Melasma is caused by melanocytes, the pigment-producing cells in your skin, becoming overactive and depositing too much pigment in patches on the face. Unlike a simple suntan, melasma involves a complex chain reaction between hormones, UV exposure, inflammation, and even the blood vessels beneath your skin. No single trigger is responsible. Instead, several factors converge to create a persistent cycle of excess pigmentation that can be difficult to reverse.
Hormones and Estrogen’s Role
Hormonal shifts are one of the most well-established triggers for melasma, which is why the condition has historically been called “the mask of pregnancy.” Elevated estrogen levels activate melanocytes, increasing both their number and the activity of enzymes that produce pigment. This explains why melasma frequently appears during pregnancy, while taking hormonal birth control, or during hormone replacement therapy.
The role of progesterone is less straightforward. Lab studies show that progesterone can actually slow melanocyte growth, partially counteracting estrogen’s stimulating effects. This may explain why not all hormonal contraceptives trigger melasma equally, and why some people develop it during pregnancy (when both hormones surge) while others don’t. The response appears to be highly individual. In one study, estrogen increased pigment cell activity in melanocytes from only three out of eight donors, suggesting your skin’s sensitivity to hormonal signals varies based on your unique biology.
UV Exposure as a Constant Driver
Ultraviolet light is the single most consistent aggravator of melasma. Sun exposure triggers the same signaling chemicals in skin cells that are found at elevated levels in melasma patches. Your outer skin cells (keratinocytes) respond to UV by releasing chemical messengers that tell nearby melanocytes to ramp up pigment production. In melasma-prone skin, this response is amplified.
What makes UV exposure particularly problematic is that it doesn’t just darken existing patches. It also drives the deeper structural changes in the skin that keep melasma coming back. UV radiation damages the elastic tissue in the dermis, disrupts the barrier between skin layers, and promotes the growth of new blood vessels, all of which feed the cycle of pigmentation. Even brief, incidental sun exposure can reactivate melasma that appeared to have faded.
Genetics and Skin Type
Your genetic background plays a significant role in whether you develop melasma. Between 33% and 50% of people with melasma report that a family member has it too, and studies of identical twins show that the vast majority of twin pairs share the condition. This strong familial pattern suggests inherited differences in how melanocytes respond to hormonal and environmental triggers.
Skin type matters as well. People with medium to olive and darker complexions (Fitzpatrick skin types III and IV) are most commonly affected, accounting for over 75% of participants in melasma clinical trials. These skin types have melanocytes that are naturally more active and responsive, which makes them more susceptible to the hormonal and UV signals that drive melasma. People with very light or very dark skin can still develop melasma, but it is less common at both ends of the spectrum.
Chronic Inflammation Beneath the Surface
Melasma is increasingly understood as more than a cosmetic pigment problem. It involves ongoing, low-grade inflammation in the skin that you can’t see or feel. When researchers examine melasma patches under a microscope, they consistently find clusters of immune cells, including T cells, macrophages, and notably high numbers of mast cells in the deeper layers of skin.
Mast cells are particularly important. When they activate, they release a potent mix of histamine, enzymes, growth factors, and inflammatory signals that directly stimulate melanocytes to produce more pigment. They also interact with sensory nerves in the skin, contributing to a form of neurogenic inflammation that further sustains the pigment-producing environment. This persistent inflammatory backdrop is a key reason melasma is so stubborn. Even after the visible darkening improves, the underlying inflammatory environment can reignite pigmentation with relatively little provocation.
The characteristics of melasma-affected skin closely mirror those of chronically sun-damaged skin: damaged elastic fibers, a disrupted boundary between the outer and inner skin layers, and increased blood vessel density. This overlap suggests that cumulative photodamage sets the stage for melasma in people who are already predisposed.
Blood Vessels and Vascular Changes
One of the less obvious but significant contributors to melasma is increased blood vessel activity in affected skin. A study of 50 women with melasma found that patches had significantly more blood vessels, and those vessels were larger and more elongated compared to nearby unaffected skin. The degree of pigmentation correlated directly with the number of vessels present.
These vascular changes are driven by elevated levels of a growth factor (VEGF) that promotes new blood vessel formation. The additional blood supply may nourish melanocytes and deliver more of the signals that keep them overproducing pigment. This vascular component helps explain why melasma can look more pronounced when your skin is flushed or warm, and why treatments targeting pigment alone sometimes fall short. The blood vessel network underneath acts as a support system for the excess pigmentation.
Medications That Can Trigger Melasma
Certain medications can cause or worsen melasma-like pigmentation. Hormonal contraceptives are the most widely recognized culprit, but anticonvulsant medications such as phenytoin and carbamazepine can also produce brownish-grey facial pigmentation that closely resembles melasma. Roughly 10% of patients on these medications develop clearly defined, symmetrical dark patches on the face and neck. The pigmentation typically fades within a few months after stopping the medication.
Any drug that makes your skin more photosensitive can theoretically worsen melasma by amplifying the effects of UV exposure. If you notice new or worsening facial pigmentation after starting a medication, that connection is worth exploring with your prescriber.
Where Melasma Sits in the Skin
Not all melasma behaves the same way, partly because the excess pigment can settle at different depths. A special UV lamp (Wood’s lamp) can help classify the type. Epidermal melasma sits in the outermost skin layer, appears more defined under the lamp, and generally responds better to topical treatments. Dermal melasma involves pigment that has dropped into the deeper skin layer, looks less distinct under the lamp, and is more resistant to treatment. Most people have a mixed type with pigment at both levels.
In people with very dark skin, the lamp examination is less useful because the high baseline pigment level makes it hard to distinguish melasma patches from surrounding skin. This doesn’t change the underlying causes, but it can affect how the condition is assessed and monitored over time.
Why Melasma Keeps Coming Back
The combination of factors driving melasma is what makes it so persistent. Hormonal sensitivity primes your melanocytes, UV exposure activates them, chronic subclinical inflammation sustains their activity, and increased blood vessel networks supply the whole process. Treating just one element, say fading the visible pigment, doesn’t address the inflammatory and vascular environment that remains ready to restart the cycle. This is why melasma commonly returns after treatment, especially with renewed sun exposure or hormonal changes. Effective long-term management typically needs to address multiple layers of this process simultaneously.