absolutely essential to the proper functioning of the immune system, the endocrine system, and the nervous system.
Copper is important for regulating the synthesis of neurotransmitters that mediate psychiatric symptoms. It is a co-factor in the chemical reaction that converts dopamine to norepinephrine. When copper levels are high, more norepinephrine and epinephrine (adrenaline) are synthesized from dopamine, which can causes feelings of agitation, anxiety and panic, overstimulation, racing thoughts, restlessness, and insomnia. In other words, it has an amphetamine-like effect, revving the nervous system into a state of overdrive. Consider that copper is often used in electrical wires because it conducts electricity well, and likewise increases nerve transmission, which is an electrical chemical process.
transduction, but ok
it’d be piss-easy to study, hair mineral analysis before meds, and after
Copper is also central to cellular energy production, and thus many patients with fibromyalgia and chronic fatigue conditions related to mitochondrial dysfunction have disorders of copper metabolism.
it all fits!
Copper overload is particularly common in women.
not anymore they just don’t check men
Estrogen can cause copper retention and accumulation, which can eventually result in toxicity. Hormonal events such as menarche, pregnancy or menopause can trigger it. These days when a patient tells me about a history of postpartum depression, severe PMS, dysmenorrhea or adverse effects related to the prescription of oral contraceptives, I immediately suspect copper overload.
Copper promotes the formation of blood vessels (angiogenesis) and when copper levels are elevated, it can predispose an individual to endometriosis and fibroid tumors, as well as increase the blood supply to other types of tumors. Excess copper can accumulate in the liver and impair its capacity for detoxification, which can result in chemical sensitivities.
I wonder if carnivores can get that?
I know it’s used in make-up a lot, as a colourant too.
Copper is carried in the blood by a specific protein called ceruloplasmin. Some patients have low levels of ceruloplasmin and thus have a large percentage of unbound copper in their blood.Unbound copper causes oxidative stress in the body. Oxidative stress is characterized by the presence of free radicals which interact with molecules in the body, damaging various cell components such as DNA, protein and lipids, and giving rise to various disease states, including autoimmune disorders, neurodegenerative disorders, and cancers, to name a few.
so it’s like poison to men, is what I’m getting
There is commonly an inverse relationship between zinc and copper in the body. Often when a patient has elevated copper, the zinc level is low. Zinc is another mineral essential to cellular function, regulation of the immune system, wound healing, and synthesis of neurotransmitters. An important ingredient in the treatment of copper overload is supplementation with zinc. This must be done very slowly and carefully, because zinc mobilizes copper stores. During this process, a person can initially feel even more anxious and symptomatic. Anti-oxidants are also used in the treatment of copper toxicity, as well as the elements molybdenum and manganese, and amino acids which promote metallothionein production. Metallothionein is another protein which binds heavy metals in the blood, and which is important for regulation of zinc and copper metabolism. It’s important to find a trained practitioner to help you with this process. A good resource is the Practitioner’s Page of the Walsh Research Institute website.
Copper toxicity is a hidden epidemic. Birth control pills and copper IUD’s contribute to excess copper in the body. For thousands of years, copper has been known to be anti-microbial in nature. Copper IUD’s work by releasing small but significant amounts of copper into the uterus. Copper immobilizes sperm as it travels to the fallopian tubes. This copper can and will enter into the blood causing all sorts of problems.
Birth control pills also tend to raise copper levels in the body. High levels of copper destroys vitamin C in the body, can deplete zinc levels, can lower iron, can cause an unusual rise in Vitamin A, and can aggravate B-vitamin metabolism. Birth control pills contain estrogen and progestin, and these powerful hormones in birth control pills turn off a woman’s ovulatory cycle. Estrogen and copper are succinctly related. Copper tends to raise estrogen in the body, and estrogen tends to cause copper to rise. Both copper and estrogen tend to feed one another.
and they give these to MINORS
but smarties have too much sugar.
There are long term consequences of both copper toxicity and excess estrogen. High levels of copper can cause numerous symptoms ranging from migraines, to PMS, chronic fatigue and allergic reactions. Copper is used in the body to produce ceruloplasmin, the major copper carrying protein, which is involved in iron utilization and the formation of hemoglobin.
Excess levels of ceruloplasmin is found among those with OCD, Schizophrenia, Angina, Alzheimer’s, Rheumatoid Arthritis and Lymphoma.
Dangers Associated with Estrogen
Copper raises estrogen and vice versa. Estrogen is touted as a therapy for numerous medical conditions such as Osteoporosis, but this mass media hype fails to identify that estrogen is stress-promoting on bones and is age-promoting. Numerous studies have shown that estrogen can produce prolactin and that prolactin can cause osteoporosis.
In short, high estrogen and low progesterone increases bone loss. Osteoarthritis is associated with excess estrogen. It is true that estrogen can cause retention of calcium. But it is now known that high levels of calcium does very little to prevent or improve symptoms of osteoporosis. Osteoporosis is not bone loss, but rather the breakdown of the collagen matrix that holds bone together, a degenerative and catabolic condition which consists of deficiencies of minerals such as boron, magnesium and phosphorous. Only if the miracle estrogen or calcium was the answer to this and other degenerative diseases. They are promoted as such but all that calcium will just end up in the toilet, and all that estrogen will displace other hormones and nutrients, causing further complications.
I have to post this now because the product push is in full swing and it could literally save tiny lives.
I can’t wait until October, all the “influencers” are pushing this online NOW. Ethically, I must put my ego aside.
A lot of Pill failures are actually in the hippy chicks taking plant “extracts”. That’s why doctors now ask young women about supplements and herbal remedies immediately after the contraception question. It wouldn’t be ethical to study pill failures but they know there’s a link.
so in context:
“How Smoking Marijuana Damages The Fetal Brain” is horrifying.
“Earlier studies have already found that children of marijuana-smoking mothers more frequently suffer from permanent cognitive deficits, concentration disorders, hyperactivity, and impaired social interactions than non-exposed children of the same age and social background.”
Weird how all these CBD products were pushed before safety studies like this, and now we have corona-chan distracting.
“A new study published in Scientific Reports, a Nature Research journal, shows how a one-time exposure during early pregnancy to cannabinoids (CBs) – both synthetic and natural—can cause growth issues in a developing embryo. This is the first research to show such a connection in mammals.” One-time. But not a drug, ya see. That makes sense.
It’s the first research to LOOK. Why was this cleared? And who calls CBD safe? Oh…. the WHO.
“In this study, the brain and facial developmental effects caused by one-time exposure to CBs—CBD and THC (the primary ingredients of marijuana)—are very similar to what is seen in fetal alcohol syndrome (FAS). Parnell and colleagues also found that when CBs and alcohol were used together, the likelihood of these birth defects more than doubled. They went on to show that these drugs may be causing defects by interacting on a basic cellular level and disrupting signaling between molecules and cells that control growth and development.” “The CBD amounts administered were within what is considered a therapeutic range for humans.”
“It is concerning how little we know about the use of marijuana, its CBs, and products like CBD oil during pregnancy,” Parnell said. “We know that there is no safe period to drink alcohol during a pregnancy, and I think this research shows the same is likely true of marijuana use.”
Drinking once doesn’t cause FAS, so this is objectively worse. Don’t expect the tradlarpers to talk about anything important re child IQ and birth rates. Nope! Let’s talk about some twit on Twitter again. I don’t care if you like your CBD rollerball, Karen! You’re better off aborting it now it’s brain damaged!
If you want to de-stress take a poxy bubble bath like a non-druggy.
I expect it causes more miscarriage too, with that effect.
With the results of these one-time exposures, Parnell and Fish are planning to now test smaller, multiple exposures throughout a pregnancy that better mimics real-life usage in human pregnancy.”
“Many women report that they use CBD oil during pregnancy in order to reduce pregnancy-related nausea.
In general, using CBD while one is pregnant is thought to be safer than smoking cannabis itself or THC-rich products.” [DS: we now know this is wrong, see above]
The hippy Karens must be stopped.
I bet it damages sperm too. That’s all the soy boys need.
There is a lack of conclusive data to determine the effects of CBD hemp oil on a fetus. However, it is known that a growing fetus is equipped with an endocannabinoid system, even when the fetus is only composed of two cells. This system is in all humans and even some animals. The endocannabinoid system is a system composed of endocannabinoids, which are neurotransmitters that bind to cannabinoid receptors.
In a study conducted on mouse embryos, researchers found that the compound THC inhibited the development of the embryos which contained less than eight cells. Another natural cannabinoid found in the human body, anandamide, also stopped the embryos from developing. CBD can increase levels of anandamide, so there may be negative effects associated with CBD use during pregnancy. It is important to note that this was a study conducted on mice and the results may not be transferable to human subjects.
If you’re gonna be a Western baby birth rate cult, talk about things like this.
“marijuana causes significant brain changes by slowing activity in the frontal and temporal lobes”
there’s a known connection to schizophrenia in men, especially those who start before 21, earlier in the teens the higher the risk
“Some argue that marijuana is not addictive, but as it demonstrates, it is a drug like any other.”
I knew this so I had to post.
Alcohol is a drug and it is addictive (alcoholism is an addiction to alcohol, not mere consumption, it’s a pattern of chronic consumption with withdrawal during cessation). As soon as they call their poison “not addictive”, you know it is. It’s like hearing “I can quit any time I want”. Cognitive dissonance, a month of cessation would be intolerable for them.
“after studying imaging of 1,000 cannabis users’ brains, there were signs of noticeable deficiencies of blood flow. The study, which included 25,168 non-cannabis users, and 100 healthy controls, shows a scary and obvious difference in blood flow levels for those that used cannabis. Additionally, those that used marijuana showed a significant lack of blood flow in the right hippocampus, the area of the brain that helps with memory formation. This part of the brain is severely affected with those that suffer from Alzheimer’s disease.”
“Our research has proven that marijuana users have lower cerebral blood flow than non-users.”
In a 2010 Italian paper published online by BioMed Central, the authors argue that disrupting the normal activities of these ECS pathways by adding cannabinoids “can significantly alter many vital in utero processes, including angiogenesis, cellular replication, tissue differentiation, and [fetal] neural cognitive development.”  ….
While THC exposure increased sexual receptivity in female hamsters and rats, it also inhibited their release of luteinizing hormones. These hormones are responsible for ovulation and the development of the corpus luteum. The latter is a hormone-secreting structure in the ovary that plays a role during very early pregnancy. 
“The results of this study show that the use of cannabis in pregnancy is associated with increased risk of adverse birth outcomes. Prevention programs that address cannabis use during pregnancy are needed.”
“With the increasing publicity of marijuana due to recent legislation, it is pertinent that the effects of fetal exposure
to the drug are assessed. While in utero cannabis exposure has been associated with early pregnancy failure, birth defects and developmental delay, the mechanisms of such outcomes are largely unexplained. Furthermore, the use of cannabinoids in cancer treatment via growth inhibition and apoptosis may indicate how cannabis exposure likely harms a growing fetus. Cannabinoid signaling is required for proper pre-implantation development, embryo transport to the uterus, and uterine receptivity during implantation. In post-implantation development, cannabinoid signaling functions in a multitude of pathways, including, but not limited to, folic acid, VEGF, PCNA, MAPK/ERK, and BDNF. Disrupting the normal activity of these pathways can significantly alter many vital in utero processes, including angiogenesis, cellular replication, tissue differentiation, and neural cognitive development. This paper aims to demonstrate the effects of cannabis exposure on a developing embryo in order to provide a molecular explanation for the adverse outcomes associated with cannabis use during pregnancy.”
The authors also argue that cannabis exposure could very likely harm a fetus due to phytocannabinoids’ effect on cells. This is because CBD and other cannabinoids are associated with cell growth inhibition and cell death, which may be good news for the treatment of cancer, but not for a growing fetus. 
These findings were based on petri dish research, but the same trend was observed in most cell cultures, not just in cancer cells. Obviously, this could mean that healthy cell growth can also be affected. 
This is speculative, however, and not an easy subject to study clinically, but it is clear that much more research is needed before any phytocannabinoid can be declared safe for use by pregnant women.
There appears to be no traceable data regarding CBD and male fertility. The available research centers mostly on marijuana and fertility in males, and it is mostly negative, except for one finding.
How are these products on the market? HOW?
It feels like a DDT style case study waiting to happen.
This research, conducted by Dr. Hans Hatt of Ruhr University in Bochum, Germany, has discovered a receptor in sperm cells that is part of the ECS.
Called the GPR18 receptor, it plays a big role in conception. Dr. Hatt explains its function very simply: “The endocannabinoid activates the spermatozoa for fertilization.” This means that it helps the sperm to fertilize the egg or the ova.
The doctor also pointed out that this receptor responds to THC and another cannabinoid, anandamide, with involvement in the sperm’s ability to penetrate the ova. This is encouraging news, but much more study is needed before phytocannabinoids can be considered a possible therapy for male infertility. 
This is also because other research points in the opposite direction for men.
Birth defects suggest it messes with the sperm’s genetics.
A total of 1,215 young Danish men aged 18-28 years were recruited between 2008 and 2012 when they attended a compulsory medical examination to determine their fitness for military service. The participants delivered a semen sample, had a blood sample drawn, and underwent a physical examination. They responded to questionnaires including information on marijuana and recreational drug use during the past 3 months (no use, use once per week or less, or use more than once per week). A total of 45% had smoked marijuana within the last 3 months. Regular marijuana smoking more than once per week was associated with a 28% (95% confidence interval (CI): -48, -1) lower sperm concentration and a 29% (95% CI: -46, -1) lower total sperm count after adjustment for confounders. The combined use of marijuana more than once per week and other recreational drugs reduced the sperm concentration by 52% (95% CI: -68, -27) and total sperm count by 55% (95% CI: -71, -31). Marijuana smokers had higher levels of testosterone within the same range as cigarette smokers. Our findings are of public interest as marijuana use is common and may be contributing to recent reports of poor semen quality.
I think we found a cause of generational infertility in men, suck up that red pill.
The inability to conceive affects both men and women equally. Among couples experiencing infertility, roughly 35 percent is due to problems in the male, while another 35 percent is due to issues in the female. Another 20 percent is a combination of issues in both the male and the female, and the remaining 10 percent is unknown.
Apart from CBD oil for fertility, a number of alternative or complementary therapies are on the rise, all with varying degrees of success.
They claim CBD is antidepressant despite cerebral flow connection to causing it. Gotta keep selling those SSRIs.
“demonstrates that marijuana can have significant negative effects on brain function. The media has given a general impression that marijuana is a safe recreational drug, this research directly challenges that notion.”
Beware anything the MSM pushes. What do druggies do? Sit around watching TV and consuming other ‘entertainment’ like Netflix.
It’s a known scandal that American farms of it are basically a monopoly.
If the effect is anti-stress, it’s a drug. If that’s the only purpose, drink tea. Put on a nicotine patch. They never explain fully the biological mechanism that makes it work like a drug, without literally being a drug. https://en.wikipedia.org/wiki/Sublingual_administration The dropper form of CBD is literally a drug, drops are used in pediatrics on babies. It’s sublingual absorption. If it’s ‘extracted’ from a drug, works like a drug and is delivered like a drug… it’s a drug.
Should adults be allowed to be druggies? Over 25, maybe. But why must I pay for stressed-out Karen’s “treatments” on the NHS? Must I pay for her alcohol too? Can she pay for my naps and chocolate?
Why not legalise morphine and laudanum and all the other naughties you used to buy over the counter before the nanny state?
Because people would grow their own poppies. That’s why. It’s too easy to extract.
The method was flawless, before AND after.
“Several studies of perfusion imaging in marijuana users have shown similar results compared to ours. A small O15 PET study in a sample of 12 marijuana users used a randomized clinical trial design to examine brain perfusion before and after marijuana use. The study results found frontal, temporal and occipital lobe hypo-perfusion – all findings concordant with our study.
Zoomers aren’t stupid, they’re polluted.
Although it is often portrayed as harmless, and sometimes even therapeutic, there has not been nearly enough studies done to prove this. In fact, marijuana is often prescribed for issues like anxiety, though studies cannot comprehensively show this to be true. Currently, the available information on the impact marijuana has on the neurophysiology of the brain show, predominantly, depressive effects.”
It’s pushed on women to harm their fetus. Skin cream lingers for hours and ends up in the blood.
stop acting like estrogen is a poison when it actually protects your body and makes your brain stress-resistant
Although the prevalence of obesity is higher among women than men, they are somewhat protected from the associated cardiometabolic consequences.
It’s easier to get a higher % when you already have a higher %. There are some of the hottest women alive under the carb loading fatties, sadly. Their natural curves predispose them to obesity.
Bring back keto!
The increase in cardiovascular disease risk seen after the menopause suggests a role for estrogens. There is also growing evidence for the importance of estrogen on body fat and metabolism in males. We hypothesized that that estrogen administration would ameliorate the adverse effects of obesity on metabolic parameters in males.
Having high T, lower E in a man can make fat more stubborn, the E cannot signal properly to clear it.
Thus, DIO induces sex-specific changes in glucose–insulin homeostasis, which are ameliorated in males treated with estrogen, highlighting the importance of sex steroids in metabolism. Given that altered peripheral glucocorticoid metabolism has been observed in rodent and human obesity, our results also suggest that sexually dimorphic expression and activity of glucocorticoid metabolizing enzymes may have a role in the differential metabolic responses to obesity in males and females.
So fatter women are healthier than fatter men. This makes sense because of baby weight. Women can lose it breastfeeding, that’s why we get it.
Plus we are naturally fatter. To grow the baby in the first place.
Estrogens play a fundamental role in the physiology of the reproductive, cardiovascular, skeletal, and central nervous systems. In this report, we review the literature in both rodents and humans on the role of estrogens and their receptors in the control of energy homeostasis and glucose metabolism in health and metabolic diseases. Estrogen actions in hypothalamic nuclei differentially control food intake, energy expenditure, and white adipose tissue distribution.
brain stuff = bitch tits
fat boys could be ruined for life, the developmental windows have closed
they may respond like girls medically, forever
Estrogen actions in skeletal muscle, liver, adipose tissue, and immune cells are involved in insulin sensitivity as well as prevention of lipid accumulation and inflammation. Estrogen actions in pancreatic islet β-cells also regulate insulin secretion, nutrient homeostasis, and survival. Estrogen deficiency promotes metabolic dysfunction predisposing to obesity, the metabolic syndrome, and type 2 diabetes. We also discuss the effect of selective estrogen receptor modulators on metabolic disorders.
I hope the fat acceptance lot don’t find this.
But not all fat is bad, especially evolved fat on women.
It makes WOMEN healthier, but never men. Classic sex differences. Women have curves.
Adipose tissue is an organ with active endocrine function involved in the regulation of energy balance and glucose homeostasis via multiple metabolic signaling pathways targeting the brain, liver, skeletal muscle, pancreas, and other organs. There is increasing evidence demonstrating that the female sex hormone, estrogen, regulates adipose development and improves systemic glucose homeostasis in both males and females. The underlying mechanism linking estrogenic regulation in adipose tissue and systemic glucose metabolism has not been fully elucidated, but is thought to include interactions of estrogen receptor signaling events involving lipolytic and/or lipogenic enzyme activity, free fatty acid metabolism, and adipocytokine production. Thus, understanding the effects of estrogen replacement on adipose tissue biology and metabolism is important in determining the risk of developing obesity-related metabolic disorders in patients undergoing treatment for sex hormone deficiency. In this report, we review literature regarding the role of estrogens and their corresponding receptors in the control of adipose metabolism and glucose homeostasis in both rodents and humans. We also discuss the effects of selective estrogen receptor modulators on glucose metabolism.
Fat is a more active organ in women.
Men taking T can have heart risks and metabolic issues, regardless of weight.
The data suggest that estrogen use in American Indian postmenopausal women may relate to deterioration of glucose tolerance. Longer duration of estrogen use among current users may relate to an increased risk of type 2 diabetes.
wouldn’t the pill do the same? is that why young women are obese with diabetes now?
The normal range of estrogen varies depending upon the patient’s age. Typically a women aged 20 to 29 will have an average level of 149 pg/ml (pictograms per milliliter). A female aged 30 to 39 will average a level of 210 pg/ml. And those over 40 but not in menopause will have an average level of 152 pg/ml. These average levels can vary day to day depending on each female’s menstrual cycle.
Yes, female estrogen peaks in the 30s.
The pedophiles like to try and bury that blood test fact by claiming nonsense about teens.
Stress also can contribute to a high estrogen level.
.According to a 2016 study in the Macedonian Journal of Medical Science, HRT could help treat insulin resistance due to low estrogen levels, although more research is needed before HRT can be said to effectively treat insulin resistance in women with low estrogen levels 13⭐
.are they suggesting fat people need more estrogen?
Signs of Insulin Resistance
According to Diabetes.co.uk, the signs of insulin resistance can include excessive fatigue, hunger, difficulty concentrating and weight gain
. Low estrogen levels may be associated with insulin resistance, which is also more likely to occur if you have gained excess weight or tend to carry fat in the belly area .
Diabetes.co.uk also states that insulin resistance can be improved by doing things like eating less carbohydrates, reducing calories, getting more exercise, reducing stress or even having weight loss surgery 13⭐
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.”
Paternal age negatively predicts offspring physical attractiveness in two, large, nationally representative datasets
Freeze your sperm at 18 for optimum freshness.
Effect of paternal age on offspring attractiveness is investigated in two datasets.
Various covariates are utilized.
Significant negative effects are found in both datasets.
Effects are independent of birth order.
Findings consistent with paternal age as a source of new mutations in offspring.
The effect of paternal age on offspring attractiveness has recently been investigated. Negative effects are predicted as paternal age is a strong proxy for the numbers of common de novo mutations found in the genomes of offspring.As an indicator of underlying genetic quality or fitness, offspring attractiveness should decrease as paternal age increases, evidencing the fitness-reducing effects of these mutations.
That’s a hard rectal red pill.
I’m sure the manosphere will try its hardest to ignore like the dead and defective babies.
Thus far results are mixed, with one study finding the predicted effect, and a second smaller study finding the opposite. Here the effect is investigated using two large and representative datasets (Add Health and NCDS),
holy Jesus a sound method
I almost fell off my high horse
both of which contain data on physical attractiveness and paternal age.
Validity! Validity! My queendom for some statistical validity!
The effect is present in both datasets, even after controlling for maternal age at subject’s birth, age of offspring, sex, race, parental and offspring (in the case of Add Health) socio-economic characteristics, parental age at first marriage (in the case of Add Health) and birth order.
The confound control is practically orgasmic, I can’t wait to see how they mansplain this one away.
That is perfect method. But it triggers butthurts and their precious feefees are hurt by the mere implication that degenerate older dads are bad for their kid’s health. Because all those upper crust respectable 1950s dads were like “60 is the new 20 lol!” Who gives a shit if your kids need you past high school? You got more priceless clubbing times you don’t remember, that’s what really matters. Not seeing your grandkids.
Class, race, sex, age at marriage, birth order, maternal age, offspring age – there’s literally nothing else to control for. Nothing. It’s flawless.
THESE. ARE. THE. STUDIES. WE. NEED.
Logically, since women are born with most of their eggs, there wouldn’t be a maternal effect. It isn’t constantly replenishing like the male gamete. Cell division’s a bitch. Male lifestyle for all his years prior
affects the child at conception (and even which sperm is conceived) far more than the details of pregnancy (minus pollutants it’s pretty much the same as in ancient times, the womb is not a new environment).
Maybe add child health although those studies already exist to cross-reference with attractiveness?
As in, are the girls more womanly as adults in WHR and the boys have more manly frames (broad shoulders, narrow waist, which should be a metric of its own)? Or less gender typical? Even androgynous, or fully gender-atypical?
Do younger or older fathers produce better-looking kids in the gendered sense?
[We can tell by looking at old photos but let’s pretend.]
Give me a time machine, please. The ugly wigger types hurt my eyes.
[I have also noted mannish looking sisters tend to be the older, “ugly” sister of two -coughs Beatrice- and the girly looking brothers tend to be the younger, usually gay one. Cannot unsee.]
“In addition to their attractiveness and intimidatory effects, human secondary sexual characters also provide cues to hormonal status and phenotypic quality consistent with the good genes model of sexual selection (which includes parasite resistance). Low waist-hip ratio is sexually attractive in women and indicates a high estrogen/testosterone ratio (which favors reproductive function). Facial attractiveness provides honest cues to health and mate value. The permanently enlarged female breast appears to have evolved under the influence of both the good genes and the runaway selection mechanisms. The male beard is not obviously related to phenotypic quality and may have evolved through a process of runaway intersexual selection.”
The beard can also be a sign of poor grade genes e.g. savages, wolf man. Overall bone structure uber alles.
Maybe factor in sexual activity of the father prior to conception? Especially partner count and STDs. STDs are known to harm attractiveness in the host [coughs David Beckham, most of Hollywood] so why not the offspring’s?
Back to the top study:
The apparent robustness of the effect to different operationalizations of attractiveness suggests high generalizability, however the results must be interpreted with caution, as controls for parental levels of attractiveness were indirect only in the present study.
aka please don’t sue us but you know it’s true
But you can wait forever because the Jews said so!
“However, birth rates are much higher in countries where the men are predominantly uncircumcised.”
There is no question that an uncircumcised man has a cooler penis than a circumcised man in the flaccid state. For some reason, removal of the foreskin is the reason for this. There seems to be some sort of temperature sensor in the foreskin that may control penile temperature. Removing the foreskin gets rid of this sensor.
It only takes a few temperature degrees of difference to damage sperm. As the penis is in close proximity to the testicles, it’s quite likely that a cooler penis would help keep the testicles cooler (Remember that men are more potent in the colder months of the year). Under these condition, if the testicles got too cold, they can always be retracted closer to the body.
Almost like God gave men a prepuce solely for this evolutionary function in reproduction.
…Now consider this: Circumcised and uncircumcised men have the same penis temperature on full erection, as we stated earlier in this article. So, clearly, there is a specific reason why a natural-uncircumcised penis remains at a cooler temperature during the flaccid state. When the penis is erect it is no longer in close proximity with the testicles, so penile temperature should not affect the testicular temperature at this phase (be the penis circumcised or uncircumcised).
Upon orgasm, the penis tends to retract more into the pelvis (at least with my experience). Due to the friction and increased blood flow that occurred during the sexual act, it makes sense that the penis will have an increase in temperature in a flaccid state post-sex than in a flaccid state previous to the sexual act. Could this retraction be another mechanism for the “heated” penis to steer clear of the testicles?
Women’s faces and voices may be cues to their reproductive potential. If so, then individual differences in indices of female fecundity and residual reproductive value, such as hormonal profiles, body composition, and age, should be associated with women’s facial and vocal attractiveness to men. However, previous research on these associations is sparse, has rendered mixed results, and is limited to Western samples. The current study therefore explored relationships between correlates of reproductive capability (testosterone levels, age, and body mass index [BMI]) and facial and vocal attractiveness in women from industrial and foraging societies. Women’s facial and vocal attractiveness was associated with each of these indicators in at least one of the two samples. The patterns of these associations suggest that women’s faces and voices provide cues to both common and unique components of reproductive potential and help explain the evolution of men’s mating preferences.
Lesson: Avoid the manjaw.
Women change their vocal pitch all the time though. European women are taught to make it lower at school (speak up = louder, lower pitch), Asians try to make it higher. The key is how they sound when hysterically upset. That’s their true level. Europeans go up, Asians down.
Attractive facial features in women are assumed to signal fertility, but whether facial attractiveness predicts reproductive success in women is still a matter of debate. We investigated the association between facial attractiveness at young adulthood and reproductive life history—number of children and pregnancies—in women of a rural community. For the analysis of reproductive success, we divided the sample into women who used contraceptives and women who did not.
So partnered, married women. Not single ones.
Introducing two-dimensional geometric morphometric methodology, we analysed which specific characteristics in facial shape drive the assessment of attractiveness and covary with lifetime reproductive success. A set of 93 (semi)landmarks was digitized as two-dimensional coordinates in postmenopausal faces. We calculated the degree of fluctuating asymmetry and regressed facial shape on facial attractiveness at youth and reproductive success. Among women who never used hormonal contraceptives, we found attractive women to have more biological offspring than less attractive women. These findings are not affected by sociodemographic variables. Postmenopausal faces corresponding to high reproductive success show more feminine features—facial characteristics previously assumed to be honest cues to fertility. Our findings support the notion that facial attractiveness at the age of mate choice predicts reproductive success and that facial attractiveness is based on facial characteristics, which seem to remain stable until postmenopausal age.
African and European perception of African female attractiveness
Dare you to do the same study with every race judging every other.
Majority of research on attractiveness is restricted to faces of European origin. The perception of attractiveness may, however, vary across communities due to variations in both facial morphology and local standards of beauty. We investigated the relative contribution of four facial markers of attractiveness based on 101 female facial portraits (standardized, non-manipulated) from Cameroon and Namibia, which were assessed by local male raters and by raters from a distant European population, the Czech Republic. Images from Cameroon include only women of Bantu origin, while Namibians are represented by women of both Bantu (Owambo/Herero) and Nama origin. While controlling for age and BMI, we explored the relationship between female attractiveness and a set of facial traits: fluctuating asymmetry, averageness, shape sexual dimorphism, and skin color (rated and measured in CIELab color space).
In the Cameroonian sample, local male raters favored lighter-skinned female faces with morphology closer to average. The attractiveness of Nama women as rated by Nama men positively correlated with lighter complexion, but this did not extend to rating by Cameroonian men. The attractiveness of Namibian Owambo/Herero women was positively associated with facial femininity and lighter complexion when judged by both Cameroonian and Nama male raters. In all samples, the attractiveness as rated by Czech men was predicted by age and BMI, but not by skin color. We found no significant association between attractiveness and fluctuating asymmetry in any of the tested samples. When controlling for age, the effect of skin color on attractiveness turned to be non-significant in the Owambo/Herrero and Nama sample, but remained significant in the Cameroonian sample. Variations in skin color thus represent an important factor of African female attractiveness within the African context, but they do not seem to affect judgements made by European raters.
They don’t want any of them.
Sensitivity to some facial markers of female attractiveness thus seems to be restricted to regional populations and/or constrained by shared ethnicity.
Paler women have more oestrogen. So duh.
Women reject old guys who’d give them dead or ugly kids:
Research in evolutionary psychology, and life history theory in particular, has yielded important insights into the developmental processes that underpin variation in growth, psychological functioning, and behavioral outcomes across individuals. Yet, there are methodological concerns that limit the ability to draw causal inferences about human development and psychological functioning within a life history framework. The current study used a simulation-based modeling approach to estimate the degree of genetic confounding in tests of a well-researched life history hypothesis: that father absence (X) is associated with earlier age at menarche (Y). The results demonstrate that the genetic correlation between X and Y can confound the phenotypic association between the two variables, even if the genetic correlation is small—suggesting that failure to control for the genetic correlation between X and Y could produce a spurious phenotypic correlation. We discuss the implications of these results for research on human life history, and highlight the utility of incorporating genetically sensitive tests into future life history research.
I don’t think debtor’s prisons will come back – but if you breed it, you should feed it. I think the abandoned women that existed since Biblical times will just hire bounty hunters to shoot the first family deserter for a share of his life insurance policy.
Patriarchs everywhere would rejoice at culling the cads. The women get a widow’s pension.
Everyone wins. Hey, you said “until death do us part”. Men used to die by their oaths.
I have noticed that immigrant men have a higher pitch than their non-immigrant relatives.
Maybe the act of immigration impairs masculinity?
Low male voice pitch may communicate potential benefits for offspring in the form of heritable health and/or dominance, whereas access to resources may be indicated by correlates of socioeconomic status, such as sociolinguistic features. Here, we examine if voice pitch and social dialect influence women’s perceptions of men’s socioeconomic status and attractiveness. In Study 1, women perceived lower pitched male voices as higher in socioeconomic status than higher pitched male voices.
A lot of PUAs get shot down for 1. being brown and feeling entitled to a white woman, the lowest miscegenation group also further sickened by repeated forced “refugee” interactions and 2. having a high pitch voice and effete face compared to their national relatives. Compare within the white race, the “Latin lover” in Italy versus Italian immigrants raised and living in London, who sound like cartoon chipmunks by comparison.
Yes, we notice.
No, you can’t change it. We notice.
Same applies to white men who moved South so it appears to be immigration. Either being an immigrant or the act itself makes a man less manly. Most obviously, torso body fat deposition like a woman of their group and the sisters become like the men at home, more athletic.
In Study 2, women independently perceived lower pitched voices and higher status sociolinguistic dialects as higher in socioeconomic status and attractiveness.
It isn’t the money, it’s the genes.
Good genes, good brains, good money. Fixating on the money is what ugly guys do – Muslim prince to Jewish media mogul.
We also found a significant interaction wherein women preferred lower pitched men’s voices more often when dialects were lower in sociolinguistic status than when they were higher in sociolinguistic status.
Capacity to protect. Not a desk jockey. The middle-class is effeminate. They want army. No cowards.
Women also perceived lower pitched voices as higher in socioeconomic status more often when dialects were higher in sociolinguistic status than when lower in sociolinguistic status.
Women know quality, really? Almost like our lives depend on it.
Finally, women’s own self-rated socioeconomic status was positively related to their preferences for voices with higher status sociolinguistic dialects, but not to their preferences for voice pitch.
Plenty of men chose to marry down to get a looker out of their genetic league, hypergamy.
Erotic capital is worth it, as you can tell by the fertility study above, even post-menopausal they’re better-looking.
Hence, women’s preferences for traits associated with potentially biologically heritable benefits, such as low voice pitch, are moderated by the presence of traits associated with resource accrual, such as social dialect markers. However, women’s preferences for language markers of resource accrual may be functionally independent from preferences for potential biological indicators of heritable benefits, such as voice pitch.
Amphetamines (and any other drugs that block dopamine indirectly) cause prolactin (yes, the milk hormone) levels to rise. Higher prolactin levels cause a reduced libido (your body* thinks it’s pregnant or postpartum) and tank your testosterone levels.
*Men are mutated women so yes this applies to you. Biology, bitch. If the template for human weren’t female (at least one X), we couldn’t give birth.
Why else do you think they wanna foist those drugs onto little boys?
Why do you think there’s a random surge in boys actually believing their girls, because the parents cleared use of amphetamines? We literally give kids amphetamines. We live in a society. This permanently alters their brain development, irreversible in adulthood.
“These results indicate that Amph is a poor PRL suppressor in either normo- or hyperprolactinemic subjects. It is proposed that this may be due to the drug’s ability to effect release of dopamine mainly from a non-granular pool of the amine.”