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Melanin and Pigmentation: How Skin Color Works and What Causes It to Change

Written by: Lindsey Walsh

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Published on

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Time to read 14 min

Skin color is one of the most visible aspects of human biology — and one of the most biologically complex. The pigmentation of skin, hair, and eyes is determined by melanin, a family of pigment molecules produced by specialized cells called melanocytes. But melanin is not merely cosmetic. It is a sophisticated biological defense system that protects cellular DNA from UV radiation damage — and its behavior in response to UV exposure, hormones, inflammation, and aging underlies a wide range of pigmentation changes that many people experience across their lifetimes.


Understanding melanin — what it is, how it is produced, what regulates it, and what disrupts it — provides the biological foundation for understanding hyperpigmentation, melasma, post-inflammatory pigmentation, the skin effects of cancer treatment, and the ingredients that support healthy, even skin tone.

What Melanin Is

Melanin is a family of biopolymer pigment molecules synthesized from the amino acid tyrosine through a multi-step enzymatic process. The word melanin comes from the Greek melas, meaning black — but melanin exists in a spectrum of colors from yellow-red to dark brown-black, depending on its chemical composition and concentration.


Melanin serves several biological functions beyond pigmentation:

  • UV photoprotection — melanin absorbs UV radiation and converts it to heat, preventing it from damaging DNA in skin cells. This is its primary biological purpose.
  • Free radical scavenging — melanin has antioxidant properties, neutralizing reactive oxygen species generated by UV exposure and other oxidative stressors.
  • Heavy metal chelation — melanin binds heavy metal ions, potentially reducing their toxicity in skin tissue.
  • Structural role — in hair and eyes, melanin contributes to the structural properties of the pigmented tissue. [1]

The Two Types of Melanin

Human skin contains two primary forms of melanin with distinct chemical compositions and biological properties:


Eumelanin — the brown-black form of melanin, dominant in darker skin tones, dark hair, and dark eyes. Eumelanin is produced in larger quantities in response to UV exposure and provides the most effective UV photoprotection. It forms larger, more compact melanosomes that disperse efficiently in keratinocytes, creating broad UV-absorbing caps over cell nuclei. [1]


Pheomelanin — the yellow-red form of melanin, dominant in fair skin, red hair, and light eyes. Pheomelanin provides significantly less UV photoprotection than eumelanin — and paradoxically, some research suggests it can generate reactive oxygen species when exposed to UV radiation, potentially contributing to oxidative damage rather than preventing it. This is one mechanism contributing to the higher skin cancer risk in fair-skinned, pheomelanin-dominant individuals. [2]


Most people produce both types of melanin — the ratio between eumelanin and pheomelanin determines the overall color and UV sensitivity of the skin.


Neuromelanin — a third form found in the brain, not relevant to skin pigmentation.

Melanocytes — Where Melanin Is Made

Melanin is produced by melanocytes — highly specialized cells that represent approximately 5-10% of the cells in the stratum basale (the deepest layer of the epidermis). Melanocytes are dendritic cells — they extend long branching processes (dendrites) into the surrounding keratinocytes, through which they transfer melanin-containing organelles called melanosomes.


The keratinocyte relationship: Melanocytes do not retain the melanin they produce — they transfer it to neighboring keratinocytes through their dendrites. Each melanocyte is in contact with approximately 36 surrounding keratinocytes, forming what is called the epidermal melanin unit. Keratinocytes position the melanosomes as caps over their nuclei — the most UV-sensitive cellular structure — providing targeted protection where it is most needed. [1]


Melanocyte density: The density of melanocytes in the epidermis is relatively consistent across different skin tones — approximately 1,000-2,000 melanocytes per square millimeter. What differs between skin tones is not the number of melanocytes but the size, number, distribution, and melanin composition of the melanosomes they produce. Darker skin has larger, more numerous melanosomes containing more eumelanin; lighter skin has smaller, fewer melanosomes containing more pheomelanin. [2]

How Melanin Is Produced — The Melanogenesis Pathway

Melanin synthesis — melanogenesis — is a multi-step enzymatic process that converts the amino acid tyrosine into melanin through a cascade of chemical reactions.


The key enzyme — tyrosinase: Tyrosinase is the rate-limiting enzyme in melanogenesis — the enzyme that initiates and controls the speed of melanin production. Tyrosinase converts tyrosine to DOPA and then DOPA to dopaquinone, which then branches into either eumelanin or pheomelanin depending on the presence of cysteine.


Tyrosinase activity is the primary target of most skin-brightening and hyperpigmentation-treatment ingredients — inhibiting tyrosinase reduces melanin production and lightens existing hyperpigmentation. [3]


What triggers melanogenesis:

  • UV radiation — the primary physiological trigger. UV exposure activates the p53 tumor suppressor pathway in keratinocytes, which upregulates the production of alpha-melanocyte stimulating hormone (α-MSH). α-MSH binds to the melanocortin-1 receptor (MC1R) on melanocytes, activating tyrosinase and increasing melanin production. This is the molecular mechanism of tanning — a protective response to UV damage. [1]
  • Inflammation — inflammatory cytokines (particularly IL-1, TNF-α, and prostaglandins) stimulate melanocyte activity through multiple pathways. This is the mechanism underlying post-inflammatory hyperpigmentation (PIH) — any inflammatory skin event (acne, eczema flare, injury, aggressive treatment) can trigger excess melanin production in the affected area. [3]
  • Hormones — estrogen, progesterone, and melanocyte-stimulating hormone (MSH) all stimulate melanocyte activity. This hormonal regulation explains melasma — the patchy hyperpigmentation triggered by pregnancy, hormonal contraceptives, and hormone therapy. Cortisol, through its activation of the HPA axis and the POMC precursor system it shares with MSH, can also stimulate pigmentation under chronic stress conditions. [4]
  • ACTH — adrenocorticotropic hormone, produced by the pituitary as part of the stress response, has structural similarity to α-MSH and can stimulate melanocyte MC1R directly. This is one mechanism through which systemic illness and treatment affect pigmentation. [4]

How Melanin Protects Skin

Melanin's primary biological function is UV photoprotection — and the mechanism is elegantly precise.


When UV radiation penetrates the epidermis, it reaches the nucleus of skin cells where it can cause DNA damage — specifically the formation of cyclobutane pyrimidine dimers (CPDs), DNA lesions that, if not repaired, can lead to mutations and eventually skin cancer. Melanin in the keratinocyte's melanosome cap absorbs UV photons before they reach the nucleus, converting their energy to heat and preventing DNA damage.


The quantifiable protection: Studies measuring CPD formation in skin of different Fitzpatrick types show dramatically less UV-induced DNA damage in darker skin types — a direct measure of melanin's photoprotective effect. The protection factor of melanin in dark skin has been estimated at approximately SPF 13.4, compared to SPF 3.4 in lighter skin — a meaningful difference but also an important reminder that melanin is not a substitute for topical sunscreen in any skin tone. [2]


Beyond UV absorption: Melanin's antioxidant properties provide additional protection against the reactive oxygen species generated by UV radiation that escape melanin's direct absorption — neutralizing free radicals that would otherwise damage cellular proteins, lipids, and DNA.

Fitzpatrick Skin Types — The Biological Meaning

The Fitzpatrick scale, developed by dermatologist Thomas Fitzpatrick in 1975, classifies skin into six types based on its response to UV exposure:


Type I — Very fair, always burns, never tans. Predominantly pheomelanin. Type II — Fair, usually burns, sometimes tans minimally. Type III — Medium, sometimes burns, always tans gradually. Type IV — Olive/medium brown, rarely burns, always tans well. Type V — Dark brown, very rarely burns, tans very easily. Type VI — Very dark brown/black, never burns, deeply pigmented. Predominantly eumelanin. [2]


The Fitzpatrick type reflects both the melanin composition (eumelanin vs. pheomelanin ratio) and the melanosome characteristics of the skin. It has important practical implications for:

  • Skin cancer risk — Types I-III carry significantly higher risk of UV-induced skin cancers
  • Hyperpigmentation tendency — Types IV-VI are more prone to post-inflammatory hyperpigmentation because their melanocytes are more reactive
  • Treatment response — laser and light-based treatments, chemical peels, and some topical actives behave differently across Fitzpatrick types
  • SPF needs — all Fitzpatrick types benefit from daily SPF, though the consequences of inadequate protection are different across the spectrum [2]

What Causes Uneven Pigmentation

The Bottom Line

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What Causes Uneven Pigmentation

Pigmentation becomes uneven when melanocyte activity becomes dysregulated — either overactive (hyperpigmentation) or underactive/absent (hypopigmentation or depigmentation) in localized areas.

  • Hyperpigmentation — excess melanin production in defined areas, producing patches, spots, or diffuse darkening darker than the surrounding skin. Causes include UV exposure, inflammation, hormonal stimulation, and certain medications and medical treatments.
  • Hypopigmentation — reduced melanin in defined areas, producing patches lighter than the surrounding skin. Causes include post-inflammatory processes (paradoxically, inflammation can produce either hyper- or hypopigmentation depending on its severity and the depth of involvement), certain infections, nutritional deficiencies, and medical treatments. [3]
  • Depigmentation — complete loss of melanin in defined areas, producing white patches. The clearest example is vitiligo, an autoimmune condition in which the immune system attacks melanocytes.



The Major Pigmentation Conditions

Melasma 

Patchy brown or grayish-brown hyperpigmentation typically affecting the cheeks, forehead, upper lip, and chin. Melasma is driven by the combination of hormonal stimulation (estrogen, progesterone, MSH) and UV exposure — either can occur alone without producing melasma, but their combination produces characteristic and often stubborn pigmentation. It is most common in women during pregnancy, while using hormonal contraceptives, or during perimenopause. [4]


Melasma is notoriously difficult to treat because it involves both epidermal (superficial, more responsive to treatment) and dermal (deeper, less responsive) melanin deposition. Consistent SPF use is the single most important management strategy.


Post-Inflammatory Hyperpigmentation (PIH) 

Hyperpigmentation that follows any inflammatory skin event — acne, eczema flares, psoriasis, injury, aggressive skincare treatments, or medical procedures. PIH occurs when the inflammatory process stimulates melanocyte activity, producing excess melanin in the affected area that persists after the inflammation has resolved. [3]


PIH is more pronounced in darker Fitzpatrick skin types (IV-VI) where melanocytes are inherently more reactive to inflammatory stimuli. It can persist for months to years without treatment and is significantly worsened by UV exposure.


Solar Lentigines (Age Spots)

Flat, well-defined brown spots that develop on sun-exposed areas (face, hands, décolletage) with accumulated UV exposure. Solar lentigines represent localized areas of increased melanocyte density and activity from years of UV stimulation — they are a direct marker of cumulative UV exposure and photoaging. [1]


Vitiligo

An autoimmune condition in which the immune system destroys melanocytes in localized areas, producing well-defined white patches of complete depigmentation. Vitiligo affects approximately 1-2% of the population across all skin tones — it is more visually apparent in darker skin types but occurs at similar rates across Fitzpatrick types. [2]


Radiation-induced pigmentation changes

Covered in detail in the cancer treatment section below — radiation produces specific and distinct pigmentation changes in the treatment field that follow a characteristic timeline.





Is Pigmentation Different in Different Skin Tones?

Yes — significantly, and in ways that have important practical implications for treatment and prevention.

  • Melanocyte reactivity: Melanocytes in darker skin tones (Fitzpatrick IV-VI) are more reactive — they produce more melanin in response to the same UV dose, inflammatory stimulus, or hormonal signal than melanocytes in lighter skin. This explains why PIH is more pronounced and persistent in darker skin: the melanocytic response to inflammation is both stronger and longer-lasting. [3]
  • Melanosome characteristics: Darker skin contains larger, more numerous, individually dispersed melanosomes that provide superior UV protection. Lighter skin contains smaller, fewer, clustered melanosomes with less photoprotective capacity.
  • Photoaging pattern: The superior photoprotection of darker skin produces a different aging pattern — less UV-induced collagen degradation, fewer wrinkles, and later development of solar lentigines. However, darker skin types develop hyperpigmentation more readily, making even-tone maintenance a more significant concern than in lighter skin.
  • Treatment sensitivity: Many laser and light-based pigmentation treatments (IPL, some lasers) carry higher risk of post-treatment PIH in darker skin types because the energy can stimulate rather than selectively destroy melanin. Treatment approaches must be calibrated for Fitzpatrick type.
  • SPF in all skin tones: A persistent misconception is that darker skin does not need SPF because its melanin provides sufficient protection. The SPF equivalent of melanin in dark skin (approximately SPF 13) provides meaningful but insufficient protection for prolonged or repeated UV exposure. Skin cancer rates are lower in darker skin types but survival rates are worse — partly because late diagnosis is more common due to the "I don't need SPF" misconception. All Fitzpatrick types benefit from daily broad-spectrum SPF. [2]




How Pigmentation Changes With Age

Pigmentation changes throughout the lifespan in characteristic and predictable ways.


Childhood and early adulthood:

Melanocyte density is relatively stable and melanin production is primarily driven by UV exposure. Even skin tone with predictable tanning and fading is characteristic.


Reproductive years:

Hormonal cycling produces cyclical variation in melanocyte activity — many women notice increased sensitivity to pigmentation triggers in the perimenstrual period when estrogen and progesterone fluctuate. Melasma may develop with pregnancy or hormonal contraceptive use.


Perimenopause and menopause:

Estrogen's regulatory influence on melanocyte activity is lost — melanocyte behavior becomes less regulated and more reactive to UV and inflammatory stimuli. Existing melasma may worsen; new solar lentigines develop more readily; skin tone becomes progressively more uneven. The simultaneous thinning of the epidermis means the melanin that remains is distributed in a thinner layer, potentially altering its appearance. [4]


Late life:

Melanocyte density progressively declines with age — the number of functional melanocytes in the epidermis decreases by approximately 8-20% per decade after age 30. Paradoxically, this can produce both areas of hyperpigmentation (where remaining melanocytes are overactive) and areas of hypopigmentation (where melanocytes have been lost entirely), producing the characteristically uneven tone of aged skin.


Hair graying reflects the same process in hair follicle melanocytes — the progressive loss of melanocyte function in the hair matrix produces the transition from pigmented to gray and eventually white hair. [1]


Cancer Treatment and Pigmentation

Cancer treatment affects pigmentation through multiple mechanisms — some direct, some indirect — producing a range of characteristic changes that are important for patients and caregivers to understand.


Chemotherapy: Many chemotherapy agents produce hyperpigmentation through direct stimulation of melanocyte activity or through their effects on the hormonal and inflammatory environment.

  • Diffuse hyperpigmentation — generalized darkening of the skin, most pronounced on sun-exposed areas, affecting 2-20% of patients depending on the agent. Commonly associated with busulfan, bleomycin, cyclophosphamide, and 5-fluorouracil.
  • Nail hyperpigmentation — darkening of nails, often in a banded pattern, associated with several chemotherapy agents.
  • Mucous membrane pigmentation — darkening of the oral mucosa and tongue.
  • The mechanism — chemotherapy-induced adrenal insufficiency can elevate ACTH, which stimulates melanocyte MC1R directly. Inflammatory cytokines from treatment-induced tissue damage further stimulate melanogenesis. [5]

Radiation therapy: Radiation produces predictable, staged pigmentation changes within the treatment field:

  • Acute (during treatment): Erythema followed by tanning-like hyperpigmentation in the radiation field, reflecting direct UV-like stimulation of melanocytes and radiation-induced inflammation. The darkening typically appears within the first 1-2 weeks of treatment.
  • Subacute (weeks to months after): Hyperpigmentation typically deepens before beginning to fade in many patients. In some areas, particularly those receiving higher doses, permanent hyperpigmentation develops.
  • Late effects: Some radiation fields develop permanent hyperpigmentation; others develop hypopigmentation as melanocytes in the heavily irradiated area are permanently damaged or destroyed. The pattern depends on radiation dose, field size, skin type, and individual response. [5]

Hormone therapy: Aromatase inhibitors and tamoxifen affect pigmentation through their modulation of estrogen signaling. Estrogen's regulatory effect on melanocyte activity is reduced, potentially improving existing melasma in some patients while altering the hormonal tone that affects overall skin pigmentation. Individual responses vary significantly. [4]


Targeted therapy: Some targeted therapies — particularly BRAF inhibitors (vemurafenib, dabrafenib) used in melanoma treatment — can produce paradoxical melanocyte activation and new pigmented lesion development as an on-target side effect of their mechanism of action. Regular skin monitoring is part of the management of patients on these agents.


Immunotherapy: Checkpoint inhibitors can produce immune-related vitiligo — depigmentation driven by the same immune activation that makes these therapies effective against melanoma. The development of treatment-associated vitiligo in melanoma patients treated with checkpoint inhibitors has been correlated with improved treatment outcomes in some studies — an interesting intersection of immune activation, pigmentation biology, and oncology. [5]


Ingredients That Support Healthy Pigmentation

Tyrosinase inhibitors — reduce excess melanin production:

  • Kojic acid — naturally derived from fungal fermentation, well-documented tyrosinase inhibitor. Found in the Turmeric Therapy Bar where it contributes to the formula's complexion-evening properties.
  • Niacinamide — inhibits the transfer of melanosomes from melanocytes to keratinocytes (a different mechanism from tyrosinase inhibition), reducing surface pigmentation without affecting melanin production itself.
  • Vitamin C — inhibits tyrosinase and has additional antioxidant properties that reduce the oxidative stimulation of melanogenesis.
  • Licorice root extract (Glycyrrhiza) — contains glabridin, a potent tyrosinase inhibitor with anti-inflammatory properties. Found in the Gentle Cleanser.
  • Azelaic acid — inhibits tyrosinase specifically in hyperactive melanocytes with relatively less effect on normally functioning ones — making it useful for pigmentation conditions without causing overall lightening.

Anti-inflammatory ingredients — reduce PIH triggers:

Any ingredient that reduces skin inflammation reduces the inflammatory stimulus for excess melanin production. Niacinamide, chamomile (Chamomilla Recutita), allantoin, and bisabolol — all found across the Juventude range — reduce the inflammatory cascades that trigger PIH. [3]


SPF — prevents UV-triggered melanogenesis:

Sun protection is the most important single intervention for both preventing new hyperpigmentation and preventing the worsening of existing pigmentation. UV exposure is a required co-factor for most hyperpigmentation conditions, including melasma and PIH — consistent SPF use significantly slows their development and progression.


Retinoids — accelerate pigment turnover:

By accelerating epidermal cell turnover, retinoids help shed hyperpigmented cells faster, improving the rate of PIH resolution and the appearance of uneven skin tone. Retinoids also inhibit tyrosinase and reduce the transfer of melanosomes to keratinocytes.


The Bottom Line

Melanin is a family of pigment molecules produced by melanocytes that serves as the skin's primary UV photoprotection system — absorbing UV radiation before it reaches and damages cellular DNA. The ratio of eumelanin to pheomelanin determines skin tone and UV sensitivity. Melanocyte activity is regulated by UV exposure, inflammation, hormones, and stress — disruptions to any of these regulatory inputs produce the hyperpigmentation, hypopigmentation, and uneven tone that represent some of the most common and persistent skin concerns. Cancer treatment affects pigmentation through direct melanocyte stimulation, hormonal disruption, inflammatory mechanisms, and immune activation — producing characteristic changes that vary by treatment type and skin tone. Supporting healthy pigmentation requires both protective strategies (SPF, anti-inflammatory skincare) and corrective approaches (tyrosinase inhibitors, cell turnover support) applied consistently over time.




Array of antioxidant-rich plants for skincare products

This article is for educational purposes only and does not constitute medical advice. Consult with healthcare professionals before starting any new skincare regimen, especially if you have existing skin conditions or are undergoing medical treatment.

Image of Lindsey Walsh, Founder of Juventude

The Author: Lindsey Walsh

Lindsey is founder and CEO of Juventude. A breast cancer survivor and cancer advocate. Lindsey built Juventude to provide effective skin care based on antioxidant-rich plants and without endocrine disrupting toxins. 

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References

  1. Brenner M, Hearing VJ. "The protective role of melanin against UV damage in human skin." Photochemistry and Photobiology, 2008; 84(3):539-549. https://doi.org/10.1111/j.1751-1097.2007.00226.x
  2. Tadokoro T, et al. "Mechanisms of skin tanning in different racial/ethnic groups in response to ultraviolet radiation." Journal of Investigative Dermatology, 2005; 124(6):1326-1332. https://doi.org/10.1111/j.0022-202X.2005.23760.x
  3. Passeron T, et al. "Hyperpigmentation disorders." Journal of the European Academy of Dermatology and Venereology, 2020; 34(Suppl 3):2-10. https://doi.org/10.1111/jdv.16242
  4. Filoni A, et al. "Melasma: Causes and management." Dermatology and Therapy, 2022; 12(8):1945-1956. https://doi.org/10.1007/s13555-022-00760-6
  5. Sibaud V. "Dermatologic reactions to immune checkpoint inhibitors." American Journal of Clinical Dermatology, 2018; 19(3):345-361. https://doi.org/10.1007/s40257-017-0336-3
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