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The origins of white skin

Discuss racial, ethnic and multicultural issues. Warning: The topics here are likely to be taboo, so if you are easily offended, you are better off not participating here.

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jaylee
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Re: The origins of white skin

Post by jaylee » October 20th, 2016, 2:00 pm

Blue Murder wrote:
jaylee wrote:Since this forum is such a magnet for severely disturbed people with extremely low IQs, I think this a good topic to post here :oops:
Which is exactly why you shouldn't waste your time. Personally, I enjoy "controversial" (lolwut) topics, but the fact that two sides cannot have intelligent discussion on HA means the bright ones like yourself are better off spending time elsewhere. That's why I don't even dish on what my "race" is. Like the poster above, he completely disregarded your article and instead wants to know what your race is so that he can "uncover your motive" or whatever lunacy he's on about.

I advise you to avoid answering.
That's okay, I'm researching mental illness here.
Mental illness researcher @ culturewhiz.org




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Kradmelder
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Re: The origins of white skin

Post by Kradmelder » October 20th, 2016, 2:24 pm

jaylee wrote:
Blue Murder wrote:
jaylee wrote:Since this forum is such a magnet for severely disturbed people with extremely low IQs, I think this a good topic to post here :oops:
Which is exactly why you shouldn't waste your time. Personally, I enjoy "controversial" (lolwut) topics, but the fact that two sides cannot have intelligent discussion on HA means the bright ones like yourself are better off spending time elsewhere. That's why I don't even dish on what my "race" is. Like the poster above, he completely disregarded your article and instead wants to know what your race is so that he can "uncover your motive" or whatever lunacy he's on about.

I advise you to avoid answering.
That's okay, I'm researching mental illness here.
Why don't you research something useful. Like if africa had more mosquito nets we could save more mosquitoes from dying from AIDS :lol:

jaylee
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Re: The origins of white skin

Post by jaylee » October 20th, 2016, 2:25 pm

Cornfed wrote:Aside from this not even being true, does this mean that the species of dogs, wolves and coyotes don't exist, since the alleles to make the other two species are largely contained within all of those species? If so, does this mean I am being irrational to react differently when confronted with a pack of Chihuahuas vs. being confronted with a pack of Timber Wolves?
Lol, that is pretty ignorant but what I expected from this board. Human variation lies on a continuum, it can't be partitioned into discrete groups because there is much more genetic variation within local groups than there is among "races" themselves. In other words, modern people are differing mixtures of multiple separate species of archaic humans.

A dog is still a wolf. Taxonomically they both belong to the species Canis lupus. Gray wolf DNA is 99.8% the same as dog DNA. Two animals are different species when they cannot produce fertile offspring with each other. "Species" is not a clear-cut term, it's pretty arbitrary and confusing (and arguably not very rigorously scientifically useful, although it may be conceptually useful on a simplistic level) - there's actually just a spectrum of genetic and phenotypic difference.

What cause different behavior in domesticated dogs is a virus hosting gene over or under activating different pathways. The domesticated dog mild-manneredness was achieved through neotony--the preservation of certain juvenile characteristics into adulthood. Dogs are to a degree perpetual pups. Wolf pups are equally friendly. They just turn into wolves at a certain point. Dogs don't.

Enteroviruses live in your intestines and they found macrophage viruses (bacteria based viruses) that live, guest where? Your gut. Think of where most of your immune system is, guess what it's protecting you from bacterial that outnumber your cells 10 to 1. lol half your feces is bacteria! That's over 70% of your immune cells and activity, meaning if you have something wrong with your bacteria balance... it starts and stops with your intestines and might take multiple issues but genes don't cause illness (too many people have "bad" genes and never get anything until something hits them hard).

Fungi, parasites, pesticides, mercury, toxins, you name it... it's your intestinal health that keeps you from getting most diseases... diabetes takes 10-12yrs of chronic immune overuse of glutamine by the immune system before its first symptoms show up. You get some bad bacteria and it slowly kills you and drains you of energy, before a few years you get cancers and brain symptoms that manifest as anxiety and then other symptoms and before you know it you have a "mental health disorder" and your doctor is like, let me refer you to a good psychologist.

Crohn's disease is a combination of two bacteria and a fungi forming a biofilm that the immune system can't penetrate that probably feeds off the intestinal lining and causes all the nasty inflammatory symptoms that are so bad doctors tend to remove large sections of the intestine because of the damage being done to it

Do you know how parasites can affects the brain and can alter human behavior? With T. gondii, affected people will mostly demonstrate subtle shifts of behavior and it has been blamed for making people more impulsive, and more prone to mental illness, including schizophrenia. But in a small number of cases, [Toxo infection] may be linked to other disturbances associated with altered dopamine levels—for example, obsessive-compulsive disorder, attention-deficit hyperactivity disorder, and mood disorders.

~genius
Mental illness researcher @ culturewhiz.org

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droid
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Re: The origins of white skin

Post by droid » October 20th, 2016, 2:42 pm

blackfag wrote:Do you know how parasites can affects the brain and can alter human behavior? With T. gondii, affected people will mostly demonstrate subtle
shifts of behavior and it has been blamed for making people more impulsive, and more prone to mental illness,
^^Case in point

Jamesbond, time to clean up :lol:
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1)Too much of one thing defeats the purpose.
2)Everybody is full of it. What's your hypocrisy?

jaylee
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Re: The origins of white skin

Post by jaylee » October 20th, 2016, 2:59 pm

droid wrote:"Jaylee" is just blackfag (aka paloaltofag). Yet again, trying over and over and over to join and get some kind of validation here. Let's dump the trash guys please.

But different populations have different proportions of each phenotype. For example, the genes related to dark hair are present in a very high rate in the Asian populations--which includes native americans--but in a much lower rate in European populations, but still there. The genes that account for racial differences (skin, hair, eye color, etc.) number only a few. That's less than a dozen out of the thousands of genes that can vary between one human and the next. That means that, while two people can both have the same color of skin, hair, and eyes, and look very similar, that similarity is only superficial. They may actually be more genetically different from each other than they are from a person of a different "race".
That's some of the dumbest crap ever posted here. If only a few genes produce such large variations it only proves how isolated groups can become so different. Of course, only skin, hair and eye color are mentioned, conveniently ignoring how just as easily "a few" genes produce differences in character and demeanor.

He might be onto something with some of his 'theories' though, I think the fungus eating this idiot's brain is advancing quite well :lol:
This one completely missed this link posted that addresses genes producing differences in character and demeanor (see below) and still clings to the false assumption concerning the nature of human variation--that is that we can be unambiguously assigned to a "race" on the basis of selected anatomical traits. In fact, when we look at specific individuals, we often run into difficulty trying to categorize them. For example, on the basis of skin color, we might put them into one "race" and on the basis of nose shape, body form, or blood type, they might go into others. The typological model (created 200 years ago) usually leads low IQ people to wrongly assume that the people within any "race" are genetically and anatomically more alike than they are like people from other "races." This all depends on the traits that are being compared. For instance, many Americans believe that people of African descent have broad noses. In fact, both the widest and the narrowest noses are found among the people of that continent.

Another major problem with the typological model is that the number of "races" you end up with depends on the number and kinds of traits employed in the classification. The more traits used, the fewer people in the world there are who share them. For example, light skin color is considered to be a defining characteristic of Europeans. However, when you add the criteria of narrow noses, straight hair, and tall stature, many Europeans would be excluded altogether or the European racial category would have to be further subdivided into several smaller "races." Since the number of "races" can be so easily changed by the way they are defined, it is clear that they do not really exist as distinct biological groupings of people. Instead, they are arbitrary creations that reflect our ethnocentric views of ourselves and other people. They are mainly cultural rather than biological groupings.

https://www.independentsciencenews.org/ ... itability/
One of the hopes and promises of the Human Genome Sequencing Project was that it would revolutionize the understanding, diagnosis, and treatment of most human disorders. It would do this by uncovering the supposed “genetic bases” of human behavior. With a few exceptions, however, the search for common gene variants -“polymorphisms” – associated with common diseases has borne little fruit. And when such associations have been found the polymorphisms seem to have little predictive value and do little to advance our understanding of the causes of disease. In a 2012 study, for example, researchers found that incorporating genetic information did not improve doctors’ ability to predict disease risk for breast cancer, Type 2 diabetes, and rheumatoid arthritis [1].

And to date, not a single polymorphism has been reliably associated with any psychiatric disorders nor any aspect of human behavior within the “normal” range (e.g., differences in “intelligence”).

To some researchers this state of affairs has given rise to a conundrum known as the “problem of missing heritability.” If traits such as intelligence are reported to be 50% heritable, goes the theory, why have no genes associated with intelligence been identified? One possible solution to the problem of missing heritability is that the heritability estimates are wrong. Another proposal is that hundreds or even thousands of genes are involved, each gene of such small effect that it cannot be identified by the standard genome-wide association study (GWAS). These problems have spurred the development of a new methodology for identifying gene variants in human populations called genome-wide complex trait analysis (GCTA).

Enter Genome-wide complex trait analysis (GCTA)
The first results of a GCTA study were published in 2010 [2]. Since then its use has rapidly expanded with the results of GCTA studies on everything from obesity to intelligence to autism regularly appearing in prestigious science journals [3-17]. Like a typical GWAS, GCTA involves scanning hundreds of thousands of polymorphisms (specifically, a common form of gene variant known as a single nucleotide polymorphism [SNP]) of thousands of persons. But instead of trying to identify individual polymorphisms more common among those who share a given trait, the goal is to determine whether or not this trait similarity can be associated with a large number of (unidentified) polymorphisms. In other words, an estimate is generated as to how much of the genetic variance (i.e., heritability) of a trait can be accounted for by shared SNPs. These heritability estimates are termed “SNP-based” and differ from standard heritability estimates that rely upon assumptions of genetic relatedness, such as twin or family studies.

For example, the much used twin study methodology is based upon the assumption that monozygotic (MZ) twins share 100% of their inherited genes, as compared to “fraternal” or dizygotic (DZ) twins who share on average 50% of their inherited genes. If MZ twins show greater concordance for a trait of interest than DZ twins, this greater concordance is ascribed to greater genetic concordance, with the presumed genetic relationship of 1 to .5 serving as the basis of the heritability estimate. By contrast, GCTA does not rely upon genetic relatedness. In fact, it is critical to GCTA that those who are studied be unrelated.

The twin study methodology has long been critiqued as being based upon a number of faulty assumptions, in particular the assumption that the environments (pre and postnatal) of MZ twins are not more alike than DZ twins. Were the environments of MZ twins more alike than those of DZ twins (as numerous studies have indicated), trait similarities ascribed to the greater genetic similarity of MZ twins might in fact be due to greater environmental similarity, significantly inflating heritability estimates. Thus far, GCTA studies appear to have proven critics of the twin study methodology right, yielding significantly lower heritability estimates (e.g., an estimation of “callous-unemotional” behavior based on the twin study methodology yielded a heritability estimate of 64%, as compared to a GCTA that yielded a heritability estimate of 7% [9]). Long-time defenders of the accuracy of twin studies can now be found speculating, in light of GCTA findings, that “the estimates of … heritability from twin and family studies are biased upwards, for example, by not properly accounting for… (common) environmental factors” [7]. GCTA studies, however, just like their twin study predecessors, suffer from serious methodological problems that call into doubt the legitimacy of their findings. They, too, are likely to generate spurious associations and faulty estimates of genetic contributions to variation in traits.

GCTA studies are highly vulnerable to confounding by population stratification
Genetic studies (by whatever method) that have so far purported to identify SNPs associated with one or another trait have more often than not been false positives [18-20]. A prime cause of this has been the failure of researchers to take adequately into account population stratification. Population stratification refers to the fact that frequencies of polymorphisms can differ in different populations and subpopulations (ethnic or geographical) due to unique ancestral patterns of migration, mating practices, and reproductive expansions and contractions. Nearly all outbred (i.e., nonfamilial) populations exhibit population stratification, including populations deemed relatively homogenous (e.g., among Icelanders). One well-known example of a false association between a polymorphism and a trait was the link between the dopamine receptor gene DRD2 and alcoholism. Initial studies suggested a strong association, but subsequent investigations found none when more effective controls for population stratification were imposed. In retrospect, it is clear why this initial result was vulnerable to confounding due to population stratification: DRD2 alleles vary widely by ethnic ancestry, and ethnic differences in alcoholism rates are pronounced.

Recall that GCTA studies are supposed to involve unrelated persons. From the standpoint of population genetics, however, relatedness is not simply a matter of being someone’s second cousin. While the designers of the GCTA method are aware of the problem posed by population stratification and attempt to correct for it, there is growing evidence that the techniques they have employed are wholly inadequate and that GCTA itself is particularly vulnerable to confounding due to population stratification [21-23].

Consider a recent GCTA study by Plomin et al., who reported a SNP-based heritability estimate of 35% for “general cognitive ability” among UK 12 year olds (as compared to a twin heritability estimate of 46%) [8]. According to the Wellcome Trust “genetic map of Britain,” striking patterns of genetic clustering (i.e. population stratification) exist within different geographic regions of the UK, including distinct genetic clusterings comprised of the residents of the South, South-East and Midlands of England; Cumbria, Northumberland and the Scottish borders; Lancashire and Yorkshire; Cornwall; Devon; South Wales; the Welsh borders; Anglesey in North Wales; Scotland and Ireland; and the Orkney Islands [8]. Now consider the title of a study from the University and College Union: “Location, Location, Location – the widening education gap in Britain and how where you live determines your chances” [9]. This state of affairs (not at all unique to the UK), combined with widespread geographic population stratification, is fertile ground for spurious heritability estimates.

Further problems of GCTA
While I have focused on population stratification, there are at least two other things to note about GCTA studies. First, GCTA assumes “additive genetic variance,” i.e., that each polymorphism contributes a tiny amount to heritability and that the “effects” of all the polymorphisms can simply be added together. This ignores widespread evidence that genes influence the effects of other genes in highly complex, non-additive ways (“G x G” interactions), and that the environment influences the manner in which genes are transcribed in equally complex ways (“G x E” interactions). Second, all GCTA estimates are derived from looking only at SNPs, but SNPs are only one form of genetic polymorphism. There are numerous other kinds of prevalent genetic variations, including copy number variations, multiple copies of segments of genes, whole genes, and even whole chromosomes. There is no rational scientific reason to assume that SNPs are the only relevant, or even the “most important” form of genetic variation (other than the fact that SNP data is easiest to obtain).

The simplistic model of additive genetic variance upon which GCTA relies (and which assumes no epistasis and no gene x environment interactions) is out of touch with current understanding of the complex, multifactorial nature of most human traits that have a genetic component. Consider Type I diabetes (T1D). Fewer than 10% of individuals who possess gene variants associated with T1D progress to the clinical disease; <40% of MZ twins are concordant for T1D; there is a more than a 10-fold difference in the disease incidence among Caucasians living in Europe; there has been a several-fold increase in the incidence over the last 50 years; and migration studies indicate that the disease incidence has increased in population groups who have moved from a low-incidence to a high-incidence region. What this indicates is not the presence of hundreds or thousands of hidden polymorphisms, but a complex interaction between genes, the developmental programming of the immune system, and an environmental “diabetogenic” trigger:

The identification of exogenous factors triggering and driving β-cell destruction [which results in the clinical disease] offers a potential means for intervention aimed at the prevention of T1D. Therefore, it is important to pursue studies on the role of environmental factors in the pathogenesis of this disease. Environmental modification is likely to offer the most powerful strategy for effective prevention of T1D, because such an approach can target the whole population or at least that proportion of the population carrying increased genetic disease susceptibility; therefore, preventing both sporadic and familial T1D, if successful [24, p. 13].

Or consider the effects of developmental stress on brain development and behavior. Monkeys generated from stressed mothers show significantly reduced hippocampal neurogenesis and significantly reduced hippocampal volume with corresponding cognitive and behavioral effects. Likewise in humans, prenatal stress has been associated with a wide array of adverse developmental cognitive and behavioral outcomes [25].

What these examples show is that if we want to understand human traits that have a genetic component, we must turn away from an excessive and offtimes exclusive focus upon genetic polymorphisms and take a more holistic approach, one in which disease and health are seen as attributes of plastic, adaptive organisms functioning within particular environments.

Advocates of GCTA, however, tell us that in order to find the multitude of polymorphisms of tiny effect underlying heritability estimates we must undertake ever larger studies involving hundreds of thousands of persons. These polymorphisms of tiny effect, however, are so many ghosts and the search for them is the last gasp of a failed paradigm. Do we really want to squander our time and resources chasing ghosts?
Mental illness researcher @ culturewhiz.org

jaylee
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Re: The origins of white skin

Post by jaylee » October 20th, 2016, 3:08 pm

Kradmelder wrote:
jaylee wrote:
Blue Murder wrote:
jaylee wrote:Since this forum is such a magnet for severely disturbed people with extremely low IQs, I think this a good topic to post here :oops:
Which is exactly why you shouldn't waste your time. Personally, I enjoy "controversial" (lolwut) topics, but the fact that two sides cannot have intelligent discussion on HA means the bright ones like yourself are better off spending time elsewhere. That's why I don't even dish on what my "race" is. Like the poster above, he completely disregarded your article and instead wants to know what your race is so that he can "uncover your motive" or whatever lunacy he's on about.

I advise you to avoid answering.
That's okay, I'm researching mental illness here.
Why don't you research something useful. Like if africa had more mosquito nets we could save more mosquitoes from dying from AIDS :lol:
I'll asked my friend who is a developmental biologist here at MIT :)
Mental illness researcher @ culturewhiz.org

pandabear
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Re: The origins of white skin

Post by pandabear » October 21st, 2016, 1:06 am

jaylee wrote:The domesticated dog mild-manneredness was achieved through neotony--the preservation of certain juvenile characteristics into adulthood. Dogs are to a degree perpetual pups. Wolf pups are equally friendly. They just turn into wolves at a certain point. Dogs don't.
Would a castrated wolf continue to behave as a puppy?

Citizen
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Re: The origins of white skin

Post by Citizen » October 21st, 2016, 8:42 am

pandabear wrote:
jaylee wrote:The domesticated dog mild-manneredness was achieved through neotony--the preservation of certain juvenile characteristics into adulthood. Dogs are to a degree perpetual pups. Wolf pups are equally friendly. They just turn into wolves at a certain point. Dogs don't.
Would a castrated wolf continue to behave as a puppy?
you mean like millions of chemically castrated and poisoned men of the USA, UK and Canada? Guess those docile puppies would willingly take jobs and be happy servants of the Bankers, Gov'ts, Churches and Cabals.
Compare to European city folk. Their food, air and water are not poisoned so European city dwellers get lots of super hot women to fck. Partying and fcking for fun to control violence.
Compare to China, Japan, and Korea...their food is not poisoned. Why? They know they are not debt slaves to the Israeli's, Catholic Church and Greeks. Those countries know they can break the banks and cabals anytime.

Moretorque
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Re: The origins of white skin

Post by Moretorque » October 21st, 2016, 11:28 pm

droid wrote:"Jaylee" is just blackfag (aka paloaltofag). Yet again, trying over and over and over to join and get some kind of validation here. Let's dump the trash guys please.

But different populations have different proportions of each phenotype. For example, the genes related to dark hair are present in a very high rate in the Asian populations--which includes native americans--but in a much lower rate in European populations, but still there. The genes that account for racial differences (skin, hair, eye color, etc.) number only a few. That's less than a dozen out of the thousands of genes that can vary between one human and the next. That means that, while two people can both have the same color of skin, hair, and eyes, and look very similar, that similarity is only superficial. They may actually be more genetically different from each other than they are from a person of a different "race".
That's some of the dumbest crap ever posted here. If only a few genes produce such large variations it only proves how isolated groups can become so different. Of course, only skin, hair and eye color are mentioned, conveniently ignoring how just as easily "a few" genes produce differences in character and demeanor.

He might be onto something with some of his 'theories' though, I think the fungus eating this idiot's brain is advancing quite well :lol:
For you it's lines of numerical code, I read years back that Africans have the most diverse genetics of all humans even though they look more similar than say a China man compared to a Kike or Whoop. The article was claiming blacks that are separated by just a few thousand miles or even less had way more genetic code variances than all the rest of the human races.

They said that is how they know blacks are by far the oldest humans and chimps even have more code than blacks and they have been here longer as well.

This may be wrong but it was an article I read.
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droid
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Re: The origins of white skin

Post by droid » October 22nd, 2016, 1:03 pm

Moretorque wrote:For you it's lines of numerical code, I read years back that Africans have the most diverse genetics of all humans even though they look more similar than say a China man compared to a Kike or Whoop. The article was claiming blacks that are separated by just a few thousand miles or even less had way more genetic code variances than all the rest of the human races.

They said that is how they know blacks are by far the oldest humans and chimps even have more code than blacks and they have been here longer as well.

This may be wrong but it was an article I read.
In which ways are they more diverse if they look more alike than compared to other groups? In behavior? this would demonstrate precisely the variability in -you guess- behavior.

That whole thing about a banana sharing most genes with humans as 'proof' that "we are all the same" is such upside down nonsense.
I'm open to these concepts but someone has to come with honest studies on how character and behavior are not affected by gene variations among groups (i.e if there are less variation on genes related to brain function), not just a pile of wishful thinking. But as it stands such studies are obviously more difficult to perform and also subject to political correctness pressure.
1)Too much of one thing defeats the purpose.
2)Everybody is full of it. What's your hypocrisy?

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Re: The origins of white skin

Post by Winston » November 17th, 2016, 9:21 pm

Here's an interesting question I never thought of. Why is the WHITE race the only race that has a diversity of colors in their hair and eyes? Other races have more homogenous colors in their hair aad eyes. This is something unique to the white race.

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