Shrek2OnDvD
I don’t really care x3 ❤️
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@PrinceLuenLeoncur
1. Skin pigmentation does not control vitamin D production.
A 2010 Journal of Investigative Dermatology study from Copenhagen University found that vitamin D levels after UVB exposure depend on baseline vitamin D and cholesterol, not on skin color. Light skin doesn’t make vitamin D faster than dark skin under the same sunlight.
2. “Light skin for vitamin D” was never shown experimentally.
No scientific paper has ever demonstrated that depigmentation genes were selected for vitamin D. It’s an old assumption from before the genetics of pigmentation were known.
3. European lightness comes from known gene mutations—specifically OCA genes.
Every major European pigmentation gene (OCA2, SLC24A5, SLC45A2, TYR, TYRP1, MC1R) belongs to the same biochemical pathway that causes Oculocutaneous Albinism.These mutations disrupt melanin synthesis—not vitamin D metabolism.
4. The same genes that cause “light skin” also cause albinism.
PubMed studies and the University of Minnesota’s Albinism Database list dozens of the same variants—like OCA2 A481T and SLC24A5 A111T.These alleles are common in Europeans but classified as albinism mutations in medical genetics.
5. The blue-eye gene suppresses OCA2.
A 2008 Human Genetics study showed that a mutation in the HERC2 gene shuts down OCA2 expression, creating blue eyes through the same melanin-loss process.That has nothing to do with vitamin D—it’s another albinism-pathway mutation.
6. These depigmenting alleles are recent and regional.
Genome mapping shows the derived “white-skin” allele (like SLC24A5 A111T) is almost fixed in Europe but rare in Africa and Asia, meaning it spread locally after migration out of Africa—not worldwide or as an adaptation.
7. The African genome contains far more variation.
As geneticist Spencer Wells wrote in The Journey of Man, “You are more likely to sample extremely divergent genetic lineages within a single African village than in all the rest of the world.”That means Europeans are simply a small, less-diverse offshoot that fixed certain mutations—not a separate evolutionary path toward better vitamin D absorption.
8. Historical descriptions match albinism traits.
Writers like Tacitus and Herodotus described early northern peoples as red-haired, blue-eyed, very pale, and sun-sensitive—classic features of partial albinism, not a sign of selective adaptation.
9. Depigmenting alleles increase, not decrease, health risks.
SLC45A2 has been identified as a melanoma-susceptibility gene in light-skinned populations.If whiteness evolved for health reasons, it wouldn’t increase vulnerability to UV damage.
10. The “turned white for sunlight” idea reverses cause and effect.
People didn’t lose pigment because they needed more vitamin D. Small isolated groups lost melanin through inherited OCA-pathway mutations that became common through genetic drift and isolation.
What’s actually correct is this:
All humans originated in Africa with fully functional melanin genes.After migration and isolation, some groups accumulated melanin-loss mutations (OCA variants).
These mutations became fixed in small northern populations, producing permanently pale skin.And experiments show no vitamin D advantage for being white—depigmentation is simply a by-product of mutation and genetic drift, not a planned adaptation.
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