rtrixie:

Whelp, guess 4chan is kill.

Whatever is the case, similar things were happening when /pol/ was deleted for the second time. Jan 2011. I never went back since. And I know others who didn’t and they lost a lot of main contributors. The only reason it was even brought back again was in a futile attempt to compete with reddit when the “toning down” of 4chan wasn’t working out. Not long after its deletion the original /new/ (/pol/, before it was renamed) was reformed, and for a period of about six months the lack of shit posters to posters with informed knowledge on various subjects was impressive for an anonymous imageboard. Fresh content was the norm, not the exception. It was though everyone who actually posted with insight on the old /new/ had converged. The new /pol/ is like /b/ - there’s no room for resourceful content, as such threads get pushed down by an over supply of poor posters who lack a strong suit on any given subject and are unable to contribute.

With the content that was being posted I put together those old “Debunking Out-of-Africa” copy-pastas on /new/, before I knew better. Many here still post what are clear extracts from them, complete with my same links/errors. You can often spot a typical 4channer from /pol/ on tumblr — with similar posts containing a series of studies, many of them outdated, one after the other to win an argument. Such data which they cannot actually uphold, or have even read. It’s mostly harmless, often serves its place, and sees people introduced to the relevant subjects. I’ve done it. However, I’ve tried to inform people such as logicd and that porcelain-doll girl about the ill-founded inconsistencies in their occasional “Out-of-Africa has been debunked” replies, but I don’t know, the multi-regional “anything other than Africa” theories have become gospel to some.

Of course, all imageboards go downhill. Eventually I signed up on tumblr - it’s a different "audience" here anyway, and the blog serves as a nice archive.

(via anarchosaur)

Remember: biology mostly doesn’t matter. The sexes have exactly equal mean abilities and interests, in fact, bias against women resolves all occupational sex differences. Moreover, toy choice and sex-typical play in children is not sexually dimorphic, but instead a product of cultural conditioning. Race doesn’t exist, so there can hardly be cognitive or behavioural differences between races. Moreover, average cranial capacity is the same in all humans. IQ is not highly heritable, so eugenics cannot work.

Homosexuality, which ought to be genetic, although nothing else ought to be, makes perfect evolutionary sense, but ethnocentrism does not. Aside from determining how we look, genes are junk, and parenting impacts how we turn out as all human behaviour is learnt. Such that practice makes perfect, with no innate mental differences (especially at the group level) and along with equal opportunity, individuals can become anything they put their minds to. Additionally, everyone has the capacity for personal responsibility, as individuals make independent choices by voluntary decision. In fact, since human behaviour is so easily moulded by the environment, we know that good people are good because they’re taught right from wrong. We thus just need to teach people the right virtues to stop them from stealing, raping, and killing.

That’s about right.


Upper-body fat has negative effects and lower-body fat has positive effects on the supply of long-chain polyunsaturated fatty acids that are essential for neurodevelopment. Thus, waist-hip ratio (WHR), a useful proxy for the ratio of upper-body fat to lower-body fat, should predict cognitive ability in women and their offspring. Moreover, because teenage mothers and their children compete for these resources, their cognitive development should be compromised, but less so for mothers with lower WHRs. These predictions are supported by data from the Third National Health and Nutrition Examination Survey. Controlling for other correlates of cognitive ability, women with lower WHRs and their children have significantly higher cognitive test scores, and teenage mothers with lower WHRs and their children are protected from cognitive decrements associated with teen births. These findings support the idea that WHR reflects the availability of neurodevelopmental resources and thus offer a new explanation for men’s preference for low WHR.http://www.cep.ucsb.edu/papers/whrlassekgaulin2008.pdf

Far from being in the eye of the beholder, the very concept of beauty and the human appreciation of attractive people is to a large degree inborn, but this hasn’t stopped campaigns (usually aimed at women) against this very concept. The cliché is that “Western” society has brainwashed us with unrealistic European standards of beauty which women in particular strive to emulate. Apparently, without this “brainwashing” we’d naturally accept people for their “inner” beauty. Not quite:
The hourglass figure is truly timeless:

It is no secret that modern culture places a premium on Barbie-doll shaped bodies. Some scientists have argued, however, that this preference only represents modern Western values. […] Written texts of all ages have the same drift when it comes to the midriff - they consistently describe women’s thin waists as attractive. The conclusion comes from an analysis of British, Indian and Chinese texts dating as far back as the first century AD. According to the researchers, the finding supports the idea that we are hardwired to prefer slender waists, which are linked to good health and fertility. […] In contrast, while breasts had the most romantic references. Apparently, it is the shape (roundness—a sign of youthfulness; Grammer et al. 2003), rather than the size, of breasts that is judged to be beautiful. 

Far from being a "culturally-conditioned" phenomena, the preference for women with slim waists was noted in the literature of three distinct cultures—China, Britain, and India—in texts dating as far back as 2000 years ago. All of the romantic references to the waist described the body part as attractively narrow. There was “not a single exception.”
Large Breasts and Narrow Waists Indicate High Reproductive Potential in Women:

Physical characteristics, such as breast size and waist–to–hip ratio (WHR), function as important features used by human males to assess female attractiveness. Here, we document that women with higher breast–to–underbreast ratio (large breasts) and women with relatively low WHR (narrow waists) have higher fecundity as assessed by precise measurements of daily levels of 17–β–oestradiol (E2) and progesterone. Furthermore, women who are characterized by both narrow waists and large breasts have 26% higher mean E2 and 37% higher mean mid–cycle E2 levels than women from three groups with other combinations of body–shape variables, i.e. low WHR with small breasts and high WHR with either large or small breasts. Such gains in hormone levels among the preferred mates may lead to a substantial rise in the probability of conception, thus providing a significant fitness benefit. […] WHR seems to be a better predictor of reproductive potential than breast size, because it correlates both with E2 and progesterone indices, whereas for breast size only its relationships with E2 are significant. […] Women from the ‘narrow waist, large breasts’ group had 26% higher values of mean E2 and 37% higher values of mean mid-cycle E2 than women from any of the other groups.

Consistent with the fitness benefits associated with low WHRs, with approx. 26% higher levels of estradiol, women with large breasts and narrow waists were found to be nearly three times more likely to get pregnant. As noted, in the middle of their menstrual cycle, this peaks at 37% higher levels than women in the other groups. Lower WHR also effects the female hormone, progesterone, but unlike WHR, breast size alone does not significantly relate to increased progesterone. Here, attractiveness appears as a useful proxy of genetic fitness.
Conversely then, the stigma attached to those with broad waists and increased abdominal fat; universally less attractive body types which are linked to poor health, should too be inborn:Pathogen-avoidance mechanisms and the stigmatization of obese people:

Humans possess pathogen-avoidance mechanisms that respond to the visual perception of morphological anomalies in others. We investigated whether obesity may trigger these mechanisms. Study 1 revealed that people who are chronically concerned about pathogen transmission have more negative attitudes toward obese people; this effect was especially pronounced following visual exposure to obese individuals. Study 2 revealed that obesity is implicitly associated with disease-connoting concepts; this effect was especially pronounced when the threat of pathogen transmission is highly salient. Evolved pathogen-detection mechanisms are hypersensitive, and they appear to play a role in the stigmatization of obese people.

Upper-body fat has negative effects and lower-body fat has positive effects on the supply of long-chain polyunsaturated fatty acids that are essential for neurodevelopment. Thus, waist-hip ratio (WHR), a useful proxy for the ratio of upper-body fat to lower-body fat, should predict cognitive ability in women and their offspring. Moreover, because teenage mothers and their children compete for these resources, their cognitive development should be compromised, but less so for mothers with lower WHRs. These predictions are supported by data from the Third National Health and Nutrition Examination Survey. Controlling for other correlates of cognitive ability, women with lower WHRs and their children have significantly higher cognitive test scores, and teenage mothers with lower WHRs and their children are protected from cognitive decrements associated with teen births. These findings support the idea that WHR reflects the availability of neurodevelopmental resources and thus offer a new explanation for men’s preference for low WHR.http://www.cep.ucsb.edu/papers/whrlassekgaulin2008.pdf

Far from being in the eye of the beholder, the very concept of beauty and the human appreciation of attractive people is to a large degree inborn, but this hasn’t stopped campaigns (usually aimed at women) against this very concept. The cliché is that “Western” society has brainwashed us with unrealistic European standards of beauty which women in particular strive to emulate. Apparently, without this “brainwashing” we’d naturally accept people for their “inner” beauty. Not quite:
The hourglass figure is truly timeless:

It is no secret that modern culture places a premium on Barbie-doll shaped bodies. Some scientists have argued, however, that this preference only represents modern Western values. […] Written texts of all ages have the same drift when it comes to the midriff - they consistently describe women’s thin waists as attractive. The conclusion comes from an analysis of British, Indian and Chinese texts dating as far back as the first century AD. According to the researchers, the finding supports the idea that we are hardwired to prefer slender waists, which are linked to good health and fertility. […] In contrast, while breasts had the most romantic references. Apparently, it is the shape (roundness—a sign of youthfulness; Grammer et al. 2003), rather than the size, of breasts that is judged to be beautiful. 

Far from being a "culturally-conditioned" phenomena, the preference for women with slim waists was noted in the literature of three distinct cultures—China, Britain, and India—in texts dating as far back as 2000 years ago. All of the romantic references to the waist described the body part as attractively narrow. There was “not a single exception.”
Large Breasts and Narrow Waists Indicate High Reproductive Potential in Women:

Physical characteristics, such as breast size and waist–to–hip ratio (WHR), function as important features used by human males to assess female attractiveness. Here, we document that women with higher breast–to–underbreast ratio (large breasts) and women with relatively low WHR (narrow waists) have higher fecundity as assessed by precise measurements of daily levels of 17–β–oestradiol (E2) and progesterone. Furthermore, women who are characterized by both narrow waists and large breasts have 26% higher mean E2 and 37% higher mean mid–cycle E2 levels than women from three groups with other combinations of body–shape variables, i.e. low WHR with small breasts and high WHR with either large or small breasts. Such gains in hormone levels among the preferred mates may lead to a substantial rise in the probability of conception, thus providing a significant fitness benefit. […] WHR seems to be a better predictor of reproductive potential than breast size, because it correlates both with E2 and progesterone indices, whereas for breast size only its relationships with E2 are significant. […] Women from the ‘narrow waist, large breasts’ group had 26% higher values of mean E2 and 37% higher values of mean mid-cycle E2 than women from any of the other groups.

Consistent with the fitness benefits associated with low WHRs, with approx. 26% higher levels of estradiol, women with large breasts and narrow waists were found to be nearly three times more likely to get pregnant. As noted, in the middle of their menstrual cycle, this peaks at 37% higher levels than women in the other groups. Lower WHR also effects the female hormone, progesterone, but unlike WHR, breast size alone does not significantly relate to increased progesterone. Here, attractiveness appears as a useful proxy of genetic fitness.
Conversely then, the stigma attached to those with broad waists and increased abdominal fat; universally less attractive body types which are linked to poor health, should too be inborn:Pathogen-avoidance mechanisms and the stigmatization of obese people:

Humans possess pathogen-avoidance mechanisms that respond to the visual perception of morphological anomalies in others. We investigated whether obesity may trigger these mechanisms. Study 1 revealed that people who are chronically concerned about pathogen transmission have more negative attitudes toward obese people; this effect was especially pronounced following visual exposure to obese individuals. Study 2 revealed that obesity is implicitly associated with disease-connoting concepts; this effect was especially pronounced when the threat of pathogen transmission is highly salient. Evolved pathogen-detection mechanisms are hypersensitive, and they appear to play a role in the stigmatization of obese people.

Upper-body fat has negative effects and lower-body fat has positive effects on the supply of long-chain polyunsaturated fatty acids that are essential for neurodevelopment. Thus, waist-hip ratio (WHR), a useful proxy for the ratio of upper-body fat to lower-body fat, should predict cognitive ability in women and their offspring. Moreover, because teenage mothers and their children compete for these resources, their cognitive development should be compromised, but less so for mothers with lower WHRs. These predictions are supported by data from the Third National Health and Nutrition Examination Survey. Controlling for other correlates of cognitive ability, women with lower WHRs and their children have significantly higher cognitive test scores, and teenage mothers with lower WHRs and their children are protected from cognitive decrements associated with teen births. These findings support the idea that WHR reflects the availability of neurodevelopmental resources and thus offer a new explanation for men’s preference for low WHR.http://www.cep.ucsb.edu/papers/whrlassekgaulin2008.pdf

Far from being in the eye of the beholder, the very concept of beauty and the human appreciation of attractive people is to a large degree inborn, but this hasn’t stopped campaigns (usually aimed at women) against this very concept. The cliché is that “Western” society has brainwashed us with unrealistic European standards of beauty which women in particular strive to emulate. Apparently, without this “brainwashing” we’d naturally accept people for their “inner” beauty. Not quite:
The hourglass figure is truly timeless:

It is no secret that modern culture places a premium on Barbie-doll shaped bodies. Some scientists have argued, however, that this preference only represents modern Western values. […] Written texts of all ages have the same drift when it comes to the midriff - they consistently describe women’s thin waists as attractive. The conclusion comes from an analysis of British, Indian and Chinese texts dating as far back as the first century AD. According to the researchers, the finding supports the idea that we are hardwired to prefer slender waists, which are linked to good health and fertility. […] In contrast, while breasts had the most romantic references. Apparently, it is the shape (roundness—a sign of youthfulness; Grammer et al. 2003), rather than the size, of breasts that is judged to be beautiful. 

Far from being a "culturally-conditioned" phenomena, the preference for women with slim waists was noted in the literature of three distinct cultures—China, Britain, and India—in texts dating as far back as 2000 years ago. All of the romantic references to the waist described the body part as attractively narrow. There was “not a single exception.”
Large Breasts and Narrow Waists Indicate High Reproductive Potential in Women:

Physical characteristics, such as breast size and waist–to–hip ratio (WHR), function as important features used by human males to assess female attractiveness. Here, we document that women with higher breast–to–underbreast ratio (large breasts) and women with relatively low WHR (narrow waists) have higher fecundity as assessed by precise measurements of daily levels of 17–β–oestradiol (E2) and progesterone. Furthermore, women who are characterized by both narrow waists and large breasts have 26% higher mean E2 and 37% higher mean mid–cycle E2 levels than women from three groups with other combinations of body–shape variables, i.e. low WHR with small breasts and high WHR with either large or small breasts. Such gains in hormone levels among the preferred mates may lead to a substantial rise in the probability of conception, thus providing a significant fitness benefit. […] WHR seems to be a better predictor of reproductive potential than breast size, because it correlates both with E2 and progesterone indices, whereas for breast size only its relationships with E2 are significant. […] Women from the ‘narrow waist, large breasts’ group had 26% higher values of mean E2 and 37% higher values of mean mid-cycle E2 than women from any of the other groups.

Consistent with the fitness benefits associated with low WHRs, with approx. 26% higher levels of estradiol, women with large breasts and narrow waists were found to be nearly three times more likely to get pregnant. As noted, in the middle of their menstrual cycle, this peaks at 37% higher levels than women in the other groups. Lower WHR also effects the female hormone, progesterone, but unlike WHR, breast size alone does not significantly relate to increased progesterone. Here, attractiveness appears as a useful proxy of genetic fitness.
Conversely then, the stigma attached to those with broad waists and increased abdominal fat; universally less attractive body types which are linked to poor health, should too be inborn:Pathogen-avoidance mechanisms and the stigmatization of obese people:

Humans possess pathogen-avoidance mechanisms that respond to the visual perception of morphological anomalies in others. We investigated whether obesity may trigger these mechanisms. Study 1 revealed that people who are chronically concerned about pathogen transmission have more negative attitudes toward obese people; this effect was especially pronounced following visual exposure to obese individuals. Study 2 revealed that obesity is implicitly associated with disease-connoting concepts; this effect was especially pronounced when the threat of pathogen transmission is highly salient. Evolved pathogen-detection mechanisms are hypersensitive, and they appear to play a role in the stigmatization of obese people.

Upper-body fat has negative effects and lower-body fat has positive effects on the supply of long-chain polyunsaturated fatty acids that are essential for neurodevelopment. Thus, waist-hip ratio (WHR), a useful proxy for the ratio of upper-body fat to lower-body fat, should predict cognitive ability in women and their offspring. Moreover, because teenage mothers and their children compete for these resources, their cognitive development should be compromised, but less so for mothers with lower WHRs. These predictions are supported by data from the Third National Health and Nutrition Examination Survey. Controlling for other correlates of cognitive ability, women with lower WHRs and their children have significantly higher cognitive test scores, and teenage mothers with lower WHRs and their children are protected from cognitive decrements associated with teen births. These findings support the idea that WHR reflects the availability of neurodevelopmental resources and thus offer a new explanation for men’s preference for low WHR.
http://www.cep.ucsb.edu/papers/whrlassekgaulin2008.pdf

Far from being in the eye of the beholder, the very concept of beauty and the human appreciation of attractive people is to a large degree inborn, but this hasn’t stopped campaigns (usually aimed at women) against this very concept. The cliché is that “Western” society has brainwashed us with unrealistic European standards of beauty which women in particular strive to emulate. Apparently, without this “brainwashing” we’d naturally accept people for their “inner” beauty. Not quite:

The hourglass figure is truly timeless:

It is no secret that modern culture places a premium on Barbie-doll shaped bodies. Some scientists have argued, however, that this preference only represents modern Western values. […] Written texts of all ages have the same drift when it comes to the midriff - they consistently describe women’s thin waists as attractive. The conclusion comes from an analysis of British, Indian and Chinese texts dating as far back as the first century AD. According to the researchers, the finding supports the idea that we are hardwired to prefer slender waists, which are linked to good health and fertility. […] In contrast, while breasts had the most romantic references. Apparently, it is the shape (roundness—a sign of youthfulness; Grammer et al. 2003), rather than the size, of breasts that is judged to be beautiful.

Far from being a "culturally-conditioned" phenomena, the preference for women with slim waists was noted in the literature of three distinct cultures—China, Britain, and India—in texts dating as far back as 2000 years ago. All of the romantic references to the waist described the body part as attractively narrow. There was not a single exception.

Large Breasts and Narrow Waists Indicate High Reproductive Potential in Women:

Physical characteristics, such as breast size and waist–to–hip ratio (WHR), function as important features used by human males to assess female attractiveness. Here, we document that women with higher breast–to–underbreast ratio (large breasts) and women with relatively low WHR (narrow waists) have higher fecundity as assessed by precise measurements of daily levels of 17–β–oestradiol (E2) and progesterone. Furthermore, women who are characterized by both narrow waists and large breasts have 26% higher mean E2 and 37% higher mean mid–cycle E2 levels than women from three groups with other combinations of body–shape variables, i.e. low WHR with small breasts and high WHR with either large or small breasts. Such gains in hormone levels among the preferred mates may lead to a substantial rise in the probability of conception, thus providing a significant fitness benefit. […] WHR seems to be a better predictor of reproductive potential than breast size, because it correlates both with E2 and progesterone indices, whereas for breast size only its relationships with E2 are significant. […] Women from the ‘narrow waist, large breasts’ group had 26% higher values of mean E2 and 37% higher values of mean mid-cycle E2 than women from any of the other groups.

Consistent with the fitness benefits associated with low WHRs, with approx. 26% higher levels of estradiol, women with large breasts and narrow waists were found to be nearly three times more likely to get pregnant. As noted, in the middle of their menstrual cycle, this peaks at 37% higher levels than women in the other groups. Lower WHR also effects the female hormone, progesterone, but unlike WHR, breast size alone does not significantly relate to increased progesterone. Here, attractiveness appears as a useful proxy of genetic fitness.

Conversely then, the stigma attached to those with broad waists and increased abdominal fat; universally less attractive body types which are linked to poor health, should too be inborn:Pathogen-avoidance mechanisms and the stigmatization of obese people:

Humans possess pathogen-avoidance mechanisms that respond to the visual perception of morphological anomalies in others. We investigated whether obesity may trigger these mechanisms. Study 1 revealed that people who are chronically concerned about pathogen transmission have more negative attitudes toward obese people; this effect was especially pronounced following visual exposure to obese individuals. Study 2 revealed that obesity is implicitly associated with disease-connoting concepts; this effect was especially pronounced when the threat of pathogen transmission is highly salient. Evolved pathogen-detection mechanisms are hypersensitive, and they appear to play a role in the stigmatization of obese people.

  • Evidence That Sex Ratios Have Long Impacted Male/Female Mating Behaviour

[…] low sex ratios at couple formation ages existed in the U.S. between 1965 and the early 1980s. The currently high sex ratios, however, will persist until the end of the century. High sex ratios appear to be associated with lower divorce rates, male commitment to careers that promise economic rewards, male willingness to engage in child care, higher fertility, and higher rates of sexual violence. Sexual selection theory calls attention to intrasexual competition in the numerically larger sex.
Secular trends in human sex ratios : Their influence on individual and family behavior

This finds that, after WWII and beginning in 1965, single men began to outnumber single women in the U.S., leading to a relatively excess of men. More men are now living throughout the entire reproductive age bracket. The same phenomena was observed in England and Wales in the 90s:

Partner supply in Britain and the US: estimates and gender contrasts

When men are scarce in a female-biased population, there is less incentive for competition among men for relationship commitment and paternal investment because male scarcity enhances their short term mating success. Females thus have less selective power and may exhibit lower thresholds for male commitment in order to have sexual relations:

Across history, female biased Operational Sex Ratios (OSRs) tend to destabilize marriages and lead to higher divorce rates, more out-of-wedlock births and single mother households, and lower paternal investment. Male biased OSRs are associated with the reverse pattern.
Male Scarcity is Differentially Related to Male Marital Likelihood across the Life Course

In the U.S., black Americans have continued to have a low sex ratio among individuals of reproductive age (because of high male mortality, high male incarceration, and low sex ratio at birth). Marriageable black women thus tend to outnumber black men:

The Divergance of Black and White Marriage Patterns

In accordance with this lower sex ratio, African Americans have a lower rate of marriage and higher rate of marriage dissolution. In a large cross-cultural analysis comparing 70 countries it was found that societies with low sex ratios had less paternal investment and marital stability:

The Sex Ratio as a Predictor of Cross-National Variation in Violent Crime

The preponderance of single men to single women (in the West) persists to this day and shows no signs of declining. There are also economic implications for male-biased sex ratios:

Male-biased sex ratios (an abundance of men) lead men to discount the future and desire immediate rewards. Male-biased sex ratios decreased men’s desire to save for the future and increased their willingness to incur debt for immediate expenditures. Sex ratio appears to influence behavior by increasing the intensity of same-sex competition for mates. Accordingly, a scarcity of women led people to expect men to spend more money during courtship, such as by paying more for engagement rings.
The Financial Consequences of Too Many Men: Sex Ratio Effects on Saving, Borrowing, and Spending

  • Figure 1. (of this post) shows the correlation between sex ratio and sociosexuality (promiscuity):

As displayed in Figure 1, cultures with more men than women are more sociosexually restricted than cultures with more women than men. […] Thus, the cultural test cases of the ISDP appear to fit well within sex ratio theory as posited by Pedersen (1991).
Sociosexuality From Argentina to Zimbabwe: A 48-Nation Study of Sex, Culture, and Strategies of Human Mating

Pedersen (1991) refers to the first study of this post. As can be seen in the figure, low sex ratios and high sociosexual levels are evident in the Baltic nations of Estonia, Latvia, and Lithuania, implying that the females there will appeal more strongly to the male ideal because the number of marriageable men in Latvia is low relative to the number of women. Males have higher sociosexuality scores than females but sociosexuality scores for females vary widely across countries. Continued:

[…] in Figure 1, it appears that once women begin to outnumber men at a sex ratio of about 95, the national level of sociosexuality becomes especially accentuated. […] Low sex ratios in the Baltics are not surprising given the high rates of male suicides and deaths from accidents within these nations (e.g., Neumayer 2003). However, even without the Baltic nations, the correlation between sex ratio and sociosexuality was significant, r(43) = -0.38, p < .01. These findings are consistent with the view that cultures with more women than men possess mating systems driven via the powers of sexual selection by men’s evolved desires for unrestricted, promiscuous sex. Figure 1 also shows that cultures with more men than women (e.g., Hong Kong, Bangladesh, and Taiwan) tend to be low on sociosexuality. In these cultures, according to sex ratio theory, the mating system is driven by women’s more potent desires for longterm, monogamous mating.

The sex differences in mating patterns, particularly the differences in short-term mating strategies, i.e., how men and women go about being promiscuous—men opt for large numbers/variety and women focus on quality—are found to be culturally universal throughout the world: Findings from a cross-cultural survey of 52 nations, 6 continents, and 13 islands find the same sex differences were evident regardless of whether mean, median, distributional, or categorical indexes of sexual differentiation were evaluated. Further studies have replicated these findings.

  • The Heritability of Sociosexuality (Promiscuity)

Finally, and perhaps most importantly, is that a bulk of influence from genes impacts individual outcomes on seemingly any measure of traits, and this includes individual promiscuity, as assessed by an Australian twin registry study:The figure above shows the estimates for the genetic (A), shared (C) and unique environment (E) influencing sociosexuality. About half the influence impacting individual promiscuity is a result of genes:

[…] Although men are substantially more interested than women in casual sex, there is ample variation in this trait (sociosexuality) within both sexes. […] A competing theory is that children acquire their mating strategy after observing their parents’ relationship. […] Parental marital instability was modestly associated with sociosexuality, but this could have been due to either genetic or environmental factors. Consistent with genetic theory, familial resemblance appeared primarily due to additive genetic rather than shared environmental factors.

Interestingly then, the causes and correlations of individual differences in sociosexuality appear to actually be similar in men and women. Demographic variables did not interact with sex in the prediction of sociosexuality. E.g., how males may behave in female-biased OSRs is impacted by genes and the unique environment. If taken in the weaker sense, some men will forgo monogamous mating if given the option, this appears to be partially true, but this is largely moderated by genes.

  • Along with individual differences, there exist differences at the group level. Associations are found between a dopamine receptor D4 (DRD4) gene variant (7R+) with both infidelity and sexual promiscuity. For one, African-Americans are found to posses significantly more of these 7R alleles. Continued here.

Moreover, sex ratios, and the subsequent male/female-driven sexual selection they produce, serve a significant place in human evolutionary history:

anarchosaur:

veryprivileged:

sweden has the second highest number of rapes in the world, and 77 percent of those rapes are perpetrated by foreigners.

image

If I recall correctly, they have a very liberal definition of rape, just as the UK has a liberal definition of “violent crime”. I could be completely wrong though; can anyone confirm or deny?

Correct. The same formula Mary Koss used to come up with the campus rape myth in the 80s. That 1-in-4 figure in Sweden is a shocking fallacy. Even with the overrepresentation of foreigners, no crime in the West, much less one as serious as rape, has a victimisation rate remotely approaching 20 or 25 percent, even over many years.

I used to state this quite often, but don’t bother now as it serves as good propaganda anyway. As do those Elin Krantz images.

The big EU study on the victimisation of women finds that the real rate is around 5%, or 1-in-20 women:

33% of women have experienced physical and/or sexual violence since the age of 15, while 5% has been raped since the age of 15.
http://fra.europa.eu/en/publication/2014/vaw-survey-main-results

Although that’s nothing to celebrate, the figure is the same as the true figure in the U.S. If you include all the other variables, such as whether women report being groped, pushed or shoved, slapped or grabbed, or had their hair pulled since they were 15, you can create any sort of fallacious figure, just by changing it from rape to “violence against women.” Even then a portion of these assaults involve a female perpetrator, so any statistic becomes misleading considering most people subconsciously link female victimhood directly to men. Well, tumblr posts and typical feminists in the media will, because such figures fit the hyperbole of the age.

laofmoonster:

Asian and Native Americans commonly have shovel-shaped incisors, which curve inward. Other human groups have more chisel-shaped incisors, which don’t curve inward.
This is caused by a variation in the EDAR gene commonly found among Asians. This allele has also been linked to thicker hair, smaller breasts, and more sweat glands, traits also common among Asians.

Good one. As the article notes, when they inserted the variant into mice they too developed phenotypes characteristic of East Asian populations: thicker hair shafts, extra sweat glands, and less breast tissue. The distinctively shaped teeth of East Asians was harder to compare in mice, but it looks like it&#8217;s probably responsible for that too.
More importantly here though is that the variant shows strong signs of selection. Adaptation to local climates is one element, but selection has often accelerated the human physical variation we see. For instance, the short frizzy hair characteristic of sub-Saharan Africans dissipates body heat and would be less adaptive in colder climates, ergo colder climates may well have made short head hair less adaptive. But when early modern humans left the Tropics, they entered environments that reduced the supply of mateable men (harsh winters; many males died hunting) and thus strengthened sexual selection of women, thereby favouring visible traits that retain male attention, such as longer hair length. It&#8217;s selection too, not just adaptation, which accelerated this.
Equally, the hair and eye hue variation in Europeans show strong signs of male sexual selection, with women having a more diverse palette of hues. Lighter skin too was under intense and persistent selection in North Eurasian populations.
Explaining the possible selective advantages characteristic of East Asians is puzzling - the authors of the study say as much with their odd theories. I mean, has any such preference for smaller breasts ever really existed? Perhaps in distinct cultures. The real advantage may well be unknown and not even related to phenotype. Whatever the real advantage is the authors compare the strength of selection to that of lactase persistence in European populations - a very advantageous allele.

laofmoonster:

Asian and Native Americans commonly have shovel-shaped incisors, which curve inward. Other human groups have more chisel-shaped incisors, which don’t curve inward.

This is caused by a variation in the EDAR gene commonly found among Asians. This allele has also been linked to thicker hair, smaller breasts, and more sweat glands, traits also common among Asians.

Good one. As the article notes, when they inserted the variant into mice they too developed phenotypes characteristic of East Asian populations: thicker hair shafts, extra sweat glands, and less breast tissue. The distinctively shaped teeth of East Asians was harder to compare in mice, but it looks like it’s probably responsible for that too.

More importantly here though is that the variant shows strong signs of selection. Adaptation to local climates is one element, but selection has often accelerated the human physical variation we see. For instance, the short frizzy hair characteristic of sub-Saharan Africans dissipates body heat and would be less adaptive in colder climates, ergo colder climates may well have made short head hair less adaptive. But when early modern humans left the Tropics, they entered environments that reduced the supply of mateable men (harsh winters; many males died hunting) and thus strengthened sexual selection of women, thereby favouring visible traits that retain male attention, such as longer hair length. It’s selection too, not just adaptation, which accelerated this.

Equally, the hair and eye hue variation in Europeans show strong signs of male sexual selection, with women having a more diverse palette of hues. Lighter skin too was under intense and persistent selection in North Eurasian populations.

Explaining the possible selective advantages characteristic of East Asians is puzzling - the authors of the study say as much with their odd theories. I mean, has any such preference for smaller breasts ever really existed? Perhaps in distinct cultures. The real advantage may well be unknown and not even related to phenotype. Whatever the real advantage is the authors compare the strength of selection to that of lactase persistence in European populations - a very advantageous allele.

Q

Anonymous asked:

The anon who stated that human evolution began in Africa is absolutely right. I'm a biology major. The evidence in support of the origins of human evolution is insurmountable. Anyone who took any entry level biology course would know about the origins of human evolution. Maybe you should educate yourself before you mock others, because it makes you sound like a fool.

A

the-porcelain-empress:

If I had a dime for every “biology major”, “science major” and other self proclaimed anonymous experts I’d be able to buy Tony Stark and make him my bitch for the weekend. 

The ones that disproved the out of Africa theory are real biologists, not tumblr biology majors. Allow me to wave bye bye in your general direction.

All of the data in genetics, archaeology and palaeoanthropology point to the African landmass for the origin of modern humans as well as the deepest lines of the genus homo. It’s also where 4 out of 5 great ape species are found (chimps, bonobos, gorillas, and humans).

See: the leaky replacement/multi-archaic populations theory. That is, rather than a single out-of-Africa dispersal scenario, early modern humans were already divided into different populations in Pleistocene Africa, after which there followed a complex migration pattern.

Every other blog I follow is wrapped up in this supposedly “debunked” Out of Africa theory, but I doubt any of you can elaborate on the current data.

You can cite all those links which "confirm" the multi-regional theory and "debunk" Out of Africa theory all you want, I’m familiar with them, perhaps because I was the one spamming most of them around 4chan 3+ years ago now. Klyosov et al., was always a favourite when that came out, and I see it still is. I also still see some of the links copied and pasted and over, in the exact same format I had originally laid them out in.

Sure, it’s fun to mock the latest anthropology graduates that universities churn out, but you all speak with such conviction about this, without really knowing the data. I tend to think that you all assume the same as those college "educated" knitwits though, in that we evolved from an African race, unchanged from times immemorial and which resembles the black Americans of today. Of course, the "blacks" we know today did not exist until relatively recently.

The original Out of Africa theory is dead because it posited zero admixture with archaic populations (because apparently they couldn’t) and a single-founder population. It has been revised, that’s all you can claim. The vast majority (~90%) of human ancestry outside of Africa derives from a population that lived in Africa on the order of 100,000 years ago. That is how things are. Multi-regionalism will not work with ancestry. So best to drop the posts which “debunk” the Out of Africa theory with links to press articles and general media tabloids. It’s becoming a little silly now.

Before They Left Africa, Early Modern Humans Were Already ‘Culturally Diverse’

archaeologicalnews:

Oxford — A new study provides fresh insights into the life of early modern humans in North Africa, the only land route into Eurasia. Researchers have carried out the biggest ever comparative study of stone tools dating to between 130,000 and 75,000 years ago found in the region between sub-Saharan Africa and Eurasia.

They have discovered there are marked differences in the way stone tools were made, reflecting a diversity of cultural traditions. The study has also identified at least four distinct populations, each relatively isolated from each other with their own different cultural characteristics.

The research paper also suggests that early populations took advantage of rivers and lakes that criss-crossed the Sahara desert. Read more.

The leaky replacement/multi-archaic populations theory certainly explains modern human origins. E.g., rather than a single out-of-Africa dispersal scenario, early modern humans were already divided into different populations in Pleistocene Africa, after which there followed a complex migration pattern.

The human biodiversity in Africa was always large, as evident here. Consider today even, those short African Pygmy populations are human relics that differ more from the Mandenka people (West Africans) than Eurasians do from the same West Africans, which should tell you enough. You also have to note that modern humans further diverged not just from adaptation and selection on the trek out of Africa, but with introgression from archaics—Eurasians with Neanderthal admixture; Melanesians with additional admixture from the Denisovans; Africans with archaic admixture that introgressed after the "to-be Eurasian" populations left Africa, 2% of which comes from a now-extinct member of the Homo genus that broke away from the modern human lineage around 700,000 years ago. Meanging that archaic admixture in modern sub-Saharan African populations likely extends beyond the H. heidelbergensis clade, which is ancestral to modern humans and Neanderthals, and may encompass late H. erectus populations.

There is a genetic basis to group identification and preferences, with groups culturally defined in terms of race and ethnicity:

Genetics, Personality, and Group Identity:

We take seriously the idea that people have an innate drive to associate with others and investigate the extent to which the impetus to associate with groups is heritable. Lewis and Bates (2010) find that the variance in group identification and favoritism is explained by genetic factors. The remaining variation is associated with the unique environment. The common environment—family socialization and culture— appear to have little influence on these attitudes. […] Our findings have implications for the study of collective action, identity politics, and the growing research program investigating social and political behavior genetics.

Evidently, ingroup/outgroup recognition, however defined, is instinctive. As always with behavioural studies, the common (shared) environment, i.e. what your parents taught you, has insignificant influence over individual attitudes reflecting ingroup/outgroup favourtism.

  • There is a genetic basis to identification and preferences, specifically for racial and ethnic groups:

Genetic Evidence for Multiple Biological Mechanisms Underlying In-Group Favoritism:

In-group favoritism is ubiquitous and associated with intergroup conflict, yet is little understood from a biological perspective. […] In a series of multivariate analyses, utilizing a large, representative sample of twins, models containing only the CAM or essentialist domains fit the data poorly. The best-fitting model revealed that a biological mechanism facilitates affiliation with arbitrary groups and exists alongside essentialist systems that evolved to process salient cues, such as shared beliefs and ancestry.

The figure of this post shows the best-fitted model. They tested influences on religious, ethnic, and racial favouritism. All paths shown are significant, and their coefficients are indicated. A = genetic influences; E = unique- environment influences. No shared-environment.

One interesting note is that the religious tend to have lower levels of ethnocentrism:

[…] Perhaps the most interesting environmental effect was that elements of the unique environment acting at the essentialist level exerted effects countervailing environmentally mediated religious favoritism, such that elevated levels of religious favoritism were associated with lowered levels of ethnic favoritism. This may reflect the influence of religious teachings, which may increase ethnic tolerance, or the possibility that religion became superordinate to coalitions based on ethnicity.

Bias is innate, universal, and thus has clear implications for diverse societies, but what benefit is group identification and what purpose would it serve? Potential evolutionary explanations include the genetic similarity theory, which has been validated by the advance in genomics:

im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes. im-just-a-reaction:

arkaimcity:

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You&#8217;re way off, but I&#8217;ll expand because I know this is so common.
Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).
Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you&#8217;re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly. 
The motivation to obtain food, and your enjoyment of food once you obtain it is what we&#8217;d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.
Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn&#8217;t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can&#8217;t walk a mile in these people&#8217;s shoes.

im-just-a-reaction:

arkaimcity:

c-a-bergamot:

It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.

Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.

You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

If your genetics make it so it’s harder for you to lose weight and easier to gain weight then you need to adjust accordingly rather than just blaming your genetics.

You’re way off, but I’ll expand because I know this is so common.

Dietary preferences are heritable between individuals. The effects of heredity can range from the most direct (metabolism) to the most indirect (levels of societal stress).

Palatability is part due to inborn preferences for a taste for sugar and energy dense foods (for example), and part by the reward system (acquired tastes). Why after you’re stuffed from a full meal can you manage to shovel down ice cream, but that one extra baked potato is just too much? Guess. This motivates food intake and the same effect can be replicated using drugs that activate these circuits directly

The motivation to obtain food, and your enjoyment of food once you obtain it is what we’d term as hunger. Surprise, this varies. Heredity influences both our susceptibility to indulging (and overindulging) in food.

Sure, why can fatties not adjust accordingly? You would. Why did that psychopath suddenly snap and kill people? You wouldn’t have done that. Chances are your genetics and life experiences differ greatly from such individuals. You can’t walk a mile in these people’s shoes.

c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one. c-a-bergamot:

“It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.
Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I&#8217;m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.
You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

c-a-bergamot:

It’s really hard to exercise" so allow me to become a fat-activist because I didn’t get it the easy way.

BMI is highly heritable though. The variance of the use-frequency of food items and food categories is explained by additive genetic and unshared environmental influences. As usual, family (shared) environment will not influence the food use of individuals in adulthood.

Diet and lifestyle too are important, but moderation between these differ among individuals, differences exist on the group (racial) level too. Although I’m sure fitness experts could probably describe in detail what amino acids are in their favourite protein shakes, I bet they know next to nothing about hereditary genetics and the way in which it impacts individual human behaviour. Not many people really do.

You can find stories of weight loss success that rely on anecdotes, cherry-picked samples and observational studies that control for precisely nothing, but randomised controlled trials lay out a different story. Invariably then, the people who say that there is a genetic causation for their obesity do have a leg to stand on, albeit a fat one.

(via anarchosaur)

  • Genetic Mutations and Intelligence Decline

De Novo Mutations Represent an Important Cause of Intellectual Disability:

Forbes: In two papers in major scientific journals, researchers today suggested pushing DNA sequencing into more routine use in the clinic, and not just as a research tool. […] The Dutch researchers sequenced 100 patients with IQs of less than 50 and their unaffected parents. The technique found genetic mutations known to cause intellectual disability in 16 patients, and genes of unknown function that appear to be the cause in another 22 patients. […] In most cases in this study, a bad copy of a gene from a parent was not to blame. One surprise is that most of the mutations that caused these cases are brand new – they didn’t exist in the parents’ genomes. In three cases, the gene was inherited from the mother via the X chromosome; because boys only have one X chromosome but women have two, such a bad copy is deleterious in boys. […] On average, every child is born with one brand new genetic mutation. Most of them don’t matter. But it may be, Brunner says, that there are 1,000 genes in which such a mutation can cause mental disability. So some unlucky kids suffer just because of the background mutation rate.

The paper in question:

Diagnostic Exome Sequencing in Persons with Severe Intellectual Disability

First and foremost, this demonstrates that it is now feasible to decode a baby’s entire genome and provide interim results back to a physician in two days. For effective detection of de novo mutations, this method extracts only known genes from DNA in the human genome (which reduces sequencing cost). They identified de novo mutations which lead to severe cognitive impairment, but there are likely many more mutations which lead to smaller impairment.

  • De novo mutations are genetic mutations that are neither parent possessed nor transmitted, this is evidence that mutational load is at least a partial factor in population variation in cognitive ability; genetic (mutational) load among all individuals is routine.

Because of previous selection (over the last millions of years), most rare gene variants affecting intelligence, for instance, will have a slightly negative effect. That is, the variants of large, positive effect (on fitness) will be found in every "normal" person, whereas variants of small negative effect will still linger at low frequency. Being smarter is actually largely a consequence of having fewer of these rare deleterious variants.

Paternal genetic load increases with age; women contribute about 15 de novo mutations independant of age, whereas men contribute more and the number increases rapidly with age.

Since intelligence is found to be highly heritable—around the same as the heritability of height (>80%) in the developed world—applying this technique of genetic testing would significantly reduce cases of intellectual disability. De novo mutations with large negative effects on IQ would never show up in any heritability study because individuals with such mutations would be removed (or never recruited in the first place). Hence forth the premise behind this study.

  • There is an unfortunate series of phenomena is occurring in the West: an increase in paternal age (thus an increase in genetic load), an increase in the brightest of women spending their reproductive years focusing on careers, and less intelligent individuals bearing the largest share of births is leading to what may be described as population-wide dysgenic fertility. Anyone who understands much about genetics would know that these circumstances are bound to have bad consequences, but there is no popular ideology based on any understanding of genetics; some strongly oppose these actual facts on the ground. Others are unaware of the data or simply don’t care about the long-term consequences.

Although such a phenomena (of less intelligent out-reproducing the intelligent leading to population-wide IQ decline) would take successive generations of dysgenic breeding, this set of circumstances is seemingly a reverse of the trend observed in the West (also observed in parts of East Asia) over the last millennium that likely determined the industrial revolution.