science proves european dna from albino - not cold adapted

[wissen85]

 

 

You can do the same thing with a potato or a lemon. It's about having an electrolyte and dissimilar metals. The battery action is from the metals, not the medium.

 

 

Um, what's "normal"?

"normal" means carbon rich as in all healthy life forms opposed to carbon recessive as in albinos.

 

the disadvantages of being white(SLC24A5) are backed up by evidence in vitro and in vivo.

 

 

 

An ideal electrode for a sodium ion battery, the type of energy storage device pioneered by Jay Whitacre, coauthor of the study, would have an anode with a surface area that can attract and support as many sodium ions as possible, and it would be redox active, capable of shuttling electrons from anode to cathode in a circuit. The spongy microstructure of natural melanin offers both.

 

The authors compared the efficiency of natural melanin taken from the ink sack of a cuttlefish with commercially available synthetic melanins. Their findings show that natural melanin, as an electrode material, has a specific capacity fifty percent larger than synthetic melanins.

 

Differences in their microstructures noted as variations in surface area could be to blame.

 

“Melanin is basically a disordered molecule, it’s very enigmatic as a structural pigment, and not all melanins are made alike,” Bettinger says. “If I get a protein from a bacteria, I can make the same protein synthetically, and it will look the same. Melanins are different. We can’t replicate the structure of natural melanin.”

 

The electronic properties of melanin are the discovery here, Bettinger adds. “We’re still unraveling how it works.” http://blog.pnas.org/2013/12/naturally-occurring-melanin-could-be-the-future-of-edible-electronics/

 

 

Edited April 23, 2016 by wissen85

[John Cuthber]

"normal" means carbon rich as in all healthy life forms opposed to carbon recessive as in albinos.

 

Yet another citation needed.

[wissen85]

Yet another citation needed.

you guys are experts in demanding citations while none of you came up with a single valid counterargument or evidence till now..

 

but anyway

 

 

Carbon forms the key component for all known life on Earth. Complex molecules are made up of carbon bonded with other elements, especially oxygen, hydrogen and nitrogen, and carbon is able to bond with all of these because of its four valence electrons. Carbon is abundant on earth. It is also lightweight and relatively small in size, making it easier for enzymes to manipulate carbon molecules.[citation needed] It is often[how often?] assumed in astrobiology that if life exists somewhere else in the universe, it will also be carbon based. https://en.wikipedia.org/wiki/Carbon-based_life

 

This study used the C. neoformans requirement of exogenous obligatory catecholamine precursors for melanization to produce isotopically enriched pigment “ghosts” and applied 2D 13C-13C correlation solid-state NMR to reveal the carbon-based architecture of intact natural eumelanin assemblies in fungal cells. http://www.jbc.org/content/290/22/13779.abstract

Edited April 23, 2016 by wissen85

[Delta1212]

I posted so much evidence of white people being oca2 albinos rather than "cold adapted". why would nature select such recessive traits for humans to be at risk of melanomas, infertility and macular degeneration by having light skin and light eyes?

,

Why would nature select for the genes that lead to malformed red blood cells in people from tropical/equatorial regions when it leads to higher rates genetic disease like sickle cell anemia?

 

The answer is that it also confirms a resistance to malaria, which is a major concern in those regions and ultimately winds up being a far deadlier killer than the genetic disease that comes along as a side effect of the resistance, at least if you live in a malaria-prone area. Move away and that advantage suddenly becomes a bigger problem than the one it is solving.

 

You keep saying that the pale skin is the result of an albinism-associated mutation "rather than" an adaptation, and that it comes with lots of health problems instead of some environmental advantage.

 

But that latter bit actually seems to imply that it does, or at least did, hold some adaptational advantage that offsets the associated problems. Traits generally don't spread and become fixed in a population if they are deleterious, especially not very large populations. Either they confirm some advantage (which may also come with some disadvantages that the advantage simply offsets, as in the case with sickle cell) or they are basically neutral and just random walked their way into the wider population without being good or bad in terms of survival.

 

Either way, nothing is ever a mutation "rather than" an adaptation, and something that is an adaptation in one environment or population may also be considered a disease in another environment or population, but the fact that something is a mutation doesn't "prove" that it's one or the other. All genetic diseases are the result of mutations and all environmental adaptations are the result of mutations.

[John Cuthber]

 

you guys are experts in demanding citations while none of you came up with a single valid counterargument or evidence till now..

 

 

You have not yet put forward anything to counter.

Anything asserted without evidence can be dismissed without evidence.

And the rest of that post does not actually support your assertion that ""normal" means carbon rich as in all healthy life forms opposed to carbon recessive as in albinos."

So you still need to cite evidence to support it.

[Strange]

So you still need to cite evidence to support it.

 

But he has posted pictures of dogs and kittens. How can anyone refute that.

[swansont]

"normal" means carbon rich as in all healthy life forms opposed to carbon recessive as in albinos.

 

Please explain how a single mutation in DNA can move you from "carbon rich" to "carbon recessive", and define those terms.

[John Cuthber]

Lets have a quick look at the first line of the OP

scientific research proved the origin of white europeans due to a albinism mutation SLC45A2/OCA2. we white people are thus not a race but mutated oculocutaneous albinos type 2.

"we white people are thus not a race but mutated oculocutaneous albinos type 2. "

If all white skinned people were albinos then there wouldn't be any albinos among the whites.

How could the melanin be more missing in a group where it's already missing?

But there are white albinos- so we know that the starting premise of this thread is wrong.

(the situation is analogous to the demise of the "mongolism"explanation of Down's syndrome when it was discovered that you could find black skinned people with Downs)

Might as well close the thread- it's not going to achieve much.

[wissen85]

Lets have a quick look at the first line of the OP

"we white people are thus not a race but mutated oculocutaneous albinos type 2. "

If all white skinned people were albinos then there wouldn't be any albinos among the whites.

How could the melanin be more missing in a group where it's already missing?

But there are white albinos- so we know that the starting premise of this thread is wrong.

(the situation is analogous to the demise of the "mongolism"explanation of Down's syndrome when it was discovered that you could find black skinned people with Downs)

Might as well close the thread- it's not going to achieve much.

with this post you just proved you have zero knowledge about genetics and biochemistry.

 

albinism has four stages, you better read about the basics of albinism before discrediting yourself by hillarious statements.

 

scientist prove that oca2 is the root of being white. second stage albinism.

Why would nature select for the genes that lead to malformed red blood cells in people from tropical/equatorial regions when it leads to higher rates genetic disease like sickle cell anemia?

 

The answer is that it also confirms a resistance to malaria, which is a major concern in those regions and ultimately winds up being a far deadlier killer than the genetic disease that comes along as a side effect of the resistance, at least if you live in a malaria-prone area. Move away and that advantage suddenly becomes a bigger problem than the one it is solving.

 

You keep saying that the pale skin is the result of an albinism-associated mutation "rather than" an adaptation, and that it comes with lots of health problems instead of some environmental advantage.

 

But that latter bit actually seems to imply that it does, or at least did, hold some adaptational advantage that offsets the associated problems. Traits generally don't spread and become fixed in a population if they are deleterious, especially not very large populations. Either they confirm some advantage (which may also come with some disadvantages that the advantage simply offsets, as in the case with sickle cell) or they are basically neutral and just random walked their way into the wider population without being good or bad in terms of survival.

 

Either way, nothing is ever a mutation "rather than" an adaptation, and something that is an adaptation in one environment or population may also be considered a disease in another environment or population, but the fact that something is a mutation doesn't "prove" that it's one or the other. All genetic diseases are the result of mutations and all environmental adaptations are the result of mutations.

 

oh dear, you just have to understand that deterious traits survived in europe due to isolation of albinos in northern europe. if two albinos procreate they cannot produce anything else than another albino, if they do it in isolation then of course you can get a large population when isolated in northern darkness, where the sun is not able to harm you so much as in other places on earth(but still scandinavia is number one in skin cancer statistics despite low uv).. of course after several tribes such as arabs, turks, mongols invaded whites got admixture of melanin hence come the different eye, hair colors..

 

by the way whites are not "very large population" we are merely 8% of all humanity, over 90% are melanated..

 

ps. albinos have same traits in every race namely blonde/red hair and blue eyes. but in other races albinos were segregated and outbred by melanin dominant individuals whereas in icy north they bred between themselves exclusively therefore it was possible for them to breed in large numbers, tacticus wrote that germanic folks never bread with foreign tribes and kept racial segregation. here you have the explanation why they could breed in such large numbers despite of their oca2.

Edited April 23, 2016 by wissen85

[andrewcellini]

albinism has four stages

citation needed.

 

And before you rail against me please note I am not an expert; I can't find this information. According to the wiki there are two types, one which affects hair, skin and eyes pigmentation and the other just the eyes (oculocutaneous and ocular respectively).

 

https://en.wikipedia.org/wiki/Albinism

 

Edit: Did find this though http://ojrd.biomedcentral.com/articles/10.1186/1750-1172-2-43

 

Is the locus (or loci) for the mutation(s) that leads to OCA albinism actually the same as that which produced european whites though? I'm having trouble finding the answer to this. Perhaps you can lead me in the right direction.

Edited April 23, 2016 by andrewcellini

[John Cuthber]

with this post you just proved you have zero knowledge about genetics and biochemistry.

 

albinism has four stages, you better read about the basics of albinism before discrediting yourself by hillarious statements.

 

It's not an issue of genetics at this point, it's one of logic.

It doesn't matter how many flavours of albinism there are- as long as they are all found in whites.

As far as I can tell, they are.

[Delta1212]

with this post you just proved you have zero knowledge about genetics and biochemistry.

 

albinism has four stages, you better read about the basics of albinism before discrediting yourself by hillarious statements.

 

scientist prove that oca2 is the root of being white. second stage albinism.

 

 

oh dear, you just have to understand that deterious traits survived in europe due to isolation of albinos in northern europe. if two albinos procreate they cannot produce anything else than another albino, if they do it in isolation then of course you can get a large population when isolated in northern darkness, where the sun is not able to harm you so much as in other places on earth(but still scandinavia is number one in skin cancer statistics despite low uv).. of course after several tribes such as arabs, turks, mongols invaded whites got admixture of melanin hence come the different eye, hair colors..

 

by the way whites are not "very large population" we are merely 8% of all humanity, over 90% are melanated..

 

ps. albinos have same traits in every race namely blonde/red hair and blue eyes. but in other races albinos were segregated and outbred by melanin dominant individuals whereas in icy north they bred between themselves exclusively therefore it was possible for them to breed in large numbers, tacticus wrote that germanic folks never bread with foreign tribes and kept racial segregation. here you have the explanation why they could breed in such large numbers despite of their oca2.

First off, 8% of humanity is over half a billion individuals. That's a huge population.

 

Secondly, if you're claiming that it's the result of founder effect derived from an initial population made up entirely of albinos, you're positing a rather major population bottle neck. The generally accepted number for a minimum viable breeding population is in the neighborhood of 500 individuals of moderately diverse genetics. I'm not sure where you're getting 500+ mostly unrelated albinos as a starting population with no or very few "melanin rich" individuals mixed in. That's not nearly a common enough mutation for that situation to arise randomly.

 

Which brings us back to the possibility that it provided some kind of selective advantage that allowed the mutation to spread throughout the population.

[wissen85]

 

Which brings us back to the possibility that it provided some kind of selective advantage that allowed the mutation to spread throughout the population.

which according to you would be?

 

if we leave out the absurd "white skin is adapted to cold" theory what else is left?

 

regarding the numbers you must consider that hardly 3% of those classified as white are blonde or red haired, majority of them are dark haired who mixed with moors, turks, arabs and asians during history. also you underestimate the fact that isolation provides a breeding ground for albinism especially the dark cold north where they can survive by hiding from the sun which makes it easy to breed in higher numbers. a life form whether healthy or albino needs only enough resources and absence of natural predators to be able to multiply, if they are provided they can easily spread in large numbers in isolation(see example of various bacteria). whites especially northerners and islanders in britain, ireland and iceland had enough isolation and resources to be able to multiply regardless of being albino. still majority of humans are melanated and not white. whites always have been minority.

It's not an issue of genetics at this point, it's one of logic.

It doesn't matter how many flavours of albinism there are- as long as they are all found in whites.

As far as I can tell, they are.

white people per se are OCA2 albinos. but of course you will also find OCA1, OCA3 and OCA4 types among whites..

 

 

Albinism affects the color of the skin, the color of the hair and the color of the eyes and it can affect the texture of the hair.

 

What this means is that there are people/Whites who are still albino WITH pigmentation. This is OCA2.

 

ANY LOSS OF PIGMENTATION IS ALBINISM. Albinism can also cause straightening of the hair

 

Good, now we've got that out of the way.

 

There are 4 types of Albinism. Each type affects the pigmentation of the hair, skin and eye color.

 

This information is NOT hard to find. I got this from the NATIONAL INSTITUTE of HEALTH: AKA NIH

 

Here is the link, it was done in 2004, it has NOW been found that the mutation of the alanine allele (SCL24A5-) accounts for the THR111 gene found in Whites and THIS IS WHY they are more genetically related to Asians.

 

Oculocutaneous albinism - Genetics Home Reference

 

 

THR111 Alleles

http://paspcr.med.umn.edu/Commentary...commentary.pdf

Allelic Variations of SLC24A5

 

There are many genes that affect skin pigmentation, what it doesn't take away is the fact that ANY LOSS IN PIGMENTATION IN THE HAIR, EYES AND SKIN, no matter how minute is in fact ALBINISM.

 

It's not meant to be mean, it's just a fact. I always though there was just one type!

 

 

Oculocutaneous Albinism Type 1

 

Disease characteristics. Oculocutaneous albinism type 1 (OCA1) is characterized by reduced synthesis of melanin in the skin, hair, and eyes, associated with ocular findings of nystagmus, reduced iris pigment with iris translucency, reduced retinal pigment, foveal hypoplasia with significantly reduced visual acuity usually in the range of 20/100 to 20/400, and misrouting of the optic nerves resulting in alternating strabismus and reduced stereoscopic vision. Individuals with OCA1A have white hair, white skin that does not tan, and fully translucent irises that do not darken with age. At birth, individuals with OCA1B have white or very light yellow hair that darkens with age, white skin that over time develops some generalized pigment and may tan with sun exposure, and blue irises that change to green/hazel or brown/tan with age. Visual acuity may be 20/60 or better in some individuals.

 

 

Oculocutaneous albinism, type 2

 

Tyrosinase-positive oculocutaneous albinism (OCA, type II) is an autosomal recessive disorder in which the biosynthesis of melanin pigment is reduced in skin, hair, and eyes. Although affected infants may appear at birth to have OCA type I, or complete absence of melanin pigment, most patients with OCA type II acquire small amounts of pigment with age. Individuals with OCA type II have the characteristic visual anomalies associated with albinism, including decreased acuity and nystagmus, which are usually less severe than in OCA type I. OCA type II is the most common type of oculocutaneous albinism in the world.

 

The gene OCA2, when in a variant form, the gene causes the pink eye color and hypopigmentation common in human albinism. Different SNPs within OCA2 are strongly associated with blue and green eyes. Hair color is the pigmentation of hair follicles due to two types of melanin, eumelanin and pheomelanin. Generally, if more melanin is present, the color of the hair is darker; if less melanin is present, the hair is lighter. Blond hair can have almost any proportion of phaeomelanin and eumelanin, but both only in small amounts. More phaeomelanin creates a more golden blond color, and more eumelanin creates an ash blond. Blond hair is common in many European peoples, but rare among peoples of non-European origin. Many children born with blond hair develop darker hair as they age. Red hair ranges from vivid strawberry shades to deep auburn and burgundy, and is the rarest fully distinct hair color on earth. It is caused by a variation in the Mc1r gene and believed to be recessive. Red hair has the highest amounts of phaeomelanin and usually low levels of eumelanin, and is the rarest natural human hair color.

 

Oculocutaneous albinism, type 3

 

Oculocutaneous albinism, type 3: A rare inherited disorder characterized by slightly reduced pigmentation in the skin, eyes and hair (due to a genetic mutation of the TYRP1 gene). Type 3 is characterized by some pigmentation of the iris despite the complete absence of tyrosinase which is needed for the production of melanin which gives the skin, hair and eyes their color. Those with OCA3 may have, Reddish-brown skin, Ginger hair, Red hair, Hazel iris, Brown iris. Type 3 also has the milder eye problems than the other types.

 

Light-skinned Whites with tyrosinase-negative albinism have pale skin and hair color ranging from white to yellow; their pupils appear red because of translucent irides. Blacks with the same disorder have hair that may be white, faintly tinged with yellow, or yellow-brown. Both Whites and Blacks with tyrosinase-positive albinism grow darker as they age. For instance, their hair may become straw-colored or light brown and their skin cream-colored or pink. People with tyrosinase-positive albinism may also have freckles and pigmented nevi that may require excision.

 

This form of albinism was referred to as 'rufous oculocutaneous albinism (ROCA)' when it was found in southern African blacks. In blacks the disorder is characterized by bright copper-red coloration of the skin and hair and dilution of the color of the iris. Manga et al. (1997) suggested that albinism caused by mutation in the TYRP1 gene should be referred to as OCA3

 

In New York City rather numerous cases are seen in Puerto Rican families from the Aguadilla-Arecibo area of northwestern Puerto Rico. Albinism in dark-skinned persons such as Puerto Ricans is not always obvious because freckled skin and reddish hair may be present. Red reflex on transillumination of the iris and nystagmus are important clues to the diagnosis.

 

In tyrosinase-variable albinism, at birth the child's hair is white, his skin is pink, and his eyes are gray. As he grows older, though, his hair becomes yellow, his irides may become darker, and his skin may even tan slightly. The skin of a person with albinism is easily damaged by the sun. It may look weather-beaten and is highly susceptible to precancerous and cancerous growths. The patient may also have photophobia, myopia, strabismus, and congenital horizontal nystagmus.

 

 

Oculocutaneous Albinism, Type 4

 

Disease characteristics. Oculocutaneous albinism type 4 (OCA4) is characterized by hypopigmentation of the skin and hair plus the characteristic ocular changes found in all other types of albinism, including nystagmus; reduced iris pigment with iris translucency; reduced retinal pigment with visualization of the choroidal blood vessels on ophthalmoscopic examination; foveal hypoplasia associated with reduction in visual acuity; and misrouting of the optic nerves at the chiasm associated with alternating strabismus, reduced stereoscopic vision, and an altered visual evoked potential (VEP). Individuals with OCA4 are usually recognized within the first year of life because of hypopigmentation of the hair and skin and the ocular features of nystagmus and strabismus. Vision is likely to be stable after early childhood. The amount of cutaneous pigmentation in OCA4 ranges from minimal to near normal. Newborns with OCA4 usually have some pigment in their hair, with color ranging from silvery white to light yellow. Hair color may darken with time, but does not vary significantly from childhood to adulthood. This form of albinism is rarer than OCA2, except in the Japanese population.

 

 

22. Squamous-cell carcinoma in situ in a patient with oculocutaneous albinism

 

Now, of course Whites are more genetically related to asians. But they they share a common ancestor. the Indian Dravidians that became you guessed it, ALBINO and that is a genetic mutation causing a difference in the allele genes. Over time they became a sub-species of the originals, all of whom were of African origin.

 

Back to topic:

 

 

Here is Whites' theory:

 

The original Black settlers of Europe TURNED WHITE because they became FARMERS, who ate only farm produce devoid of Vitamin D. And, the lessened solar duration and intensity in the Northern regions REQUIRED a Whitening of the skin for faster absorption of UV radiation and production of Vitamin D. So then, White skin absorbs Sunlight FASTER? Let's see.

 

1) Modern Whites in Europe are Germanics, Slavs, and Celts. They have nothing to do with ancient ANYBODY in Europe. They are migrants from Central Asia in the CURRENT era. Any encyclopedia will document their entry into Europe.

 

2) These Whites in Central Asia were Nomads - NOT FARMERS! Their diet was rich in Meats and FISH! Plus they had plenty of Sunshine - in Kazakhstan-south, for eight months of the year, the average UV intensity is level 8 out of a maximum 11. Thus there was no reason to turn White there!

 

3) Whites did NOT bring agriculture to Europe, Blacks and Arabs from the South did, and they did NOT turn White.

 

4) European Whites in the early current era were NOT farmers - Farming is very RECENT to European Whites!.

 

5) The Whitest of the Whites in Europe - the Anglosaxons and Irish, inhabited Costal WESTERN Europe and Scotland - regions rich in fish and game animals - ancient Germany and modern Germany are different areas.

 

The Roman historian Cornelius Tacitus (56-118 A.D.) said this about them: For my own part, I agree with those who think that the tribes of Germany are free from all taint of intermarriages with foreign nations, and that they appear as a distinct, unmixed race, like none but themselves. Hence, too, the same physical peculiarities throughout so vast a population. All have fierce blue eyes, red hair, huge frames, fit only for a sudden exertion. They are less able to bear laborious work. Heat and thirst they cannot in the least endure; to cold and hunger their climate and their soil inure them. Does THAT sound like FARMERS?

 

 

 

Moving along, let's examine some other things huh?

 

6) A Human being requires ONLY 15 minutes of Sunshine, on face or hands, TWICE a week, for good health! Thus no reason for Black people to turn White.

 

But for the sake of argument, lets accept this bit of White myth, that Blacks TURNED White because of Vitamin D deficiency - Lets test it. Think of the absurdity of this: Black humans survived in Europe for about 35,000 years, then all of a sudden, their bodies were not getting enough vitamin "D": forcing them to lighten their skin. The problem is: logically, BEFORE there could be any evolutionary movement toward lighter skin - the population would have DIED OUT from Rickets! This supports Albinism, but there were Blacks

 

Rickets

 

Rickets is a softening of bones in children due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium, potentially leading to fractures and deformity. The Roman physician Soranus reported deformation of the bones in infants as early as the first and second centuries AD. He attributed these deformities as resulting from the failure of Roman mothers to properly nurture and clean their children, but didn't directly implicate poor diet in the condition. Rickets wasn't defined as a specific medical condition until 1645, when an Englishman named Daniel Whistler gave the earliest known description of the disease while still studying medicine.

 

Rickets was very common in industrialized cities around the turn of the twentieth century, both in the United States and in Europe. It was most common among the poorer, less privileged people and often affected infants. Still, there was not a complete understanding that the condition was caused by poor nutrition, although it was considered a potential cause, along with lack of fresh air and sunshine. In the late nineteenth century, strides had been made toward finding a cure for rickets. At the London Zoo in 1889, lion cubs were fed a diet of boneless lean meat. When some cubs developed florid rickets, they were treated by the addition of cod liver oil and crushed bones to their meals, and made a full recovery.

 

What causes rickets? Regardless of the type of rickets, the cause is always either due to a deficiency of vitamin D, calcium, or phosphate. Three common causes of rickets include nutritional rickets, hypophosphatemic rickets, and renal rickets.

 

So to carry the absurdity to its logical conclusion: supposing that these Black people turning White, survived thousands of years of Rickets - in a non-deformed state, and then appeared as modern Whites. Then why would MODERN Whites STILL get Rickets? Wasn't the whole point of evolution to develop White skin, just for the "SUPPOSED" reason that Sunlight could be quickly and efficiently absorbed by the White skin, just to AVOID such things? You would have built up the resistance to sustain Rickets. Albinism is the stabilized norm for White skin, but there are variations of Albinism and not all lost total pigmentation.

 

 

Additionally, Whites don't do well in either climate hot or cold.

 

Snowburned and Sunburned Whites disprove the myth that we are adapted to either cold or hot environment, as i said all arctic animals have melanin be it polar bear, seal or arctic fox! also inuit and eskimos who live in coldest climate one earth have brown skin..

 

Edited April 23, 2016 by wissen85

[John Cuthber]

 

 

white people per se are OCA2 albinos. but of course you will also find OCA1, OCA3 and OCA4 types among whites..

 

And you get people who are white with OCA2 defects.

https://en.wikipedia.org/wiki/Angelman_syndrome

https://en.wikipedia.org/wiki/Prader%E2%80%93Willi_syndrome

But according to your idea that's impossible.

What you are saying that that these people have symptoms due to a defect in a gene they don't have.

 

Incidentally, please don't waste time on wall of text replies citing ancient Romans or a shed full of pictures of dogs.

 

You need to address the actual point.

 

How can white people have problems caused by a defect in a gene that you say they don't possess in the first place?

[swansont]

by the way whites are not "very large population" we are merely 8% of all humanity, over 90% are melanated..

 

 

Even if this is true, the percentage dropping this low is a recent development, from the trend of developed nations having low birthrates and extending medical advances to lesser-developed countries, reducing their mortality rates. In 1950, whites comprised 28% of the population. Your statistic is meaningless in the context of the discussion.

 

http://www.vdare.com/articles/whites-down-to-10-of-world-population-by-2060-does-it-matter

[wissen85]

 

 

Even if this is true, the percentage dropping this low is a recent development, from the trend of developed nations having low birthrates and extending medical advances to lesser-developed countries, reducing their mortality rates. In 1950, whites comprised 28% of the population. Your statistic is meaningless in the context of the discussion.

 

http://www.vdare.com/articles/whites-down-to-10-of-world-population-by-2060-does-it-matter

in my opinion the calssification of whites is extended to latinos, turks and other mixed population which artificially pushes the number of whites as a whole. when you consider the number of unmixed whites(real blondes and red haired) then the numbers are very low. blondes and red haired make hardly 4% of world population.. i am realistic

And you get people who are white with OCA2 defects.

https://en.wikipedia.org/wiki/Angelman_syndrome

https://en.wikipedia.org/wiki/Prader%E2%80%93Willi_syndrome

But according to your idea that's impossible.

What you are saying that that these people have symptoms due to a defect in a gene they don't have.

 

Incidentally, please don't waste time on wall of text replies citing ancient Romans or a shed full of pictures of dogs.

 

You need to address the actual point.

 

How can white people have problems caused by a defect in a gene that you say they don't possess in the first place?

you would not ask the same question over again if you have had read the post above explaining the various stages of albinism.

 

blonde/red hair and blue eyes = OCA2 = scientific evidence

 

type 2 Albinism, or (OCA2 or P type Albinism) results in a defect in the P protein, which helps tyrosinase function. As a result, tyrosinase cannot produce sufficient amounts of melanin resulting in the characteristics of albinism. OCA2 is not as severe as OCA1. People with OCA2 usually have from very light blonde to brown hair and blue eyes

 

albinism can result in various stages and symptoms. therefore you see white people with red hair, blonde hair, blue eyes, green eyes, freckles, heterochromia, waardenburg syndrome etc.

Edited April 25, 2016 by wissen85

[swansont]

in my opinion the calssification of whites is extended to latinos, turks and other mixed population which artificially pushes the number of whites as a whole. when you consider the number of unmixed whites(real blondes and red haired) then the numbers are very low. blondes and red haired make hardly 4% of world population.. i am realistic

 

 

You're also asserting this without any substantiating evidence, and beside that it's irrelevant. The fraction of the population today has little to do with a mutation that affixed itself in a portion of humans thousands of years ago.

[Arete]

blonde/red hair and blue eyes = OCA2 = scientific evidence

 

So, you're asserting that mutation in OCA2 which confers a pale skinned phenotype, introgressed from India to Europe at some point, and subsequently became fixed?

 

This explanation contains a series of testable predictions.

 

1) A diagnostic mutation/s in OCA2 is fixed in Caucasian populations.

2) This mutation/s confers the pale phenotype characteristic of Caucasian populations.

3) This mutation/s introgressed from Indian populations during (X) time.

4) The mutation/s swept to fixation since introgression.

 

To test these, you would use the following methods:

1) Compare a sample of Caucasian OCA2 sequences to other human populations to determine the diagnostic polymorphisms. There's around ~50,000 OCA2 sequences on genbank, so this should be fairly straightforward.

2) This will be tricky without a model (e.g. a knockout line of mice) However, a first step would be to determine that the mutation/s detected in 1) are non-synonymous.

3) A coalescent model like IMa2 can be used to estimate migration rates and effective population sizes, allowing you to determine if introgression during the proposed time period is plausible.

4) A Dn/Ds calculation will allow you to determine the selection coefficient for any mutation/s you determine in 1), then a Brownian model like FPG can be used to determine the probability of fixation for the timing of introgression identified in 3), given the Ne estimate from 3) and the selection coefficient.

 

Then you will have an empirical test of your hypothesis. Even better, all the software and data I've mentioned are open source, so there's nothing stopping you conducting the analyses.

 

Some speculation, however:

A) Given historical admixture between human populations, I would predict that the chances of finding a diagnostic mutation in OCA2 are pretty slim, doubly so now you've included Hispanic population in your hypothesis.

B) Demonstrating functionality will be a problem - the evidence from the suggested analysis would be correlative and certainly not definitive.

C) Based on other evidence I would predict widespread introgression between Europe and India, so I doubt this would prove troublesome to demonstrate.

D) I believe that proving fixation is plausible in a reasonable time frame will be the death blow to your hypothesis. Human populations have very large Ne values (e.g 4% of the global population is almost 300 million individuals). Large Ne values, which necessitate very long fixation times even for genes with strongly positive selection coefficients.

 

Good luck.

 

Edit:

you would not ask the same question over again if you have had read the post above explaining the various stages of albinism.

 

Is there a reference you can provide for this? There a multiple diseases with convergent symptoms described under general term "albinism", however, I can't find any reference to any diagnostic "stages" of albinism.

Edited April 25, 2016 by Arete

[John Cuthber]

in my opinion the calssification of whites is extended to latinos, turks and other mixed population which artificially pushes the number of whites as a whole. when you consider the number of unmixed whites(real blondes and red haired) then the numbers are very low. blondes and red haired make hardly 4% of world population.. i am realistic

you would not ask the same question over again if you have had read the post above explaining the various stages of albinism.

 

blonde/red hair and blue eyes = OCA2 = scientific evidence

 

type 2 Albinism, or (OCA2 or P type Albinism) results in a defect in the P protein, which helps tyrosinase function. As a result, tyrosinase cannot produce sufficient amounts of melanin resulting in the characteristics of albinism. OCA2 is not as severe as OCA1. People with OCA2 usually have from very light blonde to brown hair and blue eyes

 

albinism can result in various stages and symptoms. therefore you see white people with red hair, blonde hair, blue eyes, green eyes, freckles, heterochromia, waardenburg syndrome etc.

OK, lets just check on something.

By any conventional definition, I'm white. My ancestors are, at least for a few generations, almost entirely Scottish. (and, as it happens, my parents married in South Africa so a stupid legal system that was snotty about such things "declares" that I'm white).

So, according to you I am an albino.

 

However

I have brown eyes and dark brown hair; I tan if I go out in the sun.

So, according to any conventional definition, I am not an albino.

 

So, you are- at least by conventional use of the word "albino", wrong.

 

Are you saying that everyone else doesn't know what the word means?

Edited April 25, 2016 by John Cuthber

[wissen85]

 

The most common type of albinism, 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.[6] 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. https://en.wikipedia.org/wiki/Oculocutaneous_albinism

Edited April 25, 2016 by wissen85

[Strange]

That completely contradicts your claims.

 

1. "Overall, an estimated 1 in 20,000 people worldwide are born with oculocutaneous albinism"

 

Last time I looked 1/20,000 is a lot less than 4%

 

2. "People with OCA2 ... cannot tan"

 

All the white people I know can tan.

[wissen85]

here is a picture of a girl who has OCA2 with her sister who has OCA1..

 

http://i.imgur.com/iks6R.jpg?1

[Strange]

here is a picture of a girl who has OCA2 with her sister who has OCA1..

 

Stop doing that. It is idiotic. Please provide some peer reviewed evidence that supports your claims.

[Arete]

here is a picture of a girl who has OCA2 with her sister who has OCA1..

 

http://i.imgur.com/iks6R.jpg?1

 

OCA1 is a disease associated with mutations in the GPR143 gene, OCA 2 is a distinct form of albinism associated with mutations in the OCA2 gene.

 

There are no "stages" of Oculocutaneous albinism, there are multiple types with distinct, independent genetic causes.

Edited April 25, 2016 by Arete

[wissen85]

That completely contradicts your claims.

 

1. "Overall, an estimated 1 in 20,000 people worldwide are born with oculocutaneous albinism"

 

Last time I looked 1/20,000 is a lot less than 4%

 

2. "People with OCA2 ... cannot tan"

 

All the white people I know can tan.

not true. people with oca2 have some pheomelanin present thus are able to tan. whereas people with oca1 do not.