Agreed "the food made them white" is BS ala KIK et al.
But you still have to prove Melanin "is just sunscreen." and totally debunk the MT.
You agree with MK that vit D has little or nothing to do with skin hue. But MK has taken it a step further by citing work that demonstrates Melanin is a lot more important in human physiology and without it there are grave side-effects eg compromised human immune system, PD etc.
You dis-agree on: Albinism and Europeans white skin are the same.
quote:Originally posted by michael1010: [QUOTE]Originally posted by the lion: [qb] Also the theory is weakened by the new evidence that Europeans just began turning White max. 12,000 years ago-- *****long after the arrival of the first Africans, which would have all died of Rickets, if we were to give too much weight to that theory.****
You sneaky instigating mofo, I explained this sh*t to you a hundred times.
* The only way the immune system is compromised due to lack of melanin is due to damage of the DNA caused by what? UVA mofo, this **** was debunked on the first page. Read mofo. How can a pale person prevent this sh*t from happening---wear a whole lotta fuggin SUNSCREEN.
When the UVA damage the cells a lot of sh*t goes down, this is not the basis of the Melanin Theorist, I told ur ass this. Their position is that Europeans are albinos, and people with melanin can send each other telepathic messages, lol. Ask them mofos, why they can't predict what I'm gonna type before I type it, lol.
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I said many times we have to use ALL disciplines to get to the truth. We all know we cannot rely on conventional media to tell the truth. So we must use genetics, anthropology, archeology, linguistics AND OUR logic to understand what really went down in the past.
We as black people are unbiased, in most part, and therefore are more logical and will ALWAYS win in many of these debates. The whites in charge have the need to maintain the current status quo.
That said. What you have shown me are pictures of white skinned people. With respect, I am not sure of the significance. Are they supposed to be the same? Are you saying White Euros, African, East Asian and other Albinos ethnic groups are the same?
No! Why?. The available genetic evidence says so. As I understand it. MK may dis-agree. But more importantly each Albino of the different ethnic group (or race as you put it)looks like they belong to that race except for the skin and hair color. In summary ONLY skin color makes them "look" similar.
Using your MO one will conclude that narrow nose, straight hair and thin lips people should all be grouped together and be called . . . .Caucausians!!!!!!
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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This is the premise of RAA/Gigantic/Haitian/ and his elk.
All people with narrow nose, straight hair, thin lips should be called Cacausians. Irregardless to what modern science says, despite the genetic data, despite what the linguist says, despite what the anthroplogist says.
These guys are from the last century. And they are desperately trying to hold on to that belief.
An analogy is : all dogs that have long tale, long face and long legs are of the same group. It doesn't matter if it is a Chiwawa(?) or German Shepherd or Poodle. Three completely different line of dogs. But they are the same. stupid fighks!
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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Sneaky? HA! do want me to list the "confirmed" uses of Melanin.
You know I am not into the telepathic blacks thing. But who knows(shrug).
We are still waiting on you debunking the MANY other uses of melanin.
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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I recall on another thread asking this very question, could the original people (Blacks) carry both allele, DNA, genes, germs, etc?
However, you posted this, which science seems to be answering.
[Q}Similarly, the presence of the derived allele (albeit at low frequencies) in some sub-Saharan African populations may be due to recent gene flow from European and Central Asian populations. Alternatively, the derived allele may have existed in the ancestral human population and was lost in the ancestors of modern East Asians but retained in the ancestral European population. The allele then rose to high frequency in Europeans following the divergence of European and East Asian ancestral groups.
I wonder why it would be at a low frequency. Could it be due to the fact that it is "recessive=weak" Also notice the key words "MAY HAVE BEEN" sounds like there is a possibility.
However, this is quite interesting:
[I]The pigmentation of our skin, which is Black tending to Brown, lies deep within the science of our beginnings. The two germs, Black and Brown, were lying dormant within the original Black man, which under the right conditions produces all the other colors or races that we have in the world today.
another excerpt from the same article
He discovered in the science lab that there were in these two germs, Black and Brown, a distinct characteristic within the Brown germ that he could use to separate from the Black germ to produce other races and colors. This is somewhat like the Biblical story of Rebekah, as we read in Genesis, who struggled with twins inside her womb, the younger one struggling for dominance over the elder one. Thus, Yakub (Jacob)in his study of genetics and biology set up a law of birth control while separating the two germs.[I]
So it appears that science is baring witness to what the NOI teaches. That genetic engineering/ selective mating is what caused skin to whiten and become fixed, with the exception of dominant genetic material/DNA being [re]introduced to correct and add melanin back into the weaken recessive/albino gene pool.
Simple law, called Mendels Law: 2-Black/brown can make white and anything in between, and you best believe that you can get color from black and white; but you can't get black or any other color from 2 white.
Posts: 35 | From: ATL | Registered: Jan 2010
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quote:Originally posted by michael1010: Just because the gene for dark skin is named *derived* allele doesn't mean the original humans didn't carry this gene.
No, dipshit, the gene for darkskin is ancestral not derived. To determine whether a SNP is ancestral or derived is based on which allele is found in other primate species--usually chimpanzee. In this case chimpanzees, orangutans, and macaques all carry the G allele at this site--the A allele has not been observed in these species, hence for rs1800404, the G allele is considered ancestral while the alternative, the "A" is derived.
quote:Originally posted by michael1010: Cuz I know damn well the San are not light because they're mixed with Europeans, so the latter is the only explanation fool.
No dipshit this is your misunderstanding, there different derived alleles, this is why dumb ass nitwits like you should just sit back and listen the San carry an allele at a particular SNP in the OCA2 gene (rs1800404) which was most often found in the derived state--that is, most individuals carried one or two "A" alleles as opposed to the "G" allele which predominated in the other African populations survey.
Europeans carry the *derived alleles* at TYR, 192*A, MATP 374*G and SLC24A5 111*A.
P.s. I just knew you'd confuse the derived alleles and think what it was saying was that the San are light because of Europeans. SMH.
quote: "The lightly pigmented hunter-gatherer San populations of Southern Africa is exceptional in having a high frequency of the derived allele relative to geographically proximate and more darkly pigmented African populations (Jablonski and Chaplin 2000), further supporting the importance of OCA2 in regulating normal variation in pigmentation. The widespread distribution of the derived allele in the CEPH-Diversity Panel suggests that it is not necessarily a new mutation, nor has it been restricted to a specific geographic area. - Norton, Kittles et al."
quote:Polymorphisms in 2 genes, ASIP and OCA2, may play a shared role in shaping light and dark pigmentation across the globe , whereas SLC24A5, MATP, and TYR have a predominant role in the evolution of light skin in Europeans but not in East Asians. These findings support a case for the recent convergent evolution of a lighter pigmentation phenotype in Europeans and East Asians.
Now again, take your foot out of your mouth.
Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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It is claimed the father is "black" yet the father is not included in the photo. It is assumed that the mother is black but she may be 1/4 to 1/3 white. There is no data to support this picture. My guess on it is that the father was white and the reporters took her word for it that he was black because it made a good story. You can't build a case from one woman in Brazil. Why aren't the afrocentrics running down there to find the father?
It's foolishness and a form of lying.
Two black people with kinky hair cannot produce a child with straight hair. There are thousands of albinos in Africa. None of the Mulattoes that have kinky haired parents have straight hair. That disproves the theory right there.
Who are the contemporary Eritreans, Djibuti, Somalians,or Sudanese? It is debated by anthropologists. Regardless are they producing albinos that are both blond and have straight hair? No they are not. Look at the Chinese for instance. There are no Africans on the whole continent that have that type of very straight hair. Where are the tribes? Likewise many Caucasians have similar hair but not always black. Other times wavy or curly. Most black people in America have no North African ancestry. You mad now? It just shows you have a European like disregard for the culture of the rest of the continent. Africans don't have this problem
Posts: 42921 | From: , | Registered: Jan 2010
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Even if the father was "white" the children should still have pigmentation, due to the mother having pigmentation or dominate genes; they should look like what is deemed a "mulatto". They are Albino because both parents carry the albino (recessive) gene....meaning that people of color can carry that gene also, and without having it be reflected in their physical makeup.
quote:Originally posted by Original_Womb/man: ^^^^Lion,
Even if the father was "white" the children should still have pigmentation, due to the mother having pigmentation or dominate genes; they should look like what is deemed a "mulatto". They are Albino because both parents carry the albino (recessive) gene....meaning that people of color can carry that gene also, and without having it be reflected in their physical makeup.
Geeeezzzz!!!
you missed the point. In regard to hair two black people with kinky hair cannot produce a child with straight hair. And that particular type of very straight hair does not exist in Africa. Bushy straight coarse hair is not the same.
Posts: 42921 | From: , | Registered: Jan 2010
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quote:Originally posted by Original_Womb/man: ^^^^Lion,
Even if the father was "white" the children should still have pigmentation, due to the mother having pigmentation or dominate genes; they should look like what is deemed a "mulatto". They are Albino because both parents carry the albino (recessive) gene....meaning that people of color can carry that gene also, and without having it be reflected in their physical makeup.
Geeeezzzz!!!
you missed the point. In regard to hair two black people with kinky hair cannot produce a child with straight hair. And that particular type of very straight hair does not exist in Africa. Bushy straight coarse hair is not the same.
Dear,
You are putting to much emphasis on hair and what is deemed Negro characteristic. As it has been pointed out time and time again...Blacks/people of color via Africans or B.K.A Asiatic Black Man/woman has the highest level of diversity found in the world. That in itself should enlightened anyone questioning the different characteristics of past and modern human diversity; i.e., we did not evolve from apes/monkeys because they still exist. The question we should ask is, since apes/monkeys genetics are 99% identical to ours, did humans create apes/monkeys via bestiality? Maybe that is why it is a crime in most states.
I believe Mike has already broken down that most whites are the result of Black Asians/Indians. It has been said that the earlier Irish had nappy hair, same with Italians, Island Pacific, and Greeks, etc.
Hair can change due to diet/vitamins/minerals and environment. I know many parents who have nappy, kinky hair; however, due to diet and environment, their children's hair is totally different.
The Australian Aborigines are a perfect example of Negroid facial and body type, but straight hair.
Posts: 35 | From: ATL | Registered: Jan 2010
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quote:Originally posted by Mike111: All together now.
Damn, she's stupid!
Mike,
Brother, try to be nice. It is not her fault she has not been raised into consciousness yet; however, it is the duty of those who have to teach without insult.
It is hard accepting knowledge & wisdom that has not been propagated by the mainstream.
Posts: 35 | From: ATL | Registered: Jan 2010
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^True, but she is so forceful and persistent with her stupidity. Even a moments pause and reflection would have been cause for patience, but it never materialized.
Posts: 22721 | Registered: Oct 2005
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I think many here are just damn mentally lazy. With a topic as exciting as melanin, yet many here have not begun to research or ingest even the surface level information on the subject.
Mike & Clyde, check out Dr. Jewel Pookrum, an authority on Melanin and brain stimulation techniques. She calls herself an, immortal. Her theory is that melanin can rejuvenate the body IF we extract ourselves out of the sphere of white thought, which is detrimental to blacks.
quote:Originally posted by the lion: fakehsitory.com
This is a picture used by people to lie.
It is claimed the father is "black" yet the father is not included in the photo. It is assumed that the mother is black but she may be 1/4 to 1/3 white. There is no data to support this picture. My guess on it is that the father was white and the reporters took her word for it that he was black because it made a good story. You can't build a case from one woman in Brazil. Why aren't the afrocentrics running down there to find the father?
It's foolishness and a form of lying.
Two black people with kinky hair cannot produce a child with straight hair. There are thousands of albinos in Africa. None of the Mulattoes that have kinky haired parents have straight hair. That disproves the theory right there.
Who are the contemporary Eritreans, Djibuti, Somalians,or Sudanese? It is debated by anthropologists. Regardless are they producing albinos that are both blond and have straight hair? No they are not. Look at the Chinese for instance. There are no Africans on the whole continent that have that type of very straight hair. Where are the tribes? Likewise many Caucasians have similar hair but not always black. Other times wavy or curly. Most black people in America have no North African ancestry. You mad now? It just shows you have a European like disregard for the culture of the rest of the continent. Africans don't have this problem
Mike is right. You are very stupid!
The Jewish genetic diseases described here are autosomal recessive disorders and they result from altered genes (mutations) that are located on autosomal chromosomes. For these diseases to occur, an abnormal (mutated) gene leading to the disorder must be inherited from each parent. Carriers for an autosomal recessive disorders are individuals who have in their genetic composition one normal gene and one mutated gene for that specific disorder. Carriers are themselves healthy individuals and have no symptoms or signs of the disease for which they are carriers. The main concern for carrier individuals is that they are at risk of passing mutated genes to their children:
If both parents are carriers for the same disorder, there is a 50% likelihood with each pregnancy that the child will be a carrier (like each parent) and a 25% likelihood with each pregnancy that the child will be affected with the disorder. There is a 25% likelihood with each pregnancy that the child will be neither affected with the disorder nor a carrier for the disorder
This albino lady's husband isn't show either, but he is black and as you see, his children are not OCA1 or 2, but surely carry the OCA defective gene. The children's complexion is exactly very close to that of President Obama, who himself is the product of a union between a white woman and black man. Same as above. Posts: 2403 | Registered: Feb 2010
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quote:Originally posted by michael1010: What these scientist are trying to determine is the evolution of light skin, whether it was due to mutation outside of Africa or mutation within Africa and then increased in frequency at higher latitudes, specifically Europeans.
Which was confirmed that it didn't mutate in Africa...
The virtual absence of MATP 374*G–derived allele in the sub-Saharan African populations that we examined in the CEPH-Diversity Panel is consistent with the origin of this mutation outside of Africa after the divergence of modern Asians and Europeans.
quote:Originally posted by michael1010: They were also trying to determine if Melanesians inherited the dark skin alles from Africans, or if a different mutation is responsible for their dark skin.
Which there wasn't (a new mutation), and this shared ancestral allele at its high frequencies proves darkskin is the ancestral state of modern humans.
In contrast, the **ancestral allele** associated with **dark pigmentation** has a shared high frequency in **sub- Saharan African and Island Melanesians**.
quote:Originally posted by michael1010: This helps them to determine, if a direct route to Southern Asia along the equator was taken, or if they traveled first to central Asia adapted to this environment, and then had to re-adapt to tropical environment.
What? The authors already know from other genetic work involving uni-parentals that humans traveled along southern Asia into Island Melanesia and Australia, hence why they were candidate these people genetically represent the oldest humans living outside of Africa, because their lineages are more pristine, I.e., underived.
The discordance between our Fst-based divergence values and allele frequencies in the Melanesian CEPH populations at ASIP largely stem from the relatively low frequency of the ancestral allele in the 2 CEPH Island Melanesian populations relative to our original Island Melanesian sample. These discrepancies make it difficult to determine if ASIP truly underlies broad pigmentation differences between darkly and lightly pigmented populations or instead inter-population variation at this locus can largely be explained by differences between Africans and non-Africans. The discordance between the frequencies of the ASIP ancestral allele in our original Island Melanesian sample and the Melanesian samples from the CEPH panel may be indicative of both the complex demographic history of Island Melanesia (involving several migratory events (Spriggs 1997) and probable extensive genetic drift (Friendlaender 1975, 1987) as well as the importance of multiple loci in determining pigmentation phenotype - Norton, Kittles et al.
quote:Originally posted by michael1010: Ok, now get your highlighter out, because this part is gonna fugg u up, specifically because it's coming from the EXACT SAME STUDY YOU PRODUCED, LOL.
Similarly, the presence of the derived allele (albeit at low frequencies) in some sub-Saharan African populations may be due to recent gene flow from European and Central Asian populations. Alternatively, the derived allele may have existed in the ancestral human population and was lost in the ancestors of modern East Asians but retained in the ancestral European population. The allele then rose to high frequency in Europeans following the divergence of European and East Asian ancestral groups.
^^That is from the discussion part of the study, now read this from the RESULTS...
The distributions of the **derived and ancestral alleles** at TYR A192C, MATP C374G, and SLC24A5 A111G are consistent with the FST results suggesting strong European specific divergence at these loci.Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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These are very nasty diseases. 100x worst then Albinism, but indirectly associated with severe melanin deficiency. Since Ashkenazi Jews ARE NOT SEMITES, these diseases are not mirrored in the Arab or even the Sephardic Jew. Interesting. I find this unusually high percentage, perhaps the highest in the world of genetic defects in All peoples on the planets, very interesting and a clear marker for researching history.
1 in 5 (20%) Jews of Ashkenazi (Eastern European) descent is a carrier for one of these diseases:
* Bloom’s Syndrome
Bloom syndrome is characterized by short stature and a facial rash that develops shortly after first exposure to sun. This rash can make a butterfly-shaped patch of reddened skin on the cheeks. The rash can develop on other sun-exposed areas such as the backs of the hands. Other clinical features include a high-pitched voice; distinct facial features, such as a long, narrow face, micrognathism of the mandible, and prominent nose and ears; pigmentation changes of the skin including hypo- and hyper-pigmented areas and cafe-au-lait spots; telangiectasias (dilated blood vessels) which can appear on the skin but also in the eyes; moderate immune deficiency, characterized by deficiency in certain immunoglobulin classes, that apparently leads to recurrent pneumonia and ear infections; hypo-gonadism characterized by a failure to produce sperm, hence infertility in males, and premature cessation of menses (premature menopause), hence sub-fertility in females. However, several women with Bloom syndrome have had children.
Complications of the disorder may include chronic lung problems, diabetes, and learning disabilities. In a small number of persons, there is mental retardation. The most striking complication of the disorder is susceptibility to cancer.
* Canavan Disease
Symptoms of Canavan disease, which appear in early infancy and progress rapidly, may include mental retardation, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur.
* Cystic Fibrosis
* Familial Dysautonomia Familial dysautonomia (FD, sometimes called Riley–Day syndrome[1]) is a disorder of the autonomic nervous system which affects the development and survival of sensory, sympathetic and some parasympathetic neurons in the autonomic and sensory nervous system resulting in variable symptoms including: insensitivity to pain, inability to produce tears, poor growth, and labile blood pressure (episodic hypertension and postural hypotension). People with FD have frequent vomiting crises, pneumonia, problems with speech and movement, difficulty swallowing, inappropriate perception of heat, pain, and taste, as well as unstable blood pressure and gastrointestinal dysmotility. FD does not affect intelligence.
* Fanconi Anemia Type C
FA is primarily an autosomal recessive genetic disorder. There are at least 13 genes of which mutations are known to cause FA: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM and FANCN. FANCB is the one exception to FA being autosomal recessive, as this gene is on the X chromosome. FA is characterized by short stature, skeletal anomalies, increased incidence of solid tumors and leukemias, bone marrow failure (aplastic anemia), and cellular sensitivity to DNA cross-linking agents such as mitomycin C.
* Gaucher Disease Type 1
Gaucher's disease (pronounced /ɡoʊˈʃeɪz.dɨziːz/) is a genetic disease in which a fatty substance (lipid) accumulates in cells and certain organs.
Symptoms may include enlarged spleen and liver, liver malfunction, skeletal disorders and bone lesions that may be painful, severe neurologic complications, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelets and yellow fatty deposits on the white of the eye (sclera). Persons affected most seriously may also be more susceptible to infection. Some forms of Gaucher's disease may be treated with enzyme replacement therapy.
* Maple Syrup Urine Disease
MSUD is caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex (BCKDH), leading to a buildup of the branched-chain amino acids (leucine, isoleucine, and valine) and their toxic by-products in the blood and urine.
The disease is characterized in an infant by the presence of sweet-smelling urine, with an odor similar to that of maple syrup. Infants with this disease seem healthy at birth but if left untreated suffer severe brain damage, and eventually die.
From early infancy, symptoms of the condition include poor feeding, vomiting, dehydration, lethargy, hypotonia, seizures, ketoacidosis, opisthotonus, pancreatitis, coma and neurological decline.
* Mucolipidosis Type IV
In ML, abnormal amounts of carbohydrates or fatty materials (lipids) accumulate in cells. Because our cells are not able to handle such large amounts of these substances, damage to the cells occurs, causing symptoms that range from mild learning disabilities to severe mental retardation and skeletal deformities. Symptoms of ML can be congenital (present at birth) or begin in early childhood or adolescence. Early symptoms can include vision problems and developmental delays. Over time, many children with ML develop poor mental capacities, have difficulty reaching normal developmental milestones, and, in many cases, eventually die of the disease.
* Niemann-Pick Disease Type A
Symptoms are related to the organs in which they accumulate. Enlargement of the liver and spleen (hepatosplenomegaly) may cause reduced appetite, abdominal distension and pain as well as thrombocytopenia secondary to splenomegaly.
Sphingomyelin accumulation in the central nervous system (including the cerebellum) results in unsteady gait (ataxia), slurring of speech (dysarthria) and discoordinated swallowing (dysphagia). Basal ganglia dysfunction causes abnormal posturing of the limbs, trunk and face (dystonia) and upper brainstem disease results in impaired voluntary rapid eye movements (supranuclear gaze palsy). More widespread disease involving the cerebral cortex and subcortical structures is responsible for gradual loss of intellectual abilities causing dementia and seizures. [2]
Sleep related disorders are also seen, including gelastic cataplexy (sudden loss of muscle tone associated with laughter), and sleep inversion (sleepiness during the day and wakefulness at night).
* Glycogen Storage Disease Type 1a
Glycogen storage disease (GSD, also glycogenosis and dextrinosis) is the result of defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types.[1] GSD has two classes of cause: genetic and acquired. Genetic GSD is caused by any inborn error of metabolism (genetically defective enzymes) involved in these processes. In livestock, acquired GSD is caused by intoxication with the alkaloid castanospermine.[2]
* Tay-Sachs Disease
Tay-Sachs disease (abbreviated TSD, also known as GM2 gangliosidosis or Hexosaminidase A deficiency) is an autosomal recessive genetic disorder. In its most common variant known as infantile Tay-Sachs disease, it presents a relentless deterioration of mental and physical abilities which commences at six months of age and usually results in death by the age of four.[1
* Albinism
Albinism (from Latin albus, "white"; see extended etymology, also called achromia, achromasia, or achromatosis) is a congenital disorder characterized by the complete or partial absence of pigment in the skin, hair and eyes due to absence or defect of an enzyme involved in the production of melanin. Albinism results from inheritance of recessive gene alleles and is known to affect all vertebrates, including humans. The most common term used for an organism affected by albinism is "albino". Additional clinical adjectives sometimes used to refer to animals are "albinoid" and "albinic".
Albinism is associated with a number of vision defects, such as photophobia, nystagmus and astigmatism. Lack of skin pigmentation makes the organism more susceptible to sunburn and skin cancers.
So, when are you cats going to stop with the Vitamin D distraction/Strawman and get to debunking the Melanin theory?Posts: 2403 | Registered: Feb 2010
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^^When will you understand that you've been debunked in every possible way, yea you can play your semantic denial game with the vitamin D, but you are completely trounced by the genetics. The alleles associated with lighter skin pigmentation in Europeans, I.e., the *derived alleles* at TYR, 192*A, MATP 374*G and SLC24A5 111*A alleles are actually found at its highest frequencies amongst Europeans, not Africans or African albinos, or Indians or any other populations and arose after the ancestors of non Africans left Africa.
Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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^ my guess is you probably dont even understand what you just posted. My experience with you over the years have led me to this conclusion.
Posts: 4254 | From: dasein | Registered: Jun 2009
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^^Ok, let's see, want to test me on it? Let's see what you got.
Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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quote:Originally posted by MindoverMatter718: ^^When will you understand that you've been debunked in every possible way, yea you can play your semantic denial game with the vitamin D, but you are completely trounced by the genetics. The alleles associated with lighter skin pigmentation in Europeans, I.e., the *derived alleles* at TYR, 192*A, MATP 374*G and SLC24A5 111*A alleles are actually found at its highest frequencies amongst Europeans, not Africans or African albinos, or Indians or any other populations and arose after the ancestors of non Africans left Africa.
Come-on Mindless, this is just stupid. The "Europeans" kittles referenced were admixed Spaniards. How could you or anybody else draw complicated conclusions about European skin lightning when you see it every day and already understand it.(BTW - you DO understand that he is talking about how Black Europeans became lighter - right?).
Anyway, where is the mystery? Where is the need for quoting derived alleles and other such things? There IS NO mystery, every one of us see it on a daily basis: Black man makes a baby with a White Woman = Brown Baby. White man makes a baby with a Black woman = Brown Baby.
In this case it was Black Iberian Gauls, Berbers, and Arabs fuching White Visigoth, Vandal, and Alan Women. All the derived alleles and STRs and other such terms cannot hide the simple fact that it was about Black Men fuching White Women.
Hell, the fuching President of the United States is such a person. So give it the fuch up!!! It's a bullsh1t study by a Negro who suckered you - accept it.
Posts: 22721 | Registered: Oct 2005
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^It just occurred to me that "the Lion" may be lurking. And for sure she will ask one of her patented stupid questions - like:
Well if the Black men and White Women made "Brown" babies, why are those people almost as White as Northern Europeans today?
Because when a Black man and White Woman make a Brown Baby, if that Brown baby makes Babies with a White person, that Baby will be lighter than the Brown Baby parent.
Then, if that lighter than the Brown parent Baby, makes a Baby with a White person, that Baby will be almost as White, OR just as White, as the White parent. See how it works everyone?
quote:Originally posted by Mike111: daily basis: Black man makes a baby with a White Woman = Brown Baby. White man makes a baby with a Black woman = Brown Baby.
yes Mike you are correct like you said
A) "Black man" makes a baby with a White Woman = Brown Baby
B) White man makes a baby with a "Black" woman = Brown Baby.
(Although in most case when we say "black" we mean "dark brown")
________________________________________
unlike people with birth defects having children with normal people. examples:
C)A Polydatyly person (a person with additional fingers) makes a baby with a person with the normal ten fingers = normal baby with ten fingers
D)A person with Heterochromia (one eye a different color than the other eye) makes a baby with a normal person = normal baby with both eyes the same color
E)An Albino person makes a baby with a normal person = normal baby just as dark as the normal parent, not lighter
Posts: 42921 | From: , | Registered: Jan 2010
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quote:Originally posted by michael1010: Just because the gene for dark skin is named *derived* allele doesn't mean the original humans didn't carry this gene.
No, dipshit, the gene for darkskin is ancestral not derived. To determine whether a SNP is ancestral or derived is based on which allele is found in other primate species--usually chimpanzee. In this case chimpanzees, orangutans, and macaques all carry the G allele at this site--the A allele has not been observed in these species, hence for rs1800404, the G allele is considered ancestral while the alternative, the "A" is derived.
quote:Originally posted by michael1010: Cuz I know damn well the San are not light because they're mixed with Europeans, so the latter is the only explanation fool.
No dipshit this is your misunderstanding, there different derived alleles, this is why dumb ass nitwits like you should just sit back and listen the San carry an allele at a particular SNP in the OCA2 gene (rs1800404) which was most often found in the derived state--that is, most individuals carried one or two "A" alleles as opposed to the "G" allele which predominated in the other African populations survey.
Europeans carry the *derived alleles* at TYR, 192*A, MATP 374*G and SLC24A5 111*A.
P.s. I just knew you'd confuse the derived alleles and think what it was saying was that the San are light because of Europeans. SMH.
quote: "The lightly pigmented hunter-gatherer San populations of Southern Africa is exceptional in having a high frequency of the derived allele relative to geographically proximate and more darkly pigmented African populations (Jablonski and Chaplin 2000), further supporting the importance of OCA2 in regulating normal variation in pigmentation. The widespread distribution of the derived allele in the CEPH-Diversity Panel suggests that it is not necessarily a new mutation, nor has it been restricted to a specific geographic area. - Norton, Kittles et al."
quote:Polymorphisms in 2 genes, ASIP and OCA2, may play a shared role in shaping light and dark pigmentation across the globe , whereas SLC24A5, MATP, and TYR have a predominant role in the evolution of light skin in Europeans but not in East Asians. These findings support a case for the recent convergent evolution of a lighter pigmentation phenotype in Europeans and East Asians.
Now again, take your foot out of your mouth.
I posted from the same article, now you're just coming back to cover your dumbass. You think because the gene for light skin states *derived* it was not present in the *original* ancestors, I proved you wrong, stfu and accept it. Dark skin, hair, and eyes are *dominant traits*, light skin, eyes, and hair are *recessive traits*---dominant=ancestral, recessive=derived. Original humans carried both the dominant and the recessive traits, the recessive trait increased in frequency when they migrated to Europe. Learn to fugging comprehend. San are not mixed with European you goddamn fool, their skin color derives from the original ancestors, and increased in frequency as they migrated further from the equator towards South African forests, where the necessity for dark skin diminished. If your dumb ass don't get this, you will never fully comprehend the range of human skin colors. You think it only has to do with Vitamin D, but you proved yourself that V-D can come from food sources.
Check it out--165,000 years ago, archaeologist found evidence that modern humans in South Africa existed off a shell fish diet. There's the source of the mofo vitamin D, but yet they are still lighter. Why the fugg they're not as dark as mofo near the equator--because it's not necessary to produce more pigment. The melanocytes exist in all humans, pigment is not produced until AFTER BIRTH YOU DUMBFUCK. Can't believe I gave you too much credit, if you're too ignorant to realize newborn children are lighter than they will eventually become in a few months. If necessary, their melanocytes cells will produce more pigment depending on what they inherited from their folks. The same goes for modern humans in general they inherited the genes for light skin from the original ancestors, and it remained dormant until 12,000 years ago max. They slowly became paler, it didn't happen overnight fool. You're no different than the Melanin fools, you think overnight an albino child was born, and sexual selection for this color took place in order to survive to intake Vitamin D. Vitamin D was always needed, it didnt take 30,000 years for humans in Europe to suddenly realize this. Skin lightening was a gradual process, absorb that sh*t and let it finally sink in.
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quote:Originally posted by MelaninKing: These are very nasty diseases. 100x worst then Albinism, but indirectly associated with severe melanin deficiency. Since Ashkenazi Jews ARE NOT SEMITES, these diseases are not mirrored in the Arab or even the Sephardic Jew. Interesting. I find this unusually high percentage, perhaps the highest in the world of genetic defects in All peoples on the planets, very interesting and a clear marker for researching history.
1 in 5 (20%) Jews of Ashkenazi (Eastern European) descent is a carrier for one of these diseases:
* Bloom’s Syndrome
Bloom syndrome is characterized by short stature and a facial rash that develops shortly after first exposure to sun. This rash can make a butterfly-shaped patch of reddened skin on the cheeks. The rash can develop on other sun-exposed areas such as the backs of the hands. Other clinical features include a high-pitched voice; distinct facial features, such as a long, narrow face, micrognathism of the mandible, and prominent nose and ears; pigmentation changes of the skin including hypo- and hyper-pigmented areas and cafe-au-lait spots; telangiectasias (dilated blood vessels) which can appear on the skin but also in the eyes; moderate immune deficiency, characterized by deficiency in certain immunoglobulin classes, that apparently leads to recurrent pneumonia and ear infections; hypo-gonadism characterized by a failure to produce sperm, hence infertility in males, and premature cessation of menses (premature menopause), hence sub-fertility in females. However, several women with Bloom syndrome have had children.
Complications of the disorder may include chronic lung problems, diabetes, and learning disabilities. In a small number of persons, there is mental retardation. The most striking complication of the disorder is susceptibility to cancer.
* Canavan Disease
Symptoms of Canavan disease, which appear in early infancy and progress rapidly, may include mental retardation, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur.
* Cystic Fibrosis
* Familial Dysautonomia Familial dysautonomia (FD, sometimes called Riley–Day syndrome[1]) is a disorder of the autonomic nervous system which affects the development and survival of sensory, sympathetic and some parasympathetic neurons in the autonomic and sensory nervous system resulting in variable symptoms including: insensitivity to pain, inability to produce tears, poor growth, and labile blood pressure (episodic hypertension and postural hypotension). People with FD have frequent vomiting crises, pneumonia, problems with speech and movement, difficulty swallowing, inappropriate perception of heat, pain, and taste, as well as unstable blood pressure and gastrointestinal dysmotility. FD does not affect intelligence.
* Fanconi Anemia Type C
FA is primarily an autosomal recessive genetic disorder. There are at least 13 genes of which mutations are known to cause FA: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM and FANCN. FANCB is the one exception to FA being autosomal recessive, as this gene is on the X chromosome. FA is characterized by short stature, skeletal anomalies, increased incidence of solid tumors and leukemias, bone marrow failure (aplastic anemia), and cellular sensitivity to DNA cross-linking agents such as mitomycin C.
* Gaucher Disease Type 1
Gaucher's disease (pronounced /ɡoʊˈʃeɪz.dɨziːz/) is a genetic disease in which a fatty substance (lipid) accumulates in cells and certain organs.
Symptoms may include enlarged spleen and liver, liver malfunction, skeletal disorders and bone lesions that may be painful, severe neurologic complications, swelling of lymph nodes and (occasionally) adjacent joints, distended abdomen, a brownish tint to the skin, anemia, low blood platelets and yellow fatty deposits on the white of the eye (sclera). Persons affected most seriously may also be more susceptible to infection. Some forms of Gaucher's disease may be treated with enzyme replacement therapy.
* Maple Syrup Urine Disease
MSUD is caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex (BCKDH), leading to a buildup of the branched-chain amino acids (leucine, isoleucine, and valine) and their toxic by-products in the blood and urine.
The disease is characterized in an infant by the presence of sweet-smelling urine, with an odor similar to that of maple syrup. Infants with this disease seem healthy at birth but if left untreated suffer severe brain damage, and eventually die.
From early infancy, symptoms of the condition include poor feeding, vomiting, dehydration, lethargy, hypotonia, seizures, ketoacidosis, opisthotonus, pancreatitis, coma and neurological decline.
* Mucolipidosis Type IV
In ML, abnormal amounts of carbohydrates or fatty materials (lipids) accumulate in cells. Because our cells are not able to handle such large amounts of these substances, damage to the cells occurs, causing symptoms that range from mild learning disabilities to severe mental retardation and skeletal deformities. Symptoms of ML can be congenital (present at birth) or begin in early childhood or adolescence. Early symptoms can include vision problems and developmental delays. Over time, many children with ML develop poor mental capacities, have difficulty reaching normal developmental milestones, and, in many cases, eventually die of the disease.
* Niemann-Pick Disease Type A
Symptoms are related to the organs in which they accumulate. Enlargement of the liver and spleen (hepatosplenomegaly) may cause reduced appetite, abdominal distension and pain as well as thrombocytopenia secondary to splenomegaly.
Sphingomyelin accumulation in the central nervous system (including the cerebellum) results in unsteady gait (ataxia), slurring of speech (dysarthria) and discoordinated swallowing (dysphagia). Basal ganglia dysfunction causes abnormal posturing of the limbs, trunk and face (dystonia) and upper brainstem disease results in impaired voluntary rapid eye movements (supranuclear gaze palsy). More widespread disease involving the cerebral cortex and subcortical structures is responsible for gradual loss of intellectual abilities causing dementia and seizures. [2]
Sleep related disorders are also seen, including gelastic cataplexy (sudden loss of muscle tone associated with laughter), and sleep inversion (sleepiness during the day and wakefulness at night).
* Glycogen Storage Disease Type 1a
Glycogen storage disease (GSD, also glycogenosis and dextrinosis) is the result of defects in the processing of glycogen synthesis or breakdown within muscles, liver, and other cell types.[1] GSD has two classes of cause: genetic and acquired. Genetic GSD is caused by any inborn error of metabolism (genetically defective enzymes) involved in these processes. In livestock, acquired GSD is caused by intoxication with the alkaloid castanospermine.[2]
* Tay-Sachs Disease
Tay-Sachs disease (abbreviated TSD, also known as GM2 gangliosidosis or Hexosaminidase A deficiency) is an autosomal recessive genetic disorder. In its most common variant known as infantile Tay-Sachs disease, it presents a relentless deterioration of mental and physical abilities which commences at six months of age and usually results in death by the age of four.[1
* Albinism
Albinism (from Latin albus, "white"; see extended etymology, also called achromia, achromasia, or achromatosis) is a congenital disorder characterized by the complete or partial absence of pigment in the skin, hair and eyes due to absence or defect of an enzyme involved in the production of melanin. Albinism results from inheritance of recessive gene alleles and is known to affect all vertebrates, including humans. The most common term used for an organism affected by albinism is "albino". Additional clinical adjectives sometimes used to refer to animals are "albinoid" and "albinic".
Albinism is associated with a number of vision defects, such as photophobia, nystagmus and astigmatism. Lack of skin pigmentation makes the organism more susceptible to sunburn and skin cancers.
So, when are you cats going to stop with the Vitamin D distraction/Strawman and get to debunking the Melanin theory?
Now post the evidence that any of the above diseases are associated with lack of melanin you slick talking mother fugger. You fool the ignorant non-reading mofos, but I see right thru the bullsh*t.
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quote:Originally posted by Original_Womb/man: michael1010,
I recall on another thread asking this very question, could the original people (Blacks) carry both allele, DNA, genes, germs, etc?
However, you posted this, which science seems to be answering.
[Q}Similarly, the presence of the derived allele (albeit at low frequencies) in some sub-Saharan African populations may be due to recent gene flow from European and Central Asian populations. Alternatively, the derived allele may have existed in the ancestral human population and was lost in the ancestors of modern East Asians but retained in the ancestral European population. The allele then rose to high frequency in Europeans following the divergence of European and East Asian ancestral groups.
I wonder why it would be at a low frequency. Could it be due to the fact that it is "recessive=weak" Also notice the key words "MAY HAVE BEEN" sounds like there is a possibility.
However, this is quite interesting:
The pigmentation of our skin, which is Black tending to Brown, lies deep within the science of our beginnings. The two germs, Black and Brown, were lying dormant within the original Black man, which under the right conditions produces all the other colors or races that we have in the world today.
another excerpt from the same article
He discovered in the science lab that there were in these two germs, Black and Brown, a distinct characteristic within the Brown germ that he could use to separate from the Black germ to produce other races and colors. This is somewhat like the Biblical story of Rebekah, as we read in Genesis, who struggled with twins inside her womb, the younger one struggling for dominance over the elder one. Thus, Yakub (Jacob)in his study of genetics and biology set up a law of birth control while separating the two germs.[I]
So it appears that science is baring witness to what the NOI teaches. That genetic engineering/ selective mating is what caused skin to whiten and become fixed, with the exception of dominant genetic material/DNA being [re]introduced to correct and add melanin back into the weaken recessive/albino gene pool.
Simple law, called Mendels Law: 2-Black/brown can make white and anything in between, and you best believe that you can get color from black and white; but you can't get black or any other color from 2 white.
We already showed that 2 different types of melanin are produce- red and brown, and humans carry variations of the two, which is why we get such a wide range of complexions, eye colors, and hair colors. Brown is the dominant color of hair and eyes, possibly skin. If two parents carry the recessive gene, it increases the possibility off the offspring acquiring it. Note, that a child cannot get blue eyes unless both parents carry the gene for blue eyes, even if both parents have dark eyes, they can still carry the gene for blue eyes.
This is what I'm trying to explain, the original ancestors were dark skinned, but they carried the recessive gene for light skin, which were passed on to their European off-spring where it increased in frequency. But the gene in question is not what you all are calling the gene responsible for albinism, as this gene increased in frequency only in Africa. Most of you don't even realize that albinism is more frequent in Africa than any other country, especially in Tanzania.
Tanzania is one of the other countries besides Ethiopia where scientist are tracking the origins of modern humans.
[i]The first lineage to branch off from Mitochondrial Eve is L0. This haplogroup is found in high proportions among the San of Southern Africa, the Sandawe of East Africa. It is also found among the Mbuti people.[23][24] These groups branched off early in human history and have remained relatively genetically isolated since then. Haplogroups L1, L2 and L3 are descendents of L1-6 and are largely confined to Africa. The macro haplogroups M and N, which are the lineages of the rest of the world outside Africa, descend from L3
This is what I was trying to show Mindmatter, the San carried the original DNA and recessive alle, because they are the first ones to branch off from the original Ancestors.
This is the evidence about Tanzania and Ethiopia
Cann, Stoneking & Wilson (1987) placement of a relatively small population of humans in sub-saharan Africa, lent appreciable support for the recent Out of Africa hypothesis. The current concept places between 1,500 and 16,000 effectively interbreeding individuals (census 4,500 to 48,000 individuals) within Tanzania and proximal regions. Later, Tishkoff using data from many loci has extrapolated origins to the Angola-Namibia border region near the Atlantic Ocean (although this region has poor genetic definition), whereas Behar et al. 2008 places an ancestral population in Ethiopia. These opinions all point toward a sub-Saharan origin. More recent literature on languages and pygmy phenotype indicate that L0 and L1 were carried by click-speaking pygmies from SE Africa to Central and Western Africa, therefore explaining much of the genetic diversity in those regions. Consequently, more recent studies have tended to push the cradle of humanity more toward the South or East of Africa.Posts: 82 | Registered: May 2010
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quote:Originally posted by the lion: fakehsitory.com
This is a picture used by people to lie.
It is claimed the father is "black" yet the father is not included in the photo. It is assumed that the mother is black but she may be 1/4 to 1/3 white. There is no data to support this picture. My guess on it is that the father was white and the reporters took her word for it that he was black because it made a good story. You can't build a case from one woman in Brazil. Why aren't the afrocentrics running down there to find the father?
It's foolishness and a form of lying.
Two black people with kinky hair cannot produce a child with straight hair. There are thousands of albinos in Africa. None of the Mulattoes that have kinky haired parents have straight hair. That disproves the theory right there.
Who are the contemporary Eritreans, Djibuti, Somalians,or Sudanese? It is debated by anthropologists. Regardless are they producing albinos that are both blond and have straight hair? No they are not. Look at the Chinese for instance. There are no Africans on the whole continent that have that type of very straight hair. Where are the tribes? Likewise many Caucasians have similar hair but not always black. Other times wavy or curly. Most black people in America have no North African ancestry. You mad now? It just shows you have a European like disregard for the culture of the rest of the continent. Africans don't have this problem
Mike is right. You are very stupid!
The Jewish genetic diseases described here are autosomal recessive disorders and they result from altered genes (mutations) that are located on autosomal chromosomes. For these diseases to occur, an abnormal (mutated) gene leading to the disorder must be inherited from each parent. Carriers for an autosomal recessive disorders are individuals who have in their genetic composition one normal gene and one mutated gene for that specific disorder. Carriers are themselves healthy individuals and have no symptoms or signs of the disease for which they are carriers. The main concern for carrier individuals is that they are at risk of passing mutated genes to their children:
If both parents are carriers for the same disorder, there is a 50% likelihood with each pregnancy that the child will be a carrier (like each parent) and a 25% likelihood with each pregnancy that the child will be affected with the disorder. There is a 25% likelihood with each pregnancy that the child will be neither affected with the disorder nor a carrier for the disorder
This albino lady's husband isn't show either, but he is black and as you see, his children are not OCA1 or 2, but surely carry the OCA defective gene. The children's complexion is exactly very close to that of President Obama, who himself is the product of a union between a white woman and black man. Same as above.
You don't have any evidence that the father of the above children is a carrier you lying piece of sh*t. You just posted some other data to mask the fact that you don't know what the fugg ur talking about.
If the father is *not* a carrier, the children have a 75% chance of *not* getting the disorder. They have a 50% chance of not getting it, even if the father is a carrier. This is why her other kids are not albino.
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quote:Originally posted by michael1010: I posted from the same article, now you're just coming back to cover your dumbass. You think because the gene for light skin states *derived* it was not present in the *original* ancestors, I proved you wrong, stfu and accept it. Dark skin, hair, and eyes are *dominant traits*, light skin, eyes, and hair are *recessive traits*---dominant=ancestral, recessive=derived. Original humans carried both the dominant and the recessive traits, the recessive trait increased in frequency when they migrated to Europe. Learn to fugging comprehend. San are not mixed with European you goddamn fool, their skin color derives from the original ancestors, and increased in frequency as they migrated further from the equator towards South African forests, where the necessity for dark skin diminished. If your dumb ass don't get this, you will never fully comprehend the range of human skin colors. You think it only has to do with Vitamin D, but you proved yourself that V-D can come from food sources.
Check it out--165,000 years ago, archaeologist found evidence that modern humans in South Africa existed off a shell fish diet. There's the source of the mofo vitamin D, but yet they are still lighter. Why the fugg they're not as dark as mofo near the equator--because it's not necessary to produce more pigment. The melanocytes exist in all humans, pigment is not produced until AFTER BIRTH YOU DUMBFUCK. Can't believe I gave you too much credit, if you're too ignorant to realize newborn children are lighter than they will eventually become in a few months. If necessary, their melanocytes cells will produce more pigment depending on what they inherited from their folks. The same goes for modern humans in general they inherited the genes for light skin from the original ancestors, and it remained dormant until 12,000 years ago max. They slowly became paler, it didn't happen overnight fool. You're no different than the Melanin fools, you think overnight an albino child was born, and sexual selection for this color took place in order to survive to intake Vitamin D. Vitamin D was always needed, it didnt take 30,000 years for humans in Europe to suddenly realize this. Skin lightening was a gradual process, absorb that sh*t and let it finally sink in.
Here are the questions I asked you, and as of yet, haven't recieved any answers specifically, only dimwitted distractions from you...
Pay attention;
1) What source are you going by that states the San of southern Africa evolved their lighterskin in heavily forested areas?
2) Darken? Are you insinuating these people (south Asians) were originally lighter and became less darker? If so, source please.
3) Can you further elaborate on this because I don't quite get what you're saying here. How does the cloudy sky enable people to survive without this quality? By "this" I assume you mean melanin.
4) So the people who reside in the arctics who are in fact Asian to begin with, due to glare of sun off of the snow made them more similar to themselves? Elaborate on this please, thanks.
^^Never has anything above been answered specifically, although u did try to explain the Asian part, but otherwise no evidence has been provided by you.
I'm still waiting for you to answer them specifically, if you can.
Anyway, Wtf? Your dimwitted ass who just learned about this probably like last week is trying to school me on this?
You can't be serious. Since you are like a baby, and don't possess the capacity to answer my posts, post by post, I will deal with you in the same way.
It's been shown that the San carry a derived allele at the OCA2 loci which in turn plays a role in skin pigmentation worldwide, this is fact, you can't debunk it.
The San also carry an allele which is derived from Europeans albeit at low frequencies, this is fact and you can't debunk it.
The San also adapted to sub-tropical areas of southern Africa, which most likely had a role in their skin lightening, sorry kid but the San adapted to open areas and didn't adapt in the jungle or heavily forested areas, like you thought
On the other hand this SLC24A5 111*A derived allele is at its highest frequencies outside of Europe in geographically proximate populations in north Africa, the middle east and Pakistan, while of course it's at its highest frequency as noted in Europe, this is also fact and you can't debunk it.
It wasnt present in the ancestral population as the following also notes ...
The virtual absence of MATP 374*G–derived allele in the sub-Saharan African populations that we examined in the CEPH-Diversity Panel is consistent with the origin of this mutation outside of Africa after the divergence of modern Asians and Europeans.
I asked you for evidence from wherein you stated that the San of southern Africa received their lighter skin due to adapting under forested areas.
Were you ever able to confirm this?
Nope, you never did, instead, you stray completely off topic and post a books worth longwinded post all of which was pretty irrlevant to what I asked.
I also asked you where your proof was that south Asians less darkened because of tree covered areas. Were you able to provide any data for this? Nope.
What you did do was post that babies can darken after they're born, but wtf does that have to do with what I asked you, and what you said about south Asians less darkening because of tree covered areas?
The MATP 374*G–derived allele is virtually absent in Africa, confirming that it arose after humans left Africa and was not in the ancestral population you dipshit.
The strong European divergence at the loci in question is also strong evidence that these alleles arose outside of Africa and are specific to Europeans and not present in the ancestral population.
The distributions of the **derived and ancestral alleles** at TYR A192C, MATP C374G, and SLC24A5 A111G are consistent with the FST results suggesting strong European specific divergence at these loci.Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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quote:Originally posted by MindoverMatter718: Of course as noted, the point in question was whether or not the San carried the derived allele as noted in the study "Genetic Evidence for the Convergent Evolution of Light Skin in Europeans and East Asians" .
The following gives the definitive answer as to whether the San do in fact carry this allele or not, and if the authors were mistaking when noting it to be present.
There certainly are a few pointers I will have to address in the response from Dr. Norton, but for now, I believe she answered our question and that answer is YES the San do indeed carry the derived allele at high frequencies.
One note that I will certainly address is simply that I would see it from a point of view (as she notes some to see it) that dark skin evolved so long ago in our non anatomically modern human ancestors that the ancestral state of light pigmentation under the fur (if were to be entertained), of our non AMH ancestors if indeed was light, has nothing to do with AMH, since when AMH arose the ancestral state of dark pigmentation in our primate non AMH ancestors was already present into our physiognomy 1.2 million years ago, therefore AMH arose in a darkskin ancestral AMH state.
Also similar to the cognitive thinking which recently has been noted to be already set in homo erectus well before AMH arose, which blows the concept of cognitive thinking being an evolved trait that magically occurred 40kya when AMH entered Europe.
quote: Dear (name withheld)
Thank you for your interest in my work. I'm not sure that I fully understand your question--are you asking me if it is correct to interpret light pigmentation of the San as a derived trait, or that the A allele in the OCA2 gene (rs1800404) is derived? Let me try to address both. First, the "A" allele observed at such high frequency among the San is derived. When we talk about alleles being ancestral or derived we are basing this terminology on what allele is carried by other primates (usually chimpanzee). At this particular SNP, chimps, orangutans, and macaques all carry the G allele (to my knowledge, the A allele has not yet been observed in these species). So, for rs1800404, the G allele is considered ancestral while the alternative, the "A" is derived. Of course, this does not mean that the light pigmentation of the San is entirely due to derived alleles (for example, at the other SNPs in that study the San overwhelmingly carry the ancestral allele). Pigmentation is a complex trait that is determined by multiple genetic loci. Although we know that rs1800404 has an effect on skin pigmentation, I would be very surprised if it is responsible for all of the variation between the lightly pigmented San and more darkly pigmented neighboring African populations. It may be that in addition to carrying the derived allele at rs1800404 the San also carry ancestral alleles (those found in non-human primates) that are associated with light skin. I say "ancestral" here because many, like Jablonski and Chaplin or Rogers and Iltis would argue that humans evolved from a creature that had lightly pigmented skin under a coat of dark hair or fur. The question of whether light pigmentation in humans is derived is a bit more tricky. As I just mentioned, many assume that the ancestor of modern humans had light pigmentation under a dark coat of fur or hair, and that as you note dark pigmentation evolved when that fur was lost in response to the high UVR pressures of an African environment. In that sense, some would consider light pigmentation to be ancestral and darker pigmentation to be a derived state (with the lighter pigmentation observed in European and East Asian populations re-evolving much later in human history, most likely due to new, unique mutations such as the ones in SLC24A5 and MATP). Other people are of the opinion that dark pigmentation evolved so long ago in human history that it's acceptable to consider dark pigmentation the ancestral state. Personally I really don't think it matters as long as one is clear about which you consider to be ancestral and why. As for the environment of southern Africa influencing the pigmentation of the San, I could not say. I assume that by environment you are referring to the UVR intensity there, which is surely not as intense as it would be further north and closer to the equator. It is certainly a plausible idea, but much depends on how long the San have resided in that region and how strong selection for lighter pigmentation would have been (very strong selection could lead to a rapid change in pigmentation). If I have misunderstood your question please let me know and I'll do my best to (re)answer it. best,
~Heather Norton
Heather L. Norton Ph.D. ARL-Biotechnology 1041 East Lowell Street Bioscience West, Room 246 University of Arizona Tucson, AZ 85721
My initial e-mail for those interested...
quote: On Jan 11, 2010, at 2:36 PM, (name withheld) wrote:
Greetings, Dr, Norton.
I was recently engaged in a debate with my peers regarding your study re; "Genetic Evidence for the Convergent Evolution of Light Skin in Europeans and East Asians". We began discussing the alleles associated with darker pigmentation vs. lighter pigmentation. As you allude to in the study there are derived alleles associated with lighterskin, and an ancestral allele associated with darker skin, the ancestral allele of which dominates in Sub-Saharan Africa and Island Melanesia. Of course this dark pigmentation arose as a consequence due to loss of fur and the need to protect the skin against harmful UV rays, while also helping to preserve the folate reserves in order to produce successful offsprings in a tropical environment. The exception came when the south African San hunter gatherers were brought into play. Your study notes that the derived allele is heavily present in the San (93%), this is interesting as it specifically notes that the San of southern Africa's lighter complexion is indeed a derived state, and not the ancestral. Would I be correct in making this assessment? Also, perhaps the subtropical environment of southern Africa (which mimics temperature somewhat similar to the Mediterranean) had something to do with this lighterskin pigmentation of the San hunter gatherers? Can you please elaborate on this further, it would be most highly appreciated. Thanks in advance. Here's two snippets from the study so you can get an idea quickly of what I mean....
Genetic Evidence for the Convergent Evolution of Light Skin in Europeans and East Asians Heather L. Norton,*1 Rick A. Kittles
quote: In contrast, the **ancestral allele** associated with **dark pigmentation** has a shared high frequency in **sub- Saharan African and Island Melanesians**.A notable exception is the relatively lightly pigmented San population of Southern Africa where the **derived allele** predominates (93%), although this may be simply due to small sample size (n514). The distributions of the **derived and ancestral alleles** at TYR A192C, MATP C374G, and SLC24A5 A111G are consistent with the FST results suggesting strong Europeans pecific divergence at these loci. The *derived allele* at TYR, 192*A (previously linked with lighter pigmentation [Shriver et al. 2003]), has a frequency of 38% among European populations but a frequency of only 14% among non-Europeans. The differences between Europeans and non-Europeans for the MATP 374*G and SLC24A5 111*A alleles (both derived alleles associated with lighter pigmentation) were even more striking (MATP European 5 87%; MATP non-European 5 17%; SLC24A5 European 5 100%; SLC24A5 non-European 5 46%). The frequency of the SLC24A5 111*A allele outside of Europe is largely accounted for by high frequencies in geographically proximate populations in northern Africa, the Middle East, and Pakistan (ranging from 62% to 100%).
and if you will note...
"The lightly pigmented hunter-gatherer San populations of Southern Africa is exceptional in having a high frequency of the derived allele relative to geographically proximate and more darkly pigmented African populations (Jablonski and Chaplin 2000), further supporting the importance of OCA2 in regulating normal variation in pigmentation. The widespread distribution of the derived allele in the CEPH-Diversity Panel suggests that it is not necessarily a new mutation, nor has it been restricted to a specific geographic area. - Norton, Kittles et al."
Sincerely yours,
(name withheld).
Posts: 6572 | From: N.Y.C....Capital of the World | Registered: Jun 2008
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posted
After reading the last page. Let me surmise what I got from it.
1. Mike Jr is saying that ALL humans carry the genetic material for light skin. And it was only about 12Kya that the selective sweep occurred in Europe, specifically northern Europe. Vit D had nada(or very little) to do with skin lightening. If Vit D was so important then black Europeans would have died of rickets many times over.
This is plausible. After all it looks like San and peoples of the Americas, and Northern East Asia maintained the ability to lighten and darken depending on the environmental need. ie UV protection. Ancestral humans were probably light/white under the fur so it makes sense that the gene was always there. Melanin allowed us to adapt and progress to humans.
2. Quote by MK: So, when are you cats going to stop with the Vitamin D distraction/Strawman and get to debunking the Melanin theory?
MK is right when is this going to happen?
I think the Albino Theory is . . . nuff said. BUT the MT (most of it) still stands. Still waiting for someone to debunk it.
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After re-reading KIK last post. It seems like the Sans light skin genetic material is "different" to Europeans and East Asians. And the East Asians are also different to Europeans.
Bottomline: humans adapt. The "correct" amt of melanin is "created" depending upon the UV intensity of the environment. AND Vit D has absolutely nothing to do with it.
Now back to debunking MT. List the many uses of melanin and debunk that list. . . .
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posted
Brother, you beat up on King and Jari about religion but you do realize that "telepathic blacks" is another religion.
-------------------- Without data you are just another person with an opinion - Deming Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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He also demonstrated that human skin color is a quantitative trait. He went to Jamaica in 1912 to do an exten-sive study of children and grandchildren of parents who were interracial couples.He and his coworkers used a color wheel resembling a spinning whirligig that had different sectors of white, black, red, and yellow to pro- duce a blended blur that they would apply to the inner arm of the subjects.
When a matching color was found they would have a quantitative measure of the color rather than a subjective term to describe it. Davenport's find- ings were impressive. He exploded many folk myths about human racial hybridizing. He claimed there were two chief genes involved in human skin color and their effects were additive. There was no dominant or recessive factor for color. A person expressed as many of the color factors as were present in the genetically inferred composition (genotype) of that individ- ual. If the color factors are A and B for melanizing pigment and a and b for the virtual absence of melanin in the skin, then African males or females are AABB and white males and females (especially the Anglican whites in Jamaica) are aabb. Their children who have brown skin are AaBb. When two such brown-skinned individuals have children, their offspring form a spectrum of colors in a fixed ratio of 1 AABB: 4 AABb or AaBB: 6 AaBb or AAbb or aaBB: 4Aabb or aaBb: 1 aabb. Converting the intense melanin- producing factors into a color effect, this would be seen as 1 black: 4 dark brown: 6 brown: 4 light brown: 1 white.
Davenport rejected a myth in southern bigotry that a white person with a black ancestor later marrying a white woman with no known black ancestry could have a black baby. His work also explained why two light brown-skinned parents could have a child darker than either parent. Thus, Aabb (light brown) x aaBb (light brown) can give one-fourth of the offspring having AaBb (brown), one- fourth aabb (white), and half Aabb or aaBb (light brown).
Davenport was also the first to recognize and interpret what is called a founder effect in human genetics. He noted that families which are isolat- ed geographically, socially, or by religion become genetic isolates and marry with one another.
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quote:Originally posted by MelaninKing: I think many here are just damn mentally lazy. With a topic as exciting as melanin, yet many here have not begun to research or ingest even the surface level information on the subject.
Mike & Clyde, check out Dr. Jewel Pookrum, an authority on Melanin and brain stimulation techniques. She calls herself an, immortal. Her theory is that melanin can rejuvenate the body IF we extract ourselves out of the sphere of white thought, which is detrimental to blacks.
Thank you MK for bringing the science of melanin to this forum. It is this carbon based substance that distinguishes the hueman family. Having Knowledge of Self starts with overstanding our biology and our connection to the originator of the heavens and earth.
Although science has advanced on the study and language of melanin over the years; it was quite obvious to me in my 8th grade biology/psychology class, while studying Mendel's law, how the races game to be. I realized that whites came from blacks, via Albinism, then admixture, then selective mating to maintain light skin; Same as with the Creoles in Louisiana, and this was in the late 70's.
Also, thanks for posting Dr. Jewels links. I love the Sista!!!
Posts: 35 | From: ATL | Registered: Jan 2010
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posted
As far as I can determine, there are NO scientific studies tracing the children of mixed Albino/Pigmented parents. NONE!
This is a large world-wide population completely ignored, yet studies have been done on the most mundane and insignificant aspects of the most trivial things.
The reason for this is of course obvious:
To do such a study would quickly confirm that which is already obvious to non-Whites, i.e. Modern Whites descend from an in-breed population of Breeding Albinos with "LIMITED" admixture from "Normal" Blacks.
From the Davenport color chart:
There was no dominant or recessive factor for color. A person expressed as many of the color factors as were present in the genetically inferred composition (genotype) of that individ- ual. If the color factors are A and B for melanizing pigment and a and b for the virtual absence of melanin in the skin, then African males or females are AABB and white males and females (especially the Anglican whites in Jamaica) are aabb. Their children who have brown skin are AaBb. When two such brown-skinned individuals have children, their offspring form a spectrum of colors in a fixed ratio of 1 AABB: 4 AABb or AaBB: 6 AaBb or AAbb or aaBB: 4Aabb or aaBb: 1 aabb. Converting the intense melanin- producing factors into a color effect, this would be seen as 1 black: 4 dark brown: 6 brown: 4 light brown: 1 white.
Thus:
Albino = aabb Black = AABB
Converting the intense melanin- producing factors into a color effect, this would be seen as 1 black: 4 dark brown: 6 brown: 4 light brown: 1 white.
Therefore the MAJORITY will be BROWN (AaBb) If AaBb (brown) mates with the MAJORITY ALBINO population.
The majority of the resulting Child will be aabB.
If aabB mates with an Albino, the resulting children will likely be aab<B.
Isn't that what MOST Northern Europeans are, ALMOST Albino, but not quite?
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We already showed that 2 different types of melanin are produce- red and brown, and humans carry variations of the two, which is why we get such a wide range of complexions, eye colors, and hair colors. Brown is the dominant color of hair and eyes, possibly skin. If two parents carry the recessive gene, it increases the possibility off the offspring acquiring it.
Not true, all humans do not carry both genes. Some carry a weaker or diluted version of one or the other or both.
you posted:
[I]But the gene in question is not what you all are calling the gene responsible for albinism, as this gene increased in frequency only in Africa.[I] Most of you don't even realize that albinism is more frequent in Africa than any other country, especially in Tanzania.
Then what gene would it be? Genes can become fixed/dominant, they can mutate, change, or become diluted due to admixture; therefore, if dominant black genes, in any form, i.e. black or brown, are [re]introduced into the gene pool of... say, Albinos, well it would seem to reason that the offsprings of said Albinos would now have the advantage to now produce melanin at different diluted levels; albeit, they are now possible carriers of that recessive gene that causes Albinism.
[Q}Similarly, the presence of the derived allele (albeit at low frequencies) in some sub-Saharan African populations may be due to recent gene flow from European and Central Asian populations. Alternatively, the derived allele may have existed in the ancestral human population and was lost in the ancestors of modern East Asians but retained in the ancestral European population. The allele then rose to high frequency in Europeans following the divergence of European and East Asian ancestral groups.
The Sans people are a perfect example of Asiatic Black people, in which the so called Chinese people derived.Posts: 35 | From: ATL | Registered: Jan 2010
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quote:Originally posted by Mike111: As far as I can determine, there are NO scientific studies tracing the children of mixed Albino/Pigmented parents. NONE!
This is a large world-wide population completely ignored, yet studies have been done on the most mundane and insignificant aspects of the most trivial things.
The reason for this is of course obvious:
To do such a study would quickly confirm that which is already obvious to non-Whites, i.e. Modern Whites descend from an in-breed population of Breeding Albinos with "LIMITED" admixture from "Normal" Blacks.
THANK YOU!!!
All of the redundant fancy science language does nothing but cause more confusion to a simple HUEman equation.Posts: 35 | From: ATL | Registered: Jan 2010
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quote:Originally posted by xyyman: Brother, you beat up on King and Jari about religion but you do realize that "telepathic blacks" is another religion.
I'm not against a new religion. I'm just against a religion dating back to pre-African enslavement which was used as a tool to accomplish that very same mission. One that has seen a decline in all aspects of Africans lives since it's inception. One that worships a blue eyed blond haired albino, King of The Lepers.
One based on Melanin is solely derived from black thought. What's wrong with that?
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quote:Originally posted by MelaninKing: I think many here are just damn mentally lazy. With a topic as exciting as melanin, yet many here have not begun to research or ingest even the surface level information on the subject.
Mike & Clyde, check out Dr. Jewel Pookrum, an authority on Melanin and brain stimulation techniques. She calls herself an, immortal. Her theory is that melanin can rejuvenate the body IF we extract ourselves out of the sphere of white thought, which is detrimental to blacks.
Thank you MK for bringing the science of melanin to this forum. It is this carbon based substance that distinguishes the hueman family. Having Knowledge of Self starts with overstanding our biology and our connection to the originator of the heavens and earth.
Although science has advanced on the study and language of melanin over the years; it was quite obvious to me in my 8th grade biology/psychology class, while studying Mendel's law, how the races game to be. I realized that whites came from blacks, via Albinism, then admixture, then selective mating to maintain light skin; Same as with the Creoles in Louisiana, and this was in the late 70's.
Also, thanks for posting Dr. Jewels links. I love the Sista!!!
OW/M
Dr. Jewel Pookrum is a solid sister.
She has uncovered the mysteries of Melanin and traveled around the world preaching the magic element within blacks that makes us Godly. No doubt Whites derived from us as the substance mutated to an extreme and left a percentage of humans without. Was this due to a curse from God, because living without Melanin is a very damned state.
Whites/Jews attempt to obscure their true origins using many different deceptions, to include genetic jargon, yet, it is still very obvious from where they came, and what they hope to CORRECT in the Human Gnome program.
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it was quite obvious to me in my 8th grade biology/psychology class, while studying Mendel's law, how the races game to be.
I realized that whites came from blacks, via Albinism, . . .
The gift of Discernment is just that a gift!
REFLECT on these words of Wisdom.
Matthew 21:16 (King James Version)
And said unto him, Hearest thou what these say? And Jesus saith unto them, Yea; have ye never read, Out of the mouth of babes and sucklings thou hast perfected praise?
and
1 Corinthians 3:1-2
And I, brethren, could not speak unto you as unto spiritual, but as unto carnal, even as unto babes in Christ.
I have fed you with milk, and not with meat: for hitherto ye were not able to bear it, neither yet now are ye able.
Posts: 35 | From: ATL | Registered: Jan 2010
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posted
Seems like the the Albino Theory is only PART of the Melanin Theory. Here is homework assignment for Mike Jr. Start debunking. . .
See below
Props on the AT.
I do NOT adhere to some of these. eg S. Tishkoff explained the prevalence of hypertension in AA. The problem is being seen now in Africans IN Africa. It is gene and diet related not melanin related.
See, I gave you a head start.
• It is also claimed that, because neuromelanin, which is found in the substantia nigra (in Latin, literally "black substance") of the human brain, plays a role in the transmission of neuronal impulses, higher levels of melanin in skin enable nerve synapses to fire more quickly and efficiently as well, thereby enhancing the natural athleticism of dark skinned people.
• There is, however, a correlation between cutaneous melanin and the substantia nigra vis-a-vis Parkinson's disease, a neurological disease condition in which there is a loss of melanin-pigmented cells of the substantia nigra. Blacks have a significantly lower incidence of Parkinson's than whites, and it is believed their higher cutaneous melanin levels act as a preventative against developing the disease
• the significantly lower incidence of Parkinson's in blacks than in whites has "prompt[ed] some to suggest that cutaneous melanin might somehow serve to protect the neuromelanin in substantia nigra from external toxins
• Albino Theory(AT):’One of the notions of melanin theory is that white people are "mutants", that white skin is an aberration, a form of albinism
• Welsing also posits that, because it is so easy for whiteness to be lost genetically during interracial breeding, light-skinned peoples developed an aggressive colonial urge, and their societies militaristically dominated others in order to preserve this light-skinned purity.
• Melanin gives humans the ability to FEEL because it is the absorber of all frequencies of energy. Since whites have the least amount of Melanin, this is why they are perceived by People of Color as generally being rigid, unfeeling (heartless), cold, calculating, mental, and "unspiritual
• Recent studies by Roger Allen at the University of Maryland show that, after being subjected to stress, Blacks exhibit elevated blood pressure at least ten times as long as do Whites. Welsing also claims that the prevalence of high blood pressure among African Americans is due to the fact that melanin exchanges "black photons" with other electrons and, therefore, picks up the negative energy vibrations from white people
• The role that melanin deficiency plays in such disorders remains under study: • Mortality also is increased in patients with Hermansky-Pudlak syndrome and Chediak-Higashi syndrome. Patients with Hermansky-Pudlak syndrome have a bleeding diathesis secondary to platelet dysfunction and also experience restrictive lung disease (pulmonary fibrosis), inflammatory bowel disease, cardiomyopathy, and renal disease. Patients with Chediak-Higashi syndrome are susceptible to infection and also can develop lymphofollicular malignancy.[10]
• The evidence is that melanin concentrating hormone (MCH) binds chemically to receptors in the brain to amplify addiction response. A 2008 study of cocaine addiction in rats conducted by researchers at Johns Hopkins University School of Medicine found: there is an established link between one aspect of melanin-related biology and drug and alcohol. Also, Injecting MCH potentiates cocaine-induced hyperactivity in mice. Mice lacking MCH1R exhibit decreased cocaine-induced conditioned place preference, as well as cocaine sensitization
• Additionally, researchers in the journal Pharmacology, Biochemistry and Behavior concluded that, while the mechanism for nicotine addiction is not fully understood, melanin has a "biochemical affinity for nicotine," and that the "greater the amount of melanin people have, the harder it could be for them to quit smoking. Other evidence indicates that "even though African Americans smoke fewer cigarettes than some other groups, they have a higher intake of nicotine from each cigarette
• Eumelanin is found in hair, areola, and skin, and colors hair grey, black, yellow, and brown. In humans, it is more abundant in peoples with dark skin.
• Pheomelanin is also found in hair and skin and is both in lighter skinned humans and darker skinned humans. Pheomelanin also may become carcinogenic when exposed to the ultraviolet rays of the sun.
• Neuromelanin is the dark pigment present in pigment bearing neurons of four deep brain nuclei: the substantia nigra (in Latin, literally "black substance") - • The loss of pigmented neurons from specific nuclei is seen in a variety of neurodegenerative diseases. In Parkinson's disease there is massive loss of dopamine producing pigmented neurons in the substantia nigra.
• Under the microscope melanin is brown, non-refractile and finely granular with individual granules having a diameter of less than 800 nanometers.
• Freckles and moles are formed where there is a localized concentration of melanin in the skin. They are highly associated with pale skin.
• People with gray, blue, and green eyes are more at risk for sun-related eye problems.
• Recent research by J.D. Simon et al.[22] suggests that melanin may serve a protective role other than photoprotection. Melanin is able to effectively ligate metal ions through its carboxylate and phenolic hydroxyl groups, in many cases much more efficiently than the powerful chelating ligand ethylenediaminetetraacetate (EDTA).
• In 1963, D.E Weiss and coworkers reported[23][24][25] high electrical conductivity in a melanin, iodine-doped and oxidized polypyrrole "Black".
• Likewise, melanin is the best sound-absorbing material known[26], because of its strong electron-phonon coupling. This may be related to melanin's presence in the inner ear.
• Suboptimal conditions for the effective polymerization of melanin monomers may lead to formation of lower-molecular-weight, pro-oxidant melanin that is has been implicated in the causation and progression of macular degeneration.
• Recent[update] experiments by researchers at McGill University, Montreal, Canada with mutant yellow-orange mice and human redheads, both with non-functional MC1R, show that both genotypes display reduced sensitivity to noxious stimuli and increased analgesic responsiveness to morphine-metabolite analgetics.[17]
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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posted
Hope you are NOT Homeylu.. . . cause that is a sista that is tight.
Now the bible
quote:Originally posted by Original_Womb/man:
quote:Originally posted by xyyman:
quote:Originally posted by Original_Womb/man:
it was quite obvious to me in my 8th grade biology/psychology class, while studying Mendel's law, how the races game to be.
I realized that whites came from blacks, via Albinism, . . .
The gift of Discernment is just that a gift!
REFLECT on these words of Wisdom.
Matthew 21:16 (King James Version)
And said unto him, Hearest thou what these say? And Jesus saith unto them, Yea; have ye never read, Out of the mouth of babes and sucklings thou hast perfected praise?
and
1 Corinthians 3:1-2
And I, brethren, could not speak unto you as unto spiritual, but as unto carnal, even as unto babes in Christ.
I have fed you with milk, and not with meat: for hitherto ye were not able to bear it, neither yet now are ye able.
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posted
Whites/Jews attempt to obscure their true origins using many different deceptions, to include genetic jargon, yet, it is still very obvious from where they came, and what they hope to CORRECT in the Human Gnome program. [/QB][/QUOTE]
As THEM teaches, they have and are attempting to graft themselves back to the original man. DEEEEEPPPPPP!!!
This thread can not and will not be DEBUNKED!Posts: 35 | From: ATL | Registered: Jan 2010
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posted
^ Yes xyyman, and even this is just the tip of the iceberg. It has been medically proven that a lack of melanin affects the brain in creating many psychological disorders, to include;
Hate doing this to your brother. But let's put this Albino thing to bed and move on to other aspects of the Melanin Theory. Let white people make fools of themselves.. . .if they wish. We are better than that.
Quote: So far, however, the MC1R is the only gene that is known to explain physiological variation in human pigmentation (rather than just rare Mendelian phenotypes such as albinism) (8, 9).
The majority of red-heads are, therefore, compound heterozygote for loss-of function alleles of the MC1R.
In other words the extreme of white people simply "turned it off. . .completely"
from:
The Melanocortin 1 Receptor (MC1R): More Than Just Red Hair JONATHAN L. REES Uni6ersity of Edinburgh, Edinburgh, United Kingdom *Address reprint requests to Professor Jonathan Rees, Dermatology, Uni6ersity of Edinburgh, Lauriston Buildings, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, United Kingdom. E-mail: jonathan.rees@ed.ac.uk Received 6 March 2000; in final form 17 March 2000
I hope we all understand what the above means.
Posts: 12143 | From: When you have eliminated the impossible, whatever remains, however improbable | Registered: Jun 2007
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posted
I believe what the above paper is stating is that ALL humans carry the MC1R genotype. And it is NOT transmistted by Mendelian pattern(cf to Albinism).
The function of MC1R is essentially to "make" Melanin. So in other words this MC1R was there from the beginning of humankind. However as humans moved futher away from the high UV parts of the earth the MC1R essentially ceased to function properly resulting in the extreme of red hair and corresponding de-pigmented skin.
But as MK and others pointed out or asked: WHERE and WHY is the natural environment for such phenotype.
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