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National Geographic - Still Lying

 

What does an old liar do after promising to stop lying?

LIE!

 

In the case of National Geographic – we know how it ends – with a lie of course: But where do we begin? They freely admit that they were Racists for decades previously, but National Geographic is 130 years old (founded 1888), does that mean that in the previous 100 years or so, they were NOT Racists? If so, then what made them Racists? (Just having fun with the hypocrisy).


 

 

The promise to stop being Racist appears to have been brought-on by this story:

 

 

 

 

The Race Issue


There’s No Scientific Basis for Race—It's a Made-Up Label

It's been used to define and separate people for millennia.

But the concept of race is not grounded in genetics.

The four letters of the genetic code —A, C, G, and T—are projected onto Ryan Lingarmillar, a Ugandan.

DNA reveals what skin color obscures: We all have African ancestors.

 

 

By Elizabeth Kolbert
Photographs by Robin Hammond

In the first half of the 19th century, one of America’s most prominent scientists was a doctor named Samuel Morton. Morton lived in Philadelphia, and he collected skulls. He wasn’t choosy about his suppliers. He accepted skulls scavenged from battlefields and snatched from catacombs. One of his most famous craniums belonged to an Irishman who’d been sent as a convict to Tasmania (and ultimately hanged for killing and eating other convicts). With each skull Morton performed the same procedure: He stuffed it with pepper seeds—later he switched to lead shot—which he then decanted to ascertain the volume of the braincase.

Morton believed that people could be divided into five races and that these represented separate acts of creation. The races had distinct characters, which corresponded to their place in a divinely determined hierarchy. Morton’s “craniometry” showed, he claimed, that whites, or “Caucasians,” were the most intelligent of the races. East Asians—Morton used the term “Mongolian”—though “ingenious” and “susceptible of cultivation,” were one step down. Next came Southeast Asians, followed by Native Americans. Blacks, or “Ethiopians,” were at the bottom. In the decades before the Civil War, Morton’s ideas were quickly taken up by the defenders of slavery.

 

What National Geographic won't say is that this is consistent with Albinos trying to place themselves at the height of humanity, with a sliding scale for those closest in color to them: and declaring their disease "Albinism" as a positive evolutionary mutation. Rather than the truth, which is that their disease makes them incapable of providing for themselves by working outdoors (Farming) in most areas of the world. This disadvantage precipitated their need for "Dark skinned Slaves" to do that work for them. Unwilling to admit to their need, Albinos turned to Racial lies to cover their deficiency. Note - even in Europe, skin Cancer still kills them.

 

 

 

“He had a lot of influence, particularly in the South,” says Paul Wolff Mitchell, an anthropologist at the University of Pennsylvania who is showing me the skull collection, now housed at the Penn Museum. We’re standing over the braincase of a particularly large-headed Dutchman who helped inflate Morton’s estimate of Caucasian capacities. When Morton died, in 1851, the Charleston Medical Journal in South Carolina praised him for “giving to the negro his true position as an inferior race.”

Today Morton is known as the father of scientific racism. So many of the horrors of the past few centuries can be traced to the idea that one race is inferior to another that a tour of his collection is a haunting experience. To an uncomfortable degree we still live with Morton’s legacy: Racial distinctions continue to shape our politics, our neighborhoods, and our sense of self. This is the case even though what science actually has to tell us about race is just the opposite of what Morton contended - (sounds promising but we know that Albinos will never admit the truth).

Morton thought he’d identified immutable and inherited differences among people, but at the time he was working—shortly before Charles Darwin put forth his theory of evolution and long before the discovery of DNA—scientists had no idea how traits were passed on. Researchers who have since looked at people at the genetic level now say that the whole category of race is misconceived. Indeed, when scientists set out to assemble the first complete human genome, which was a composite of several individuals, they deliberately gathered samples from people who self-identified as members of different races. In June 2000, when the results were announced at a White House ceremony, Craig Venter, a pioneer of DNA sequencing, observed, “The concept of race has no genetic or scientific basis.”

Over the past few decades, genetic research has revealed two deep truths about people. The first is that all humans are closely related—more closely related than all chimps, even though there are many more humans around today. Everyone has the same collection of genes, but with the exception of identical twins, everyone has slightly different versions of some of them. Studies of this genetic diversity have allowed scientists to reconstruct a kind of family tree of human populations. That has revealed the second deep truth: In a very real sense, all people alive today are Africans.

 

This is of course true: simply because the modern Human,

Homo-Sapien-Sapien is a Black or Brown Skinned creature native to Africa.

 

Our species, Homo sapiens, evolved in Africa—no one is sure of the exact time or place. The most recent fossil find, from Morocco, suggests that anatomically modern human features began appearing as long as 300,000 years ago. For the next 200,000 years or so, we remained in Africa, but already during that period, groups began to move to different parts of the continent and become isolated from one another—in effect founding new populations.

In humans, as in all species, genetic changes are the result of random mutations—tiny tweaks to DNA, the code of life. Mutations occur at a more or less constant rate, so the longer a group persists, handing down its genes generation after generation, the more tweaks these genes will accumulate. Meanwhile, the longer two groups are separated, the more distinctive tweaks they will acquire.

By analyzing the genes of present-day Africans, researchers have concluded that the Khoe-San, who now live in southern Africa, represent one of the oldest branches of the human family tree. The Pygmies of central Africa also have a very long history as a distinct group. What this means is that the deepest splits in the human family aren’t between what are usually thought of as different races—whites, say, or blacks or Asians or Native Americans. They’re between African populations such as the Khoe-San and the Pygmies, who spent tens of thousands of years separated from one another even before humans left Africa.

All non-Africans today, the genetics tells us, are descended from a few thousand humans who left Africa maybe 60,000 years ago. These migrants were most closely related to groups that today live in East Africa, including the Hadza of Tanzania. Because they were just a small subset of Africa’s population, the migrants took with them only a fraction of its genetic diversity.

 

There is no real basis for this statement: Albinos sample the genes of Albinos like themselves, and their "Near" Mulattoes, then declare their nonsense. Chinese, Koreans, Japanese and the like, are Albino and Mulatto people. Just like Europeans, South Europeans, Turks, many North Africans, Middle-Easterners, and the Turks and Turk mulattoes of Arabia. In all of those same places there are skeletons of the "Original" Black people who settled those lands. They undoubtedly had diverse genes.

 

Somewhere along the way, perhaps in the Middle East, the travelers met and had sex with another human species, the Neanderthals; farther east they encountered yet another, the Denisovans. It’s believed that both species evolved in Eurasia from a hominin that had migrated out of Africa much earlier. Some scientists also believe the exodus 60,000 years ago was actually the second wave of modern humans to leave Africa. If so, judging from our genomes today, the second wave swamped the first.

In what was, relatively speaking, a great rush, the offspring of all these migrants dispersed around the world. By 50,000 years ago they had reached Australia. By 45,000 years ago they’d settled in Siberia, and by 15,000 years ago they’d reached South America. As they moved into different parts of the world, they formed new groups that became geographically isolated from one another and, in the process, acquired their own distinctive set of genetic mutations.

Most of these tweaks were neither helpful nor harmful. But occasionally a mutation arose that turned out to be advantageous in a new setting. Under the pressure of natural selection, it spread quickly through the local population. At high altitudes, for instance, oxygen levels are low, so for people moving into the Ethiopian highlands, Tibet, or the Andean Altiplano, there was a premium on mutations that helped them cope with the rarefied air. Similarly, Inuit people, who adopted a marine-based diet high in fatty acids, have genetic tweaks that helped them adapt to it.

Sometimes it’s clear that natural selection has favored a mutation, but it’s not clear why. Such is the case with a variant of a gene called EDAR (pronounced ee-dar). Most people of East Asian and Native American ancestry possess at least one copy of the variant, known as 370A, and many possess two. But it’s rare among people of African and European descent

At the University of Pennsylvania’s Perelman School of Medicine, geneticist Yana Kamberov has equipped mice with the East Asian variant of EDAR in hopes of understanding what it does. “They’re cute, aren’t they?” she says, opening the cage to show me. The mice look ordinary, with sleek brown coats and shiny black eyes. But examined under a microscope, they are different from their equally cute cousins in subtle yet significant ways. Their hair strands are thicker; their sweat glands are more numerous; and the fat pads around their mammary glands are smaller.

Kamberov’s mice help explain why some East Asians and Native Americans have thicker hair and more sweat glands. (EDAR’s effect on human breasts is unclear.) But they don’t provide an evolutionary reason. Perhaps, Kamberov speculates, the ancestors of contemporary East Asians at some point encountered climate conditions that made more sweat glands useful. Or maybe thicker hair helped them ward off parasites. Or it could be that 370A produced other benefits she’s yet to discover and the changes she has identified were, in effect, just tagalongs. Genetics frequently works like this: A tiny tweak can have many disparate effects. Only one may be useful—and it may outlive the conditions that made it so, the way families hand down old photos long past the point when anyone remembers who’s in them. “Unless you have a time machine, you’re not going to know,” Kamberov sighs.

 

 

THERE’S MORE DIVERSITY IN AFRICA THAN ON ALL THE OTHER CONTINENTS COMBINED.

That’s because modern humans originated in Africa and have lived there the longest. They’ve had time to evolve enormous genetic diversity—which extends to skin color. Researchers who study it sometimes use Africa’s linguistic diversity—it has more than 2,000 languages as a guide. Photographer Robin Hammond followed their lead, visiting five representative language communities. His portraits span the color spectrum from Neilton Vaalbooi (top left in photo grid above), a Khoe-San boy from South Africa, to Akatorot Yelle (bottom right), a Turkana girl from Kenya. “There is no homogeneous African race,” says geneticist Sarah Tishkoff of the University of Pennsylvania. “It doesn’t exist.” The prehistoric humans who left Africa some 60,000 years ago—giving rise over time to the other peoples of the world—reflected only a fraction of Africa’s diversity.

 

Factually True in part - but with false implication. This is explained below.

 

DNA is often compared to a text, with the letters standing for chemical bases—A for adenine, C for cytosine, G for guanine, and T for thymine. The human genome consists of three billion base pairs—page after page of A’s, C’s, G’s, and T’s—divided into roughly 20,000 genes. The tweak that gives East Asians thicker hair is a single base change in a single gene, from a T to a C.

 

STRs and SNPs

 

Two types of Genetic material are the basis for all DNA results:

STRs (short tandem repeats) and SNPs (single nucleotide polymorphisms)

 

 

Y-DNA Tests use STR markers (and SNPs): A short tandem repeat (STR or microsatellite) is a pattern of two or more nucleotides that are repeated directly adjacent to each other. The repeats can range in length from 2 to 6 base pairs/repeat. A short tandem repeat polymorphism occurs when homologous STR loci differ in the number of repeats between individuals. By identifying repeats of a specific sequence at specific locations in the genome, it is possible to create a genetic profile of an individual. They report your STR marker results as the measured number of repeats for each marker. In the example below, the marker DYS393 has 12 repeats.

 

 

Family Tree DNA says: By themselves, Y-chromosome DNA (Y-DNA) short tandem repeat (STR) markers from a Y-DNA test do not have any particular meaning. The value of testing Y-DNA STR markers comes from creating a Y-DNA signature (haplotype) with them and comparing that Y-DNA signature to others in a database. They are useful for genetic genealogy because your Y-DNA signature distinguishes your paternal lineage from others. They can then be used with Family Tree DNA’s comparative database to discover genealogical connections or historic ancestry.


DNA testing companies or labs in certain cases use different nomenclatures to designate the same Y-STR allele. Thus, a conversion must be applied in these cases to accurately compare Y-STR results obtained from different companies. The most common nomenclature is based on guidance provided by NIST for Y-STR markers historically reported differently by various companies. The NIST standard is the proposal of ISOGG (International Society of Genetic Genealogy) for genetic genealogy companies. DYS454 is the least diverse, and multi-copy marker DYS464 is the most diverse Y-STR marker. Genealogical DNA test labs CAN examine up to 442 Y-STRs.

So, what it is the difference between a gene and an allele?

The short answer is that an allele is a variant form of a gene. Explained in greater detail, each gene resides at a specific locus (location on a chromosome) in two copies, one copy of the gene inherited from each parent. The copies, however, are not necessarily the same. When the copies of a gene differ from each other, they are known as alleles. A given gene may have multiple different alleles, though only two alleles are present at the gene’s locus in any individual.

Alleles can sometimes result in different phenotypes (observable traits), with certain alleles being dominant (overriding the traits of other alleles) or, in some cases, multiple alleles acting in a codominant fashion. An example of the latter is the human ABO blood group system, in which persons with type AB blood have one allele for A and one for B (persons with neither allele are type O). An example of dominant allele expression is flower color in pea plants. A plant with purple flowers actually has a genotype (genetic makeup) consisting of a gene with a dominant P and a recessive p allele.

 

SNPs

 

 

What are single nucleotide polymorphisms (SNPs)?

From: U.S. Department of Health & Human Services - Single nucleotide polymorphisms, frequently called SNPs (pronounced “snips”), are the most common type of genetic variation among people. Each SNP represents a difference in a single DNA building block, called a nucleotide. For example, a SNP may replace the nucleotide cytosine (C) with the nucleotide thymine (T) in a certain stretch of DNA.

Nucleotide Definition

A nucleotide is one of the structural components, or building blocks, of DNA and RNA. A nucleotide consists of a base (one of four chemicals: adenine, thymine, guanine, and cytosine) plus a molecule of sugar and one of phosphoric acid. More: C, T, and U are called pyrimidines and each has a single nitrogen-containing ring. A and G are called purines and each has two nitrogen-containing rings. Definition from the National Human Genome Research Institute (NHGRI)

SNPs occur normally throughout a person’s DNA. They occur once in every 300 nucleotides on average, which means there are roughly 10 million SNPs in the human genome. Most commonly, these variations are found in the DNA between genes. They can act as biological markers, helping scientists locate genes that are associated with disease. When SNPs occur within a gene or in a regulatory region near a gene, they may play a more direct role in disease by affecting the gene’s function.

Most SNPs have no effect on health or development. Some of these genetic differences, however, have proven to be very important in the study of human health. Researchers have found SNPs that may help predict an individual’s response to certain drugs, susceptibility to environmental factors such as toxins, and risk of developing particular diseases. SNPs can also be used to track the inheritance of disease genes within families. Future studies will work to identify SNPs associated with complex diseases such as heart disease, diabetes, and cancer.


Here’s a simplified example of how AncestryDNA turns those trends into an ethnicity estimate. AncestryDNA looks at about 700,000 markers in your DNA sample. Those markers are called SNPs (pronounced snips). And each snip is made up of a pair of letters, either some combination of A and/or T or C and/or G. Let’s say that at SNP rs122 there are two possibilities: A and T. Because you get one letter (or allele) from each parent, you can have an AA, AT, or TT. Each possible outcome at each SNP has a probability for how likely it is to show up in each region represented by the reference panel. We’ll pretend that rs122 occurs in three populations—Native American, Swedish, and English—at the following frequencies: A = appears 5% of the time in Native American populations, 75% in English populations, and 80% in Swedish T = appears 95% of the time in Native American populations, 25% in English populations, and 20% in Swedish. So, if you have AA at rs122, it seems you are more likely to be Swedish than Native American. If your DNA reads TT, the opposite seems more likely. One SNP doesn’t tell us much about your ethnicity, but when we apply the same process to thousands of SNPs, and then do the math, the grand total becomes the basis for your ethnicity estimate.


You Contain a Range of Possibilities: When you get your ethnicity estimate, the first thing you look for are the region names and percentages, right? “I’m 32% Ireland! 24% Native American! 9% Benin/Togo—where’s Benin/Togo?” But there are some other numbers that are just as important. Here’s an example of an AncestryDNA ethnicity estimate for someone with strong ties to northern Europe: These results say that AncestryDNA estimates that 99% of this customer’s DNA comes from Europe. The next level includes Great Britain, Ireland, and Scandinavia. Each of these regions has a percentage and a range. AncestryDNA determines the range by analyzing each DNA sample an extra 40 times. Each time, a few randomly selected portions of the sample are left out to help improve statistical validity of the first analysis, which is done with the entire sample. The percentage you get is the average of those 40 tests. The range reflects most of the results of those 40 analyses, with extreme outliers left out.

In the example above, those 40 analyses showed that as little as 14% and as much as 46% of this customer’s DNA appears to match the Ancestry Irish reference panel, with an average percentage of 30%. The likelihood that this user’s actual genetic Irish ethnicity is exactly 30% is not very high. However, AncestryDNA has relatively high confidence that this person’s genetic ethnicity falls within the range.

 

 

The Bottom line: none of this is really very accurate, and because there is little or none of Ancient Black DNA from the Americas, Europe, Asia, Oceania: and little "NORMAL" Black DNA from everywhere, including Africa: this type of science should be viewed as mostly a curiosity rather than serious science. To put it another way: consider the ridiculousness of less than 13% of the population, with a disease (Albinism), presuming to type the whole (including those without disease) based on themselves. Isn't it so preposterous that it becomes silly comedy?

 

 

Similarly, the mutation that’s most responsible for giving Europeans lighter skin is a single tweak in a gene known as SLC24A5, which consists of roughly 20,000 base pairs. In one position, where most sub-Saharan Africans have a G, Europeans have an A. About a decade ago a pathologist and geneticist named Keith Cheng, at Penn State College of Medicine, discovered the mutation by studying zebrafish that had been bred to have lighter stripes. The fish, it turned out, possessed a mutation in a pigment gene analogous to the one that is mutated in Europeans.

 

Albinos simply can't bring themselves to admit what SLC24A5 REALLY IS!

An Albinism mutation!

 

Studying DNA extracted from ancient bones, paleogeneticists have found that the G-to-A substitution was introduced into western Europe relatively recently—about 8,000 years ago—by people migrating from the Middle East, who also brought a newfangled technology: farming. That means the people already in Europe—hunter-gatherers who created the spectacular cave paintings at Lascaux, for example—probably were not white but brown. The ancient DNA suggests that many of those dark-skinned Europeans also had blue eyes, a combination rarely seen today.

 

 

 

“What the genetics shows is that mixture and displacement have happened again and again and that our pictures of past ‘racial structures’ are almost always wrong,” says David Reich, a Harvard University paleogeneticist whose new book on the subject is called Who We Are and How We Got Here. There are no fixed traits associated with specific geographic locations, Reich says, because as often as isolation has created differences among populations, migration and mixing have blurred or erased them.

Across the world today, skin color is highly variable. Much of the difference correlates with latitude. Near the Equator lots of sunlight makes dark skin a useful shield against ultraviolet radiation; toward the poles, where the problem is too little sun, paler skin promotes the production of vitamin D. Several genes work together to determine skin tone, and different groups may possess any number of combinations of different tweaks. Among Africans, some people, such as the Mursi of Ethiopia, have skin that’s almost ebony, while others, such as the Khoe-San, have skin the color of copper. Many dark-skinned East Africans, researchers were surprised to learn, possess the light-skinned variant of SLC24A5. (It seems to have been introduced to Africa, just as it was to Europe, from the Middle East.) East Asians, for their part, generally have light skin but possess the dark-skinned version of the gene. Cheng has been using zebrafish to try to figure out why. “It’s not simple,” he says.

 

 

After all of these years, we can't believe National Geographic would actually bring back this old bullshit which has been debunked many, many, times!

paler skin promotes the production of vitamin D.

 

NO IT DOES NOT!!!

 

 

 

WHAT PALE SKIN (Albinism) DOES PROMOTE IS "SKIN CANCER"!

 

 

 

 

When people speak about race, usually they seem to be referring to skin color and, at the same time, to something more than skin color. This is the legacy of people such as Morton, who developed the “science” of race to suit his own prejudices and got the actual science totally wrong. Science today tells us that the visible differences between peoples are accidents of history. They reflect how our ancestors dealt with sun exposure, and not much else.

“We often have this idea that if I know your skin color, I know X, Y, and Z about you,” says Heather Norton, a molecular anthropologist at the University of Cincinnati who studies pigmentation. “So I think it can be very powerful to explain to people that all these changes we see, it’s just because I have an A in my genome and she has a G.”

About an hour away from Morton’s collection, at West Chester University, Anita Foeman directs the DNA Discussion Project. On a bright fall morning, she’s addressing the latest participants in the project—a dozen students of varying hues, each peering at a laptop screen. A few weeks earlier the students had filled out questionnaires about their ancestry. What did they believe their background to be? The students had then submitted saliva samples for genetic testing. Now, via their computers, they are getting back their results. Their faces register their reactions.

One young woman, whose family has lived in India as far back as anyone can recall, is shocked to discover some of her ancestry is Irish. Another young woman, who has grown up believing one of her grandparents was Native American, is disappointed to learn this isn’t so. A third describes herself as “confused.” “I was expecting a lot more Middle Eastern,” she says.

Foeman, a professor of communications, is accustomed to such responses. She started the DNA Discussion Project in 2006 because she was interested in stories, both the kind that families tell and the kind that genes tell. From early on in the project, it was clear these were often not the same. A young man who identified as biracial was angry to discover his background was, in fact, almost entirely European. Several students who had been raised in Christian households were surprised to learn some of their ancestors were Jewish.

“All these stories that have been suppressed pop out in the genes,” Foeman says. Even Foeman, who identifies as African-American, was caught off guard by her results. They showed that some of her ancestors were from Ghana, others from Scandinavia.

“I grew up in the 1960s, when light skin was really a big deal,” she explains. “So I think of myself as being pretty brown skinned. I was surprised that a quarter of my background was European.” “It really brought home this idea that we make race up,” she says.

Of course, just because race is “made up” doesn’t make it any less powerful. To a disturbing extent, race still determines people’s perceptions, their opportunities, and their experiences. It is enshrined in the U.S. census, which last time it was taken, in 2010, asked Americans to choose their race from a list that reflects the history of the concept; choices included “White,” “Black,” “American Indian,” “Asian Indian,” “Chinese,” “Japanese,” and “Samoan.” Racial distinctions were written into the Jim Crow laws of the post-Reconstruction South and are now written into statutes like the Civil Rights Act, which prohibits discrimination on the basis of race or color. To the victims of racism, it’s small consolation to say that the category has no scientific basis.

Genetic sequencing, which has allowed researchers to trace the path of human migration and now allows individuals to trace their own ancestry, has introduced new ways of thinking about human diversity. Or at least so Foeman hopes. The DNA Discussion Project gives participants insight into their own background, which is generally a lot more complicated than they’d been led to believe. And this, in turn, opens up a conversation about the long, tangled, and often brutal history that all of us ultimately share. “That race is a human construction doesn’t mean that we don’t fall into different groups or there’s no variation,” Foeman says. “But if we made racial categories up, maybe we can make new categories that function better.”

 

 

 

 

 

As a reminder:

 

 

Above, National Geographic implies that the REASON European Albinos and Mongols have so little genetic diversity, is because they all descend from the SMALL group of Africans who left Africa to settle the rest of Planet Earth. Well, on the face of it, those actually thinking about it know that can't be true. For years the Albinos have been telling us how different Black people OUTSIDE of Africa, like Australians, Oceanians, Americans, are from Africans. Now they want to tell us how SIMILAR they are!

As we have learnt over the years, it is our good fortune that Albinos cannot plan or coordinate their lies with each other. So it is often the case that just as one group is mixing their lies with some truth (the best lies always have some truth) on one subject, another group is doing the same thing with a DIFFERENT subject: leaving us to simply PLUCK the truth from the lies. Such is the case with the Genome studies of Native Australians and Native Mexicans.

 

 

See - lots of "DIVERSITY" here

 

Australian Aborigines

 

 

 

 

 

 

 

 

Australians on the nearby Island of Tasmania - ALL DEAD!

 

   

 

 

 

 

See - lots of "DIVERSITY" here

 

 

 

Ancient Mexicans

 

 

 

Note this ancient Mongol in Guerrero

 

 

 

 

 

 

 

 

 

 

Please note the presence of Mongols in the Mayan Empire

 

 

 

 

 

 

Pictures of Modern Indigenous Mexicans

 

 

 

   

 

 

 

 

 

 

The Mestizo

 

 

After Mexico's Albinos and their "Near" Mulattoes (Mestizos), Killed-off

most of the Blacks and Dark Mongols, this is what they tried to do.

 

Mestizo
From Wikipedia, the free encyclopedia

The large majority of Mexicans can be classified as "Mestizos", meaning in modern Mexican usage that they identify fully neither with any indigenous culture nor with a particular non-Indigenous heritage, but rather identify as having cultural traits incorporating both indigenous and European elements. In Mexico, Mestizo has become a blanket term which not only refers to mixed Mexicans but includes all Mexican citizens who do not speak indigenous languages even Asian Mexicans and Afro-Mexicans. By the deliberate efforts of post-revolutionary governments the "Mestizo identity" was constructed as the base of the modern Mexican national identity, through a process of cultural synthesis referred to as mestizaje. Mexican politicians and reformers such as José Vasconcelos and Manuel Gamio were instrumental in building a Mexican national identity on the concept of mestizaje (the process of race homogenization).

 

Even today, Native People or their mulatto descendants, often Rebel: with the usual results - Death!

Wiki: The Chiapas conflict refers to the 1994 Zapatista Uprising and its aftermath, and tensions between the indigenous peoples and subsistence farmers in the Mexican state of Chiapas in the 1990s and 1980s. The Zapatista uprising started in January 1994, and lasted less than two weeks before the government pacified the area. Negotiations between the government and Zapatistas led to agreements being signed. But these agreements were not complied with in the following years and the peace process stagnated. This resulted in an increasing division between communities with ties to the government and communities that sympathized with the Zapatistas. Social tensions, armed conflict and para-military incidents increased, culminating in the killing of 45 people in the village of Acteal in 1997 by para-militaries. Though at a low level, rebel activity continues and violence occasionally erupts between Zapatista supporters and anti-Zapatista militias along with the government. The last related incident occurred in 2014, when a Zapatista-affiliated teacher was killed and 15 more wounded in Chiapas.

 

 

 

As these two studies above clearly show - National Geographic lied

as to why Albino Europeans and Mongols have LITTLE genetic diversity.

 

 

That's because the Black people who settled Europe WERE NOT dark skinned White people as the Albinos now imply! They were just ordinary looking Africans from many different parts of the continent (Africans entered Europe through Gibraltar in the West, and through the Middle-East). And as these studies show, the same was true of the African settlers of Asia, the Americas, and lands South - in varying degrees of course. So clearly this "LACK" of diversity involves ONLY "White" or "Light" skinned people, not the Paleo Africans around the world.

 

Okay, but that doesn't tell us "WHY" Albino Europeans and Mongols have so LITTLE genetic diversity you say. For the answer to that question, we need to reference another Albino source - Wikipedia. From their article on "Oculocutaneous Albinism Type 2 (OCA2)" we get this Quote:

The prevalence of OCA type 2 is estimated at 1/38,000-1/40,000 in most populations throughout the world, with a higher prevalence in the African population of 1/3,900-1/1,500. Did everyone get that, in certain African populations: 1 in 3900 Africans may be an Albino! Now lets leave it there, while related material is introduced.

 

 

 

 

 

 

The Bi-racial Twins above explained

 

OCA2

Oculocutaneous Albinism Type 2 (OCA2)

From Wikipedia, the free encyclopedia

(Formerly called the P gene)

The most common type of Albinism, it is caused by mutation of the P gene. People with OCA2 generally have more pigment and better vision than those with OCA1, but cannot tan like some with OCA1b. A little pigment can develop in freckles or moles. People with OCA2 usually have fair skin but often not as pale as OCA1, and pale blonde to golden, strawberry blonde, or even brown hair, and most commonly blue eyes. Affected people of African descent usually have a different phenotype (appearance): yellow hair, pale skin, and blue, gray or hazel eyes. About 1 in 15,000 people have OCA2. The gene MC1R doesn't cause OCA2, but does affect its presentation.


The "P" protein, also known as melanocyte-specific transporter protein or pink-eyed dilution protein homolog, is a protein that in humans is encoded by the oculocutaneous albinism II (OCA2) gene. The P protein is believed to be an integral membrane protein involved in small molecule transport, specifically tyrosine - a precursor of melanin. Certain mutations in OCA2 result in type 2 oculocutaneous albinism. OCA2 encodes the human homologue of the mouse p (pink-eyed dilution) gene. In human, the OCA2 gene is located on the long (q) arm of chromosome 15 between positions 12 and 13.1 The human OCA2 gene is located on the long arm (q) of chromosome 15, specifically from base pair 28,000,020 to base pair 28,344,457 on chromosome 15.

Function
OCA2 provides instructions for making the protein called P protein which is located in melanocytes which are specialized cells that produce melanin. Melanin is responsible for giving color to the skin, hair, and eyes. Moreover, melanin is found in the light-sensitive tissue of the retina of the eye which plays a role in normal vision. The exact function of protein P is unknown, but it has been found that it is essential for the normal coloring of skin, eyes, and hair; and likely involved in melanin production. This gene seems to be the main determinant of eye color depending on the amount of melanin production in the iris stroma (large amounts giving rise to brown eyes; little to no melanin giving rise to blue eyes).


Clinical significance
Global frequency distribution of the OCA2 gene's ancestral allele (blue) and derived His615Arg allele (yellow).
Mutations in the OCA2 gene cause a disruption in the normal production of melanin; therefore, causing vision problems and reductions in hair, skin, and eye color. Oculocutaneous albinism caused by mutations in the OCA2 gene is called oculocutaneous albinism type 2. The prevalence of OCA type 2 is estimated at 1/38,000-1/40,000 in most populations throughout the world, with a higher prevalence in the African population of 1/3,900-1/1,500. Other diseases associated with the deletion of OCA2 gene are Angelman syndrome (light-colored hair and fair skin) and Prader-Willi syndrome (unusually light-colored hair and fair skin). With both these syndromes, the deletion often occurs in individuals with either syndrome.


A mutation in the HERC2 gene adjacent to OCA2, affecting OCA2's expression in the human iris, is found common to nearly all people with blue eyes. It has been hypothesized that all blue-eyed humans share a single common ancestor with whom the mutation originated. The His615Arg allele of OCA2 is involved in the light skin tone and the derived allele is restricted to East Asia with high frequencies, with highest frequencies in Eastern East Asia (49-63%), midrange frequencies in Southeast Asia, and the lowest frequencies in Western China and some Eastern European populations.

 

What Causes Albinism? - The Nemours Foundation.

Albinism is inherited. People are born with albinism because they inherit an albinism gene or genes from their parents. In the most common forms of oculocutaneous albinism, both parents must carry the albinism gene for a child to be born with the condition. Even if both parents carry the gene, the chance of each of their children being born with albinism is one in four.

If just one parent has the gene and the other parent has a normal pigment gene, their children won't have oculocutaneous albinism. But each child will have a one in two chance of being a "carrier" of an albinism gene. If a child who carries the gene grows up to have a baby with someone who also does, there's a one in four chance that their baby may have albinism. Since most people who carry an albinism gene don't show any signs of the condition, a baby with albinism can be born to parents whose coloring is typical for people of their ethnic group.

 

What neither National Geographic nor most other Albino

sources will tell you, is that an Albino (White Skinned) couple, such as Europeans:

can ONLY make Albino (White) babies - because that inescapably explains them!

 

Blacks of course, make White Babies

- of every Phenotype -

every minute of every day

 

The Lie of all Albinos having Bad Eyesight

Albino scientists have created the lie that Albinism and poor Eyesight was "cause and effect". That lie was created so that they could say: "See we are not Albinos, because Albinos have "Bad Eyesight" and we have "Normal" Eyesight: while that is often true for OCA1 Albinos (the most severe type of Albinism), it is false for the others as a rule. And that lie is very easy to debunk, by simply looking. Note this Albino family, are any of them wearing glasses? Next Google "Albino images". The search will return pictures of hundreds of Albinos, some with terrible Skin Cancer, but next to none wearing glasses.

 

 

 

Having established a factual background, we can now discuss the perfectly common

"Mixed" Twins that National Geographic found so mystifying.

 

 

 

 

 

Twins - identical and fraternal

 

There are two types of twins – identical (monozygotic) and fraternal (dizygotic).

To form identical twins, one fertilized egg (ovum) splits and develops two babies with exactly the same genetic information. This differs from fraternal twins, where two eggs (ova) are fertilized by two sperm and produce two genetically unique children, who are no more alike than individual siblings born at different times. THAT'S ALL THE "MIXED" TWINS REALLY ARE!

 

 

Amanda Wanklin Biggs is an Albino, which is a "Recessive" gene condition.

Michael Biggs is a normal Black man except for one thing, he is a "CARRIER" for Albinism.

 

Autosomal Dominant Inheritance


Humans have 46 chromosomes in each cell in their body. These are arranged in 23 pairs. One chromosome in each pair is inherited from the mother and one from the father. 22 of the pairs are identical in males and females, and these are known as the "autosomes". The 23rd pair consists of the two sex chromosomes, which determine the sex of the child.
Conditions described as "autosomal" are those in which the defective gene (mutation) that causes the disorder is located on one of the 44 chromosomes other than the two sex chromosomes. Autosomal conditions affect both males and females equally.


If a condition is dominant, that means that a single copy of the affected gene is enough to cause the condition, even if the matching gene in the pair is normal. The abnormal gene "dominates" the pair of genes. So a child inheriting the abnormal gene from an affected parent will also have the condition. If just one parent has a dominant gene defect, each child has a 50% chance of inheriting the disorder. The image below shows the inheritance pattern for autosomal dominant disorders. Further information about genetics can be found in the links section to the left.

 

As we can see from this Punnett graphic, when the Mother/Father is Albino AND

the other parent is a "CARRIER" for Albinism, the is a 50% chance that at least ONE child will be an Albino.

 

 

 

 

So what happens when BOTH Parents are CARRIERS?

 

The image below shows the inheritance pattern for autosomal recessive disorders

where both parents are carriers but neither is affected.

 

 

 

Autosomal Recessive Inheritance


Humans have 46 chromosomes in each cell in their body. These are arranged in 23 pairs. One chromosome in each pair is inherited from the mother and one from the father. 22 of the pairs are identical in males and females, and these are known as the "autosomes". The 23rd pair consists of the two sex chromosomes, which determine the sex of the child.
Conditions described as "autosomal" are those in which the defective gene (mutation) that causes the disorder is located on one of the 44 chromosomes other than the two sex chromosomes. Autosomal conditions affect both males and females equally.


Examples: spinal muscular atrophy, congenital muscular dystrophy, limb girdle muscular dystrophy (some types)
If a condition is recessive, that means that it will not usually cause any symptoms in people who have a normal copy of the gene as well as a defective one, because the normal copy is able to compensate for the defective one. This means that people can be "carriers" of the disease without knowing it. The mutation may be passed from parents to their children, but the child will only be affected if both parents pass on a mutated copy of the gene.

 

 

 

 

But what happens when a "Healthy"

Black (not a carrier) mates with an Albino?

 

When an individual affected by an autosomal recessive condition has a child, that child will of necessity be at least a carrier of the condition, since the parent has no "normal" copy of the gene to pass on. But if the other parent is neither affected nor a carrier of the condition, the child will receive one normal copy of the gene from that parent and so will not be affected themselves. This means that the majority children born to people with a recessive condition are not affected. If the second parent happens to be a carrier, there is a 50% chance that the couple will have an affected child. If both parents are affected, all their children will be affected too.

 

 

Thus the "MULATTO" is born!

 

 

 

 

 

 

 

 

Now getting back to why White Europeans and the Chinese have so little genetic diversity, it's really quite simple. Recalling from the Wiki article on OCA2: The prevalence of OCA type 2 is estimated at 1/38,000-1/40,000 in most populations throughout the world, with a higher prevalence in the African population of 1/3,900-1/1,500.

Did everyone get that, in certain African populations: 1 in 3900 Africans may be an Albino! That means that 4 x that number are either Carriers or Albinos. And it is from this SMALL population of "effected" Africans, from whence White Europeans (Central Asians actually) and Chinese (East Asians) derive. Of course today's Europeans and Chinese are admixed, the Chinese much more so, (they used to be called the "Yellow Race"): and few Europeans are "Classic" OCA2 Albinos, but that's where they all come from, and that's why they have so little genetic diversity.

 

 

 

 

 

Definitions - Background Facts - Questions and Answers

 

Recessive traits


Recessive traits can be carried in a person's genes without appearing in that person. For example, a dark-haired person may have one gene for dark hair, which is a dominant trait, and one gene for light hair, which is recessive.

Dominant Traits


Dominant traits are those that are expressed or seen when a heterozygous genotype is present. Heterozygous just means having two different alleles for a gene. One is usually dominant while one is recessive. Remember, recessive alleles are masked by dominant alleles.

EXAMPLES
In genetics, a dominant trait will appear in the offspring if one of the parents contributes it. (Compare recessive trait.) Note: In humans, dark hair is a dominant trait; if one parent contributes a gene for dark hair and the other contributes a gene for light hair, the child will have dark hair, ditto skin, eyes, etc.

Q: Is straight hair a dominant or recessive trait?
A: It has been long established that Curly hair is a dominant trait in Caucasians and Straight hair is Recessive.

Q: Are blue or brown eyes more dominant?
A: The brown version of a gene is dominant over the blue one.

Two dominant traits or Homozygous


If an organism is heterozygous (heterozygous refers to a pair of genes where one is dominant and one is recessive — they're different), for that trait, or possesses one of each allele, then the dominant trait is expressed. Alternative forms of a given gene are called alleles, and they can be dominant or recessive. When an individual has two of the same allele, whether dominant or recessive, they are homozygous.

Q: What is an example of a homozygous recessive genetic disorder?
A: Many disorders are homozygous recessive, from cystic fibrosis to Albinism.

Q: What is homozygous recessive parent?
A: When a trait is recessive, an individual must have two copies of a recessive allele to express the trait: because having just a single dominant trait, would cause that trait to show.

THIS IS WHY ALBINOS LIKE EUROPEANS CAN ONLY MAKE MORE ALBINOS!

In order to make pigmented Humans, Albinos MUST mate with Pigmented Humans to provide a dominant gene or genes.
Not surprisingly there is no question and answer to be found for the question: "Which is Dominant Black Skin or White Skin"?

How is skin color determined in babies? Can white and black parents give birth to a white child?

Q: How is skin color determined in babies?"

American Society for Biochemistry and Molecular Biology
The Regulation of Skin Pigmentation - Yuji Yamaguchi, Michaela Brenner, and Vincent J. Hearing.

Visible pigmentation of the skin, hair, and eyes depends primarily on the functions of melanocytes, a very minor population of cells that specialize in the synthesis and distribution of the pigmented biopolymer melanin. Melanocytes are derived from precursor cells (called melanoblasts) during embryological development, and melanoblasts destined for the skin originate from the neural crest. The accurate migration, distribution, and functioning of melanoblasts/melanocytes determine the visible phenotype of organisms. At this time, more than 125 distinct genes are known that regulate pigmentation either directly or indirectly. Many of those affect developmental processes critical to melanoblasts, others regulate the differentiation, survival, etc. of melanocytes, and yet others regulate distinct processes that affect pigmentation. Many of those genes (>25 at latest count) affect the biogenesis or function of melanosomes, the discrete membrane-bound organelles within which melanins are synthesized. Melanosomes, which are closely related to lysosomes and are within the family of lysosome-relatedg organelles (LROs),3 require a number of specific enzymatic and structural proteins to mature and become competent to produce melanin

Suffice it to say that the critical enzymes include tyrosinase (TYR), Tyrp1, and Dct, mutations of which dramatically affect the quantity and quality of melanins synthesized. Critical structural proteins include Pmel17 (also known as gp100) and MART1, both of which are required for the structural maturation of melanosomes. A large number of proteins are involved in the sorting/trafficking of proteins to melanosomes, and mutations in any of those typically lead to inherited hypopigmentary disorders (Hypopigmentation is the loss of skin color). Melanocytes can produce three distinct kinds of melanins: two types of eumelanin, which are the predominant pigments found in dark skin and black hair, and pheomelanin, which is associated with the red hair/freckled skin phenotype.

*Actually there are three basic types of melanin: Eumelanin, Pheomelanin, and Neuromelanin. The most common type is eumelanin, of which there are two types—brown eumelanin and black eumelanin. Pheomelanin is a cysteine-derivative that contains polybenzothiazine portions that are largely responsible for the color of red hair, among other pigmentation. It contains sulfur and is alkali soluble; elevated levels are found in the rufous type of Oculocutaneous Albinism. Neuromelanin is found in the brain, though its function remains obscure.

 

PREDICTING SKIN COLOR

Skin color is an example of polygenic inheritance, which means that multiple genes collectively influence phenotypic expression of the trait. There are actually several different genes that regulate a variety of processes of melanin production. Therefore, there is no one gene that determines skin color. In the simplest example: The more "high pigmentation" genes a person has, the darker their skin; whereas an Albino has very little pigmentation and has White Skin. Black + White = Brown. This is why most Black/Albino mixed-race children have an intermediate skin tone between their parents. But since there are no people who are 100% Black or 100% White there is an almost endless variety in Human Skin Tone. The Davenport Skin Color Predictor was very useful in its time. It showed that the mating of a Black Man and a White Woman, at the extremes, had only one chance of a Black Baby and only one chance of a White Baby: All the other Babies would be some shade of BROWN!

 

Davenport Skin Color Predictor

 

 


But now the IrisPlex System for predicting Eye Color using DNA

may soon be perfected, and adapted to predict Skin Color.

 

 

 

Explanation of DNA used by the IrisPlex System

HERC2 - Wikipedia
HERC2 is an enzyme that in humans is encoded by the HERC2 gene. A mutation in the HERC2 gene adjacent to OCA2, affecting OCA2's expression in the human iris, is found common to nearly all people with blue eyes.

LOC105370627 (Uncharacterized LOC105370627) is an RNA Gene, and is affiliated with the ncRNA class.
A non-coding RNA (ncRNA) is a functional RNA molecule that is transcribed from DNA but not translated into proteins.

SLC45A2
This gene encodes a transporter protein that mediates melanin synthesis. The protein is expressed in a high percentage of melanoma cell lines. Mutations in this gene are a cause of oculocutaneous albinism type 4, and polymorphisms in this gene are associated with variations in skin and hair color. Multiple transcript variants encoding different isoforms have been found for this gene.


TYR
The TYR gene provides instructions for making an enzyme called tyrosinase. This enzyme is located in melanocytes, which are specialized cells that produce a pigment called melanin. Melanin is the substance that gives skin, hair, and eyes their color. Melanin is also found in the light-sensitive tissue at the back of the eye (the retina), where it plays a role in normal vision.
Tyrosinase is responsible for the first step in melanin production. It converts a protein building block (amino acid) called tyrosine to another compound called dopaquinone. A series of additional chemical reactions convert dopaquinone to melanin in the skin, hair follicles, the colored part of the eye (the iris), and the retina.

IRF4 - From Wikipedia.
Interferon regulatory factor 4 also known as MUM1
In melanocytic cells the IRF4 gene may be regulated by MITF. IRF4 is a transcription factor that has been implicated in acute leukemia. This gene is strongly associated with pigmentation: sensitivity of skin to sun exposure, freckles, blue eyes, and brown hair color. A variant has been implicated in greying of hair.

 

 

 

 

 

 

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