Melasma on the face is caused by melanocytes (the pigment-producing cells in your skin) going into overdrive, generating far more melanin than surrounding skin. The result is patches of brown, tan, or grey-blue discoloration, most often across the cheeks, forehead, upper lip, and bridge of the nose. What pushes those cells into overdrive is rarely one thing. It’s typically a combination of sun exposure, hormonal shifts, genetics, inflammation, and even increased blood vessel activity beneath the skin’s surface.
Sun Exposure Is the Single Biggest Trigger
Ultraviolet radiation is the most important factor in the development of melasma. When UV light hits your skin, it triggers the production of reactive oxygen species, which are unstable molecules that damage cell membranes and signal melanocytes to ramp up pigment production. UV light also prompts your skin cells to release chemical messengers, including hormones and proteins like endothelin-1, that tell melanocytes to keep producing melanin long after you’ve gone indoors.
What makes melasma particularly stubborn is that standard sunscreens blocking only UVB rays (the ones responsible for sunburn) aren’t enough. Longer wavelengths, including UVA and even visible light in the 320 to 700 nanometer range, also stimulate melanocytes. This is why people with melasma can notice their patches darkening on cloudy days, through car windows, or even from the blue light emitted by screens, and why broad-spectrum protection with iron oxide-tinted sunscreens is often recommended.
Hormones Drive Pigment Production
Hormonal fluctuations are the second most recognized cause, which is why melasma is sometimes called “the mask of pregnancy.” Estrogen and progesterone both directly activate the enzymes melanocytes use to manufacture pigment. When estrogen binds to receptors on melanocytes, it switches on the genes for key pigment-building enzymes, essentially telling the cell to produce more melanin at the genetic level. Progesterone works through a separate but equally powerful pathway, activating a chain of signals that ultimately boosts the same pigment enzymes.
This explains why melasma so frequently appears during pregnancy, when both estrogen and progesterone surge dramatically. It also explains flare-ups linked to hormonal birth control pills, hormone replacement therapy, and IVF treatments. Clinical trial data reflects this hormonal connection clearly: roughly 97% of melasma clinical trial participants are female, though men do develop the condition as well, particularly those with darker skin tones.
Genetics Set the Stage
Your family history plays a larger role than many people realize. In one hospital-based study, 62% of melasma patients had a family history of the condition. A separate global survey found the number closer to 48%. Either way, having a parent or sibling with melasma significantly raises your risk. The genetic component likely influences how reactive your melanocytes are to UV light and hormonal signals, which is why two people with the same sun exposure and hormone levels can have very different outcomes.
Skin tone matters too. People with medium to olive complexions, classified as Fitzpatrick skin types III and IV, are the most commonly affected, accounting for over 75% of patients in clinical studies. Darker skin types (V and VI) are also at elevated risk. Lighter-skinned individuals can develop melasma, but it’s far less common because their melanocytes are generally less active at baseline.
Blood Vessels Beneath the Patches
Melasma isn’t purely a pigment problem. Research has shown that the skin underneath melasma patches contains more blood vessels, and those vessels are larger than in surrounding normal skin. The number of vessels directly correlates with the degree of pigmentation, meaning more blood vessel growth tends to mean darker patches.
These blood vessels aren’t just bystanders. The cells lining them actively release signaling molecules, including endothelin-1 and stem cell factor, that stimulate nearby melanocytes to produce more pigment. UV exposure amplifies this process by activating those same endothelial cells. This vascular component is one reason melasma can be so difficult to treat. Addressing pigment alone without calming the blood vessel activity underneath often leads to recurrence.
Chronic Inflammation in the Skin
A growing body of evidence now frames melasma not just as a pigment disorder but as a chronic inflammatory condition of the skin’s microenvironment. Surrounding skin cells, including keratinocytes (the cells forming your skin’s outer barrier), fibroblasts (the structural cells deeper in the skin), and immune cells all release inflammatory signals that push melanocytes toward overproduction. These signals include growth factors and cytokines that bind to receptors on melanocytes and activate pigment-producing pathways.
Fibroblasts in the deeper dermal layer appear to play a particularly important role. Melasma lesions show overexpression of specific growth factor receptors that are believed to increase pigment production from below. This “crosstalk” between the upper and lower layers of skin helps explain why melasma can involve pigment deposited at different depths, making some cases harder to treat than others.
Thyroid Disorders and Other Medical Links
Thyroid dysfunction, particularly hypothyroidism and autoimmune thyroid disease, shows up more often in people with melasma than in the general population. In one case-control study of women aged 20 to 50, thyroid disorders were present in nearly 38% of those with melasma compared to just 11% of those without it, making the odds of having a thyroid condition almost five times higher if you have melasma. The exact mechanism isn’t fully mapped, but thyroid hormones influence skin cell metabolism and may alter how melanocytes respond to other triggers.
Certain medications can also contribute by making your skin more sensitive to light. Common culprits include some antibiotics (particularly doxycycline and sulfonamides), anti-seizure medications, thiazide diuretics, and certain NSAIDs like piroxicam. Tricyclic antidepressants, some anti-anxiety medications, and the heart drug amiodarone are also known photosensitizers. If you’ve noticed melasma developing after starting a new medication, that connection is worth exploring.
Heat as an Overlooked Trigger
Heat itself, independent of UV light, can worsen melasma. Infrared radiation and high temperatures stimulate melanocytes and promote blood vessel dilation in the skin. This is why some people notice their melasma flaring after cooking over a hot stove, using a sauna, or exercising outdoors in summer. The combination of heat and UV light together is more damaging than either alone, which makes hot, sunny climates particularly challenging for people prone to melasma.
Epidermal vs. Dermal Melasma
Not all melasma sits at the same depth in the skin, and the depth affects both appearance and how well it responds to treatment. Epidermal melasma, where excess pigment is concentrated in the skin’s outer layer, appears as sharply defined brown or black patches. Dermal melasma, where pigment has dropped into the deeper skin layer, looks more like diffuse grey-blue discoloration and doesn’t enhance as clearly under a Wood’s lamp (the ultraviolet light dermatologists use to evaluate pigment depth). Most people have mixed melasma, with pigment at both levels, which is one reason treatment often requires a multi-pronged approach addressing UV protection, inflammation, and pigment simultaneously.