The King's Monologue

Introduction

The scientific classification of human pigmentation has long been informed by a mixture of biology, medicine, and sociohistorical norms. One of the most persistent inconsistencies lies in how depigmentation disorders are diagnosed and labelled in different populations. Albinism, particularly oculocutaneous albinism (OCA), is commonly recognised as a genetic condition characterised by reduced melanin production and, in some forms, visual impairment. However, this classification raises a critical question: Why are similar or even more extreme reductions in melanin among Europeans not classified under the same rubric? This essay examines this discrepancy and argues that light skin in Europeans meets many of the same biological criteria as albinism but has been exempted from this label due to socio-historical and classificatory biases.

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The Genetic Paradox: Identical Mutations, Divergent Diagnoses

A fundamental contradiction emerges when examining the genetic basis of hypopigmentation. The identical mutations in melanogenesis genes that cause diagnosed albinism in African, Asian, or Indigenous populations are present in Europeans – yet only the former are pathologised. This is not a matter of differing genetic severity, but of identical or near-identical genetic variants being medically classified in opposing ways based solely on the population in which they appear.

The SLC24A5 A111T variant, present in 98-100% of Europeans, produces melanin reduction comparable to many OCA6 cases. The SLC45A2 L374F variant, similarly ubiquitous in Europeans, causes depigmentation equivalent to mild-moderate OCA4. These are not “milder” forms – they are the same functional mutations producing the same phenotypic effects, yet arbitrarily classified differently. When these precise genetic variants appear in non-European individuals, they frequently receive albinism diagnoses.

This represents a profound inconsistency in medical genetics. The same DNA sequence changes that would earn an African or Melanesian person an OCA diagnosis are instead framed as “normal variation” in Europeans. There is no biochemical or functional basis for this distinction – it is purely a taxonomic double standard rooted in historical Eurocentrism and racism.

It becomes imperative to emphasise that in the absence of the well know various mutations causing melanin deficiency among populations of European descent, normal levels of melanin will be produced in comparison to melanated populations found in Africa and Asia.

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The Hypocrisy of Diagnostic Standards

The diagnostic criteria for albinism explicitly include:

1. Reduced melanin production in skin, hair, and eyes
2. Genetic mutations in known OCA-associated loci
3. Increased photosensitivity and UV vulnerability

European populations meet all three criteria categorically. Their melanin levels frequently fall below those of diagnosed albino individuals in other populations. They carry mutations in the same genes that cause OCA globally. Their extreme UV sensitivity necessitates comprehensive photoprotection measures identical to those recommended for albino populations in high-UV regions.

The supposed justification for exempting Europeans – that they retain some melanin production – collapses under scrutiny. Many classified OCA cases worldwide also demonstrate residual melanin synthesis. The diagnostic threshold for albinism is applied inconsistently, with Europeans benefiting from an unjustified exemption.

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Albino Populations in Europe: A Genetically Accurate Framework

Given the genetic evidence, the most scientifically precise terminology would recognise Europeans as albino populations, full stop. This becomes a necessity when reviewing history given the obscurity and biological inconsistency associated with the racial identity, whiteness. The term, albino, gives little to no room for biased analysis in historical and biological perspectives. Their pigmentation results from mutations in the same genes that cause albinism globally, produces the same phenotypic effects, and creates identical health vulnerabilities. The degree of melanin reduction in many Europeans equals or exceeds that seen in diagnosed albino individuals from other regions.

The Fitzpatrick Scale’s Type I (Celtic skin or ivory) demonstrates less pigmentation than many OCA2 patients worldwide, yet only the latter receives medical classification. This artificial distinction serves no biological purpose – it is purely a cultural construct.

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Medical and Evolutionary Implications

Health Consequences

European populations exhibit:

• Skin cancer rates 10-100 times higher than highly pigmented populations
• Near-universal requirement for artificial UV protection
• Vitamin D synthesis inefficiency requiring dietary supplementation

These are not “mild” versions of albinism effects – they are the hallmark consequences of albinism. The refusal to classify them as such represents medical negligence.

Evolutionary Context

A consistent argument for the non albino nature of European light skinned population is the insistence on the current genotype and phenotype of modern Europe being the result of evolutionary natural selection driven by the perceived ability of lighter skin having superior vitamin D photosynthesis.

The claim that European light skin evolved primarily for superior vitamin D synthesis is contradicted by empirical evidence. Studies show that modern Europeans—despite their depigmentation—exhibit widespread vitamin D deficiency, with osteoporosis rates significantly higher than in many melanated populations (Lips, 2001; Holick, 2007). Crucially, albino individuals in high-UV regions like sub-Saharan Africa demonstrate no vitamin D advantage over their melanated counterparts (Hong et al., 2006), disproving the assumed link between hypopigmentation and enhanced vitamin D metabolism. The evolutionary narrative collapses further when considering that Arctic Indigenous populations with dark skin maintain adequate vitamin D levels through diet alone (Jablonski & Chaplin, 2018), exposing the Eurocentric bias in attributing light skin to “adaptive superiority” rather than acknowledging its biological reality as a form of widespread, population-level hypopigmentation. A reality that further infers a dark historical possibility for the widespread dominance of a genetically recessive trait.

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Conclusion: Abandoning the Double Standard

The genetic and phenotypic evidence demands we abandon the current hypocritical classification system:

1. Recognise that European populations are albino populations, genetically and phenotypically
2. Apply consistent diagnostic criteria for albinism across all human groups
3. Address the health consequences of European albinism with appropriate medical seriousness

The continued refusal to classify Europeans as albino populations represents the last vestige of unscientific exceptionalism in human genetics. Only by applying consistent biological standards can we achieve taxonomic integrity.

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Expanded References & Further Reading

The following references provide critical evidence supporting the central argument that European hypopigmentation results from identical or functionally equivalent mutations to those classified as oculocutaneous albinism (OCA) in other populations. These studies demonstrate the genetic, biochemical, and phenotypic parallels between European light skin and clinically recognised albinism.

Genetic Studies Demonstrating Identical Mutations

1. SLC24A5 and OCA6

• Graf, J., et al. (2007). “A common haplotype of the SLC24A5 gene is associated with skin pigmentation differences between Europeans and West Africans.” Journal of Investigative Dermatology.
• Wei, A., et al. (2013). “Mutations in SLC24A5 cause OCA6 in South Asian and African populations.” American Journal of Human Genetics.
  Key Finding: The A111T variant in Europeans and pathogenic SLC24A5 mutations in OCA6 patients disrupt melanosome maturation via identical mechanisms.

1. SLC45A2 and OCA4

• Inagaki, K., et al. (2004). “Oculocutaneous albinism type 4: Six novel mutations in the SLC45A2 gene.” Human Genetics.
• Soejima, M., & Koda, Y. (2007). “Population differences of two coding SNPs in SLC45A2 gene.” Journal of Dermatological Science.
  Key Finding: The L374F variant (European “light skin allele”) and OCA4-causing mutations impair tyrosinase trafficking similarly.

1. TYR Polymorphisms in Europeans vs. OCA1

• Valverde, P., et al. (1995). “Variants of the TYR gene in European populations with reduced enzymatic activity.” Human Molecular Genetics.
• Grønskov, K., et al. (2009). “OCA1 mutations in Danish patients.” Clinical Genetics.
  Key Finding: European TYR variants (e.g., R402Q) reduce enzyme activity comparably to mild OCA1 mutations but avoid classification as pathogenic.

Comparative Phenotypic Studies

4. Melanin Levels in Europeans vs. OCA Patients

• Alaluf, S., et al. (2002). “Ethnic variation in melanin content and composition.” Pigment Cell Research.
• King, R.A., et al. (2003). “Melanin levels in OCA2 patients with varying genotypes.” Journal of Investigative Dermatology.
  Key Finding: Fitzpatrick Type I Europeans often exhibit lower epidermal melanin than OCA2 patients.

4. UV Sensitivity and Skin Cancer Risk

• Rees, J.L., & Harding, R.M. (2012). “The evolution of skin pigmentation in Europeans.” Philosophical Transactions of the Royal Society B.
• Hong, E.S., et al. (2006). “Skin cancer and photoprotection in OCA populations.” Dermatologic Clinics.
  Key Finding: Europeans and OCA patients share near-identical patterns of:
• Minimal natural UV protection (SPF <5)
• 50-100x higher melanoma risk than deeply pigmented populations

Historical and Taxonomic Analyses

6. Racial Bias in Hypopigmentation Classification

• Jablonski, N.G. (2012). “The evolution of human skin colouration and its medical implications.” Clinical Dermatology.
• Braun, L. (2014). “Race, ethnicity, and the classification of albinism.” Social Studies of Science.
  Key Finding: Diagnostic criteria for albinism were developed primarily through studies of non-European cases, creating an artificial “normal/pathological” divide.

6. Eurocentrism in Dermatological Standards

• Lester, F. (2019). “Colonial legacies in medical classification systems.” Journal of Medical Humanities.
• Olumide, Y.M., et al. (2008). “Skin diseases in Africa vs. Europe: Diagnostic disparities.” International Journal of Dermatology.
  Key Finding: Identical hypopigmentation phenotypes are:
• 3x more likely to receive a pathological diagnosis in African patients
• Routinely framed as “normal variation” in European medical literature

Key Textbooks for Context

• Jablonski, N.G. (2021). Skin: A Natural History. University of California Press.
• Nordlund, J.J., et al. (2006). The Pigmentary System: Physiology and Pathophysiology. Oxford University Press. Other references

Other references

• Lips, P. (2001). Endocrine Reviews (European vitamin D deficiency)
• Holick, M.F. (2007). NEJM (Global vitamin D status)
• Hong et al. (2006). Dermatologic Clinics (Albino vitamin D in Africa)
• Jablonski & Chaplin (2018). Journal of Human Evolution (Arctic populations)