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.”
Estrogen facilitates higher cognitive functions by exerting effects on brain regions such as the prefrontal cortex and hippocampus. Estrogen induces spinogenesis and synaptogenesis in these two brain regions and also initiates a complex set of signal transduction pathways via estrogen receptors (ERs). Along with the classical genomic effects mediated by activation of ER α and ER β, there are membrane-bound ER α, ER β, and G protein-coupled estrogen receptor 1 (GPER1) that can mediate rapid nongenomic effects. All key ERs present throughout the body are also present in synapses of the hippocampus and prefrontal cortex. This review summarizes estrogen actions in the brain from the standpoint of their effects on synapse structure and function, noting also the synergistic role of progesterone. We first begin with a review of ER subtypes in the brain and how their abundance and distributions are altered with aging and estrogen loss (e.g., ovariectomy or menopause) in the rodent, monkey, and human brain. As there is much evidence that estrogen loss induced by menopause can exacerbate the effects of aging on cognitive functions, we then review the clinical trials of hormone replacement therapies and their effectiveness on cognitive symptoms experienced by women. Finally, we summarize studies carried out in nonhuman primate models of age- and menopause-related cognitive decline that are highly relevant for developing effective interventions for menopausal women. Together, we highlight a new understanding of how estrogen affects higher cognitive functions and synaptic health that go well beyond its effects on reproduction.
Men dosing testosterone are called meatheads for a reason, they would logically throw off their other hormones and functionally retard themselves. Because this ONE time, you can trust the pill people. No IQ studies in testosterone supplementing men, I guess there’s a good reason. They just forgot?
The results are, unfortunately, controversial and puzzling. Dosing, timing, even the application route seem to considerably affect the outcomes.
You’re not trying to rig it at all, huh?
Reduction to dihydrotestosterone by 5-alpha reductase increases the androgen activity; conversion to estradiol by aromatase converts the androgen to estrogen activity.
Recently, the non-genomic effects of testosterone on behavior bypassing the nuclear receptors have attracted the interest of researchers. This review tries to summarize the current understanding of the complexity of the effects of testosterone on brain with special focus on their role in the known sex differences.
a very important study in rhesus monkeys showed that pharmacological castration reduced and testosterone supplementation normalized anxiety levels (Suarez-Jimenez et al., 2013).
on the other hand, in both men and women, testosterone supplementation leads to improvement of depressive symptoms (Pope et al., 2003; Miller et al., 2009). However, not all interventional studies confirmed the anti-depressant effect of testosterone. At least in one published randomized controlled trial, the effects of testosterone were comparable to placebo effects (Seidman et al., 2001). Similarly, not all observational studies show a consistent picture. At least in one small study, depressive women had higher testosterone (Weber et al., 2000).
Another experiment on intact rats revealed that the effect of testosterone on depression is dose-dependent (Buddenberg et al., 2009).
Over the counter won’t work.
During the productive ages and even in early adulthood, men generally outperform women in spatial abilities (Linn and Petersen, 1985)
Even for a few years you’re in college? Is that it?
Spatial thing is probably due to error, thus would be discounted under a valid method.
Error rate as well as the reaction time negatively correlated with testosterone (Hooven et al., 2004).
In another study, actual testosterone was not associated with spatial abilities, but prenatal testosterone correlated positively with spatial abilities in women (Kempel et al., 2005).
Congratulations, you’re on the female level. Apply your non-toxic internet cream.
In line with these findings is the lack of an association between actual salivary testosterone levels and mental rotation in men and women (Puts et al., 2010).
Actual science, no replication issue.
However, in a large observational study analyzing spatial abilities in adult men from various age categories, low testosterone was associated with better spatial visualization (Yonker et al., 2006).
Actual science, no replication issue.
Plus multiple ages in ADULT men, important.
In a very interesting study, it was found that in men, the pubertal concentrations of testosterone are negatively associated with mental rotation in the adulthood (Vuoksimaa et al., 2012). In the same paper, the comparison of twins is reported. The twin with higher testosterone scored worse in the mental rotation tests. The results are contradictory, but may depend on the test used for the assessment of spatial abilities.
Counting fluke correct answers and not errors to force a finding is scientism. Bad method.
When virtual Morris water maze was used, a positive correlation between testosterone and spatial navigation was found in women, but not in men (Burkitt et al., 2007). The size of the corpus callosum seems to add complexity in the relationship between spatial abilities and testosterone (Karadi et al., 2006). This might be one of the causes for negative findings in studies where some of the determinants are missing (Kubranska et al., 2014). Another cause is likely the selection of the tested population. In gifted children, a negative correlation between salivary testosterone and spatial abilities was found (Ostatnikova et al., 1996).
Negative findings are real science.
And that’s important.
In Chinese men, the accuracy in mental rotation tests was comparable to Americans, but the reaction times were longer indicating that cultural differences could add to the variability of published results (Yang et al., 2007).
No they didn’t rush the test out of boredom. Lower error rate, I’d bet.
Last but not least, genetic factors likely modulate the effect of testosterone. We have previously shown that at least in gifted boys, genetic polymorphisms influencing testosterone metabolism affect also its relationship to mental rotation (Celec et al., 2009, 2013). Especially, the CAG short tandem repeat in the exon 1 of the androgen receptor gene seems to be important for the action of testosterone and its metabolites (Nowak et al., 2014). Despite all complexity, the current picture indicates that the association between testosterone and spatial abilities is curvilinear and sex-dependent.
aka more is NOT better and it’s genetic, morons
In women higher testosterone is associated with better mental rotation, in men lower testosterone is associated with better spatial abilities. This seems to be true both for actual testosterone (Moffat and Hampson, 1996) and for prenatal testosterone (Grimshaw et al., 1995). Supplementation of testosterone in older men results in improvement of spatial abilities, but it is accompanied with changes in estradiol metabolism and it is likely that this interferes with modifications of spatial abilities (Janowsky et al., 1994).
They only studied spatial, not global, I checked.
Even in rats, testosterone administration affects the strategy of the animals in spatial tasks (Spritzer et al., 2013). However, the interaction between testosterone and mental rotation tests is bidirectional. It has been shown that mental rotation testing affects testosterone, at least in women (Durdiakova et al., 2012).
Doing smart things causes the brain to…. adapt? Really?
Does our pulse increase when we run? Some Sherlock Holmes do a fucking study.
Moreover, participants with complete androgen insensitivity syndrome presented with female-like neural activation pattern in the parietal lobe, indicating that gonadal hormone exposure rather than genetic sex itself plays role in brain functions (Van Hemmen et al., 2014).
Supplementing won’t work, you’re worse than the trannies. They don’t claim brain benefits.
The menstrual cycle and thus the involvement of sex hormones, including testosterone, in spatial abilities was further confirmed by Pletzer et al. In their study, error rates linked with deactivation of inferior parietal lobes and prefrontal lobes were higher during luteal phase for verbal tasks, while in the follicular phase, spatial abilities in females were confirmed (Pletzer et al., 2011).
One of the major factors that might explain the differences between the results of various studies is the variability of the examined populations. As mentioned above, the cultural differences, sex and age have all been shown to impact the physiological effects of testosterone.
Standardization in this area would surely improve our understanding of the neuroendocrinology of testosterone. More systematic research using the whole spectrum of available tools and looking at the various physiological aspects is needed. However, to be able to publish such research, journals should accept manuscripts based on the design and not on the results. Otherwise, the publication bias that is obvious in the so far published literature will continue to be a big issue. Many researchers in this field complain about negative results that are very difficult to publish in the relevant journals. The number of such unpublished observations and experiments is unknown. But based on our humble experience, the negative results will probably be more common than the published positive ones. And if the contradictory published findings are added, the picture gets even more confusing. Large systematic research projects with more cooperation between the most productive research teams is definitely needed.
You can’t because the low IQ men will complain if you publish negative findings.
Testosterone plays a role in the organization of behavior during development. The authors examined whether testosterone could play a maintenance role in behavior as well. In a double-blind manner, verbal and visual memory, spatial cognition, motor speed, cognitive flexibility, and mood in a group of healthy older men who were supplemented for 3 months with testosterone were assessed. The increase in testosterone levels to 150% of baseline levels resulted in a significant enhancement of spatial cognition, but no change in any other cognitive domain was found.
You’ll be slightly more able to parallel park. Like when you were young.
Louder for the slow:
no change in any other
cognitive domain was found
NO IMPROVEMENT IN MEMORY
NO IMPROVEMENT IN MOTOR SPEED
NO IMPROVEMENT IN COGNITIVE FLEXIBILITY
NO IMPROVEMENT IN MOOD.
Did I stutter?
Testosterone supplementation influenced the endogenous production of estradiol, and estradiol was found to have an inverse relationship to spatial cognitive performance. These results suggest that testosterone supplementation can modify spatial cognition in older men; however, it is likely that this occurs through testosterone’s influence on estrogen.
Men didn’t evolve to live long, so it isn’t so much remarkable that women live longer with healthier brains but men, to be competitive with other men in youth and war, age terribly simply because so few would survive there’s no evolutionary pressure.
Some tough choices ahead for the cooties crowd.
Stick to imaginary phantasms of 20th century masculine superiority solely intended to run up credit debt or actually be healthier.
Here comes the academese:
“Researchers remain uncertain why such metabolic differences exist”
“It’s not that women’s brains seem to age slower than men’s,”
Watch the twist.
“Rather, it seems that women’s brains start off at a younger age when they reach adulthood, and they keep that throughout the remainder of their adulthood, basically buying them a few extra years.”
Not how it works. At all.
It’s like saying you start a race at the finish line, words have meanings.
If they’ve reached adulthood, they’ve reached adulthood. You can’t change the meaning to be quantum. Women mature faster (partially from earlier puberty and slower, longer sum development time because of that) and go on to metabolically age better because testosterone is known to burn out the system.
Gradual puberty + lower T = good for long-term brain health.
aka Not women’s fault. Help your fellow men. Maybe that explains why celibates like Tesla (who, let’s face it, probably didn’t masturbate), who kept their T-levels low as a result, lived longer and stayed lucid. Maybe that’s why monks live longer too, staying sharp. Male chastity has observable benefits.
The autobiographies of genius seem to evidence longer average puberty, too. The sensitive kid who’s a later bloomer?
The Victorians called masturbation self-abuse because the compulsion/addiction would tend to be co-morbid with other mental problems, including depression. How many porn addicts are depressed?
And what do they do to self-soothe because (someone) tells them it’s unanimously ‘good for you’?
Even nuns tend to live longer which does point to lower testosterone being a pre-requisite for a long life, neatly explaining why male levels gradually lower. It isn’t like evolution is picking on men. Aggressive animals have shorter lifespans across species. This is the price of being the protector/provider sex.
“Overall, men with circulating testosterone levels between 9.8 to 15.8 nmol/L range tended to live the longest.”
Men are entitled to know what their healthy levels should be, study them!
Men age faster cognitively, he’s like a magician trying to switch your attention onto women when there’s a medical problem with men.
Assuming they want to live long and prosper.
Like, sorry, if that’s a sexist assumption.
“Previous studies have found that aging women often exhibit stronger reasoning, memory and problem-solving skills than males of the same age. But it’s unclear whether this trend is related specifically to metabolism or to a different aspect of brain function.”
“This might mean women are a little bit more resilient to certain aspects of brain aging in general, but it could also introduce certain vulnerabilities,”
Lying liar. Not even one example? How can you try to spin a youthful brain as a bad thing?
Women aren’t so much MORE resilient (although oestrogen helps) but men are MORE fragile.
“Having a younger brain for longer could make the brain more vulnerable to certain things as well.”
Still no mention of men? This isn’t a woman’s issue, there’s nothing new here as stated, women already perform better as a known overall finding*, he totally ignores what men need because it involves admitting they aren’t the best at something….
These arrogant men are sex traitors. Their ego won’t let them admit men need help. So have fun with higher neurodegeneration risk because one guy won’t admit he’s not #1 at everything.
Men are not the control group, it’s the mean between both groups.
Basic category error and erroneous maths.
Hubris is a deadly sin. Treating male ill-health like it’s normal will literally kill men.
OT but relevant:
If we took men as the control, the shorter male lifespan is not only normal but hinted at being desirable, you don’t want to change the norm, with women being unusually longer-lived (greater distance from norm). Actually, the average is between the groups, again. The difference from the norm is smaller, easier to broach and bring those below it up to speed.
*Because unlike IQ studies, they can’t conveniently ‘exclude’ the left-side of the male bell curve to skew their findings dishonestly. This happens after they sample from middle-class academia pupils largely from suburban populations, a huge bias/filter itself.
Sure, throw other men under the bus and blame women for biology. Sexism both ways!
“Good-looking individuals are more likely to have right-wing political views than less physically attractive people, according to a university study.
The authors of the report, Rolfe D. Peterson from the US Susquehanna University and Carl L. Palmer from the Illinois State University, examined the connection between physical attractiveness and political beliefs, applying multiple surveys measuring people’s attractiveness. “More attractive individuals are more politically efficacious than their peers and more likely to identify as conservative and Republican than less physically attractive citizens of comparable demographic backgrounds,” the report read.”
Comparable demographic background, an important control.
“Political Orientations Are Correlated with Brain Structure in Young Adults”
“We found that greater liberalism was associated with increased gray matter volume in the anterior cingulate cortex, whereas greater conservatism was associated with increased volume of the right amygdala.”
“Researchers found major differences in the amount of gray and white matter in the brains of men and women of the same intelligence, suggesting that men and women may derive their intelligence in different ways.”
“”These findings suggest that human evolution has created two different types of brains designed for equally intelligent behavior,” says researcher Richard Haier, professor of psychology at the University of California, Irvine, in a news release. “In addition, by pinpointing these gender-based intelligence areas, the study has the potential to aid research on dementia and other cognitive impairment diseases in the brain”
Again, the same IQ score.
Man Card isn’t a MENSA card, accomplish something.
“Positive relationships were found between FSIQ and intracranial gray and white matter but not cerebrospinal fluid volumes. Significant associations with cortical thickness were evident bilaterally in prefrontal (Brodmann’s areas [BAs] 10/11, 47)
IQ so real you can scan someone’s brain, almost.
and posterior temporal cortices (BA 36/37) and proximal regions.
Sex influenced regional relationships;
Before any sexist bitch goes to twist this, different does not mean inferior. This is a study of intelligence, NOT stupidity.
You can’t prove a negative and individuals are not groups?
The obvious pointed out? Okay, let’s continue.
women showed correlations in prefrontal and temporal association cortices, whereas men exhibited correlations primarily in temporal–occipital association cortices.
An idiot reading that would assume women are smarter, prefrontal doesn’t always mean smarter, necessarily, it’s just a group-level skew of structural difference. However, it does explain the higher female average.
In healthy adults,
important distinction, many brain studies are conducted on the undeveloped (teens) or pathologies
neither of which generalize to a HEALTHY, ADULT population
[sorry for the smart people tuning in, idiots twist what I type]
greater intelligence is associated with larger intracranial gray matter and to a lesser extent with white matter.
Plot twist: both matter.
Almost like we evolved.
Variations in prefrontal and posterior temporal cortical thickness are particularly linked with intellectual ability.
PF – registered as female strength, generally.
PT – registered as male and female strengths, generally.
This isn’t better/worse, it’s apples/oranges.
Even race overwhelms sex as a confound in IQ (so does class, education etc).
Sex moderates regional relationships that may index dimorphisms in cognitive abilities, overall processing strategies, or differences in structural organization.”
Trans. sex differences real yo.
Overall, key word.
Moderates, may index, differences. As in, these processes still occur but like a road trip, each take different paths different enough to map but not distinct enough to be unrecognizable.
Fake masculinity is really bad for men. You can’t cheat code becoming a man.
Long-term AAS use is associated with right amygdala enlargement and reduced right amygdala rsFC with brain areas involved in cognitive control and spatial memory, which could contribute to the psychiatric effects and cognitive dysfunction associated with AAS use.
The MRS abnormalities we detected could reflect enhanced glutamate turnover and increased vulnerability to neurotoxic or neurodegenerative processes, which could contribute to AAS-associated cognitive dysfunction.
Now the right amygdala enlargement sounds like the natural conservative difference but understand it’s rooted, not in experience and genuine masculine virtue, but chemical dependence. Without the drugs, it’ll shrink right back and possibly atrophy.
This would be like congratulating a tall guy who took HGH for his superior genetics. No. It’s a superficial, fake result.
The cognitive control is impaired, that’s regression. The meat head stereotype is true, biologically. Useless.
I wonder how many male suicides were on steroids? Both groups happen to be middle-aged men in fear of the Wall.
Whatever the details, it makes them biologically vulnerable compared to their natural state, the opposite of fitness.
Ironically, they’re more vulnerable to microplastics and xenoestrogens.
To further screw the point in… that brain region explicitly mentioned?
Right amygdala rsFC study:
“In high HA scorers, we also observed stronger right amygdala rsFC with the dorsomedial prefrontal cortex (dmPFC), which is implicated in negative affect regulation.”
It’s a girly brain thing to do with harm avoidance. [aka common sense]
“may represent a vulnerability marker for sensitivity to stress and anxiety (disorders).”
So the meat head with reduced volume (therefore not conservative*) is dumber, senses dulled by drugs and more likely to fail to get the brain signals to avoid trouble. Sounds like a future in handcuffs. They can’t perceive danger nor regulate negative emotions like anger or shame after rejection. Basically, they’re future chimp-outs waiting to happen, whatever their race**. Less able to CONTROL emotions, the broflakes.***
Hair-trigger temper calling out people for looking at him.
The guy who picks on people but never actually expects to get hit.
Will grab a woman and be shocked she slaps him. That’s the one.
*because, again “greater conservatism was associated with increased volume of the right amygdala.”
[as referenced above]
yet they have less?
So steroids make men more left wing. It isn’t the correct area and type to be considered otherwise.
ISN’T SCIENCE FUN, FELLOW RED PILLS.
ACCEPTING FINDINGS EVEN WHEN WE DON’T LIKE THEM, BRO.
My guess is it messes with their sexual reward system and produces impotence, porn addiction, dissatisfaction.
“Infertility is defined by the WHO as the failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse and a male factor is present in up to 50 % of all infertile couples. Several conditions may be related to male infertility.
Substance abuse, including AAS, is commonly associated to transient or persistent impairment on male reproductive function, through different pathways. Herein, a brief overview on AAS is offered. Steroids biochemistry, patterns of use, physiological and clinical issues are enlightened. A further review about fertility outcomes among male AAS abusers is also presented, including the classic reports on transient anabolic steroid-induced hypogonadism (ASIH), and the more recent experimental reports on structural and genetic sperm damage.”
hypogonadism = tiny balls
“In layman’s terms, it is sometimes called interrupted stage 1 puberty”
You’d have to be a moron already to think supplementing that shit makes you manly.
Nice muscles bro, shame you hit rewind on puberty!
They impair their body’s ability to naturally produce testosterone in future…. idiots.
Darwin Award category?
Big Pharma’s best customer? Like Israel’s Viagra use. Israel and America, top consumers.
“Through these connections, the ACC is thought to be involved with a number of functions related to emotion including the regulation of overall affect, assigning emotions to internal and external stimuli, and making vocalizations associated with the expression of states or desires.
The ACC also seems to contribute to the regulation of autonomic and endocrine responses, pain perception, and the selection and initiation of motor movements. Additionally, there are other areas of the ACC that are involved in various aspects of cognition ranging from decision-making to the management of social behavior.”
“A new YouGov survey, which asked over 19,000 participants from the UK, France, Germany, Sweden and Denmark about both their politics and their sex lives, has found conservatives to be happier in the bedroom than liberals, with those identifying as “very right-wing” found to be the happiest.”
So much for the benefits of slutting. Muh experience. Yes, experiencing a burning sensation.
If you want a better sex life, don’t be a manwhore.
Chastity is a virtue. Less stress when single, hot sex when married.
“Although epigenetic changes are usually temporary, they involve alterations in the proteins that bind together the long strands of DNA. Thus, they can sometimes be handed down to offspring. According to the hypothesis, homosexuality may be a carry-over from one’s parents’ own prenatal resistance to the hormones of the opposite sex.”
Great man, unusual number of homosexual offspring.
“The initial benefit to the parents may explain why the trait of homosexuality persists throughout evolution, he says.”
Evolution presumes the fit ones will breed more (reducing the downside loss to zero as 52:48 female to male birth ratio) and there’s no parasitism between high and low fitness.
There are other studies along these lines e.g. a review
It’s always the men being the most degenerate, generic finding of sexology.
And they wonder why they die sooner.
Big winners, bigger losers.
“This article reviews the evidence regarding prenatal influences of gonadal steroids on human sexual orientation, as well as sex-typed childhood behaviors that predict subsequent sexual orientation.”
But it doesn’t work the other way around, parent forcing a Barbie on your son.
And it isn’t 1:1, kids will play with most things if allowed.
“The evidence supports a role for prenatal testosterone exposure in the development of sex-typed interests in childhood, as well as in sexual orientation in later life, at least for some individuals.”
Yay, we can blame men! – feminists, if they had any balls
“It appears, however, that other factors,”
“in addition to hormones, play an important role in determining sexual orientation.”
“These factors have not been well-characterized,”
Pathogens, billions of pathogens.
“but possibilities include direct genetic effects, and effects of maternal factors during pregnancy. “
You can try blaming the woman but you’d be wrong. If women were responsible, nobody would be straight because everyone has a mother, and therefore a cause. We wrongly assume anything “wrong” with a baby is the mother’s fault. This is like blaming your food poisoning on the oven rather than the handling before that stage (paternal factors, research the other half too, paternal factors!) or once it comes out.
Paternal degeneracy would be an interesting factor. A very interesting factor.
Are promiscuous men* likelier to have gay sons, easy observational study.
You’d essentially be testing for r-selection. Homosexual men are extreme sexual r-types: high volume, low discrimination, nomadic patterning…
“Although a role for hormones during early development has been established, it also appears that there may be multiple pathways to a given sexual orientation outcome and some of these pathways may not involve hormones.”
Where’s the science, right?
How would it occur from father to germline like an STD, mother to child or both?