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Washington’s Dermatology Divide Is Leaving Rural Patients Behind

26 Best Small Towns in Washington State with Tons of Character - The Emerald Palate

If you live in Seattle, getting a weird mole or rash checked out by a dermatologist might just mean a quick trip across town. But if you live in a small town in eastern Washington—or don’t have a car, reliable internet, or time off work—that same appointment could take months to get and hours to reach. For many people in our state, especially in rural areas, skin care just isn’t easy to access.

And that’s a problem. Skin conditions aren’t always just about appearance—they can be uncomfortable, painful, or even life-threatening. Skin cancer, for example, is one of the most common cancers in the U.S., but it’s also one of the most treatable when caught early. Yet in rural areas, access to dermatologists is alarmingly scarce—with only 0.085 dermatologists per 100,000 people, compared to 4.11 per 100,000 in urban regions across Washington and Oregon. So why are so many Washingtonians still waiting to get care?

Here’s where teledermatology can help. It’s a fancy word, but the idea is simple: it’s a way for skin doctors (dermatologists) to look at rashes, moles, acne, and other skin issues through photos or video calls instead of in-person visits. Patients can send in pictures of their skin problem or meet with a doctor over a video call to get answers without needing to leave their home.

During the COVID-19 pandemic, teledermatology took off out of necessity—and it worked surprisingly well. Many skin issues are visible, which makes them easier to diagnose from a screen than, say, a heart condition. And patients who used telehealth often said they liked it. It saved them gas money, time off work, and long drives just to get care.

But now that we’re out of the emergency phase of the pandemic, we risk losing a good thing. Not everyone in Washington can access teledermatology easily. In some rural towns, there’s no reliable internet. Some insurance plans still don’t cover online dermatology visits the same way they cover in-person ones. And some people—especially older adults—don’t feel confident using video calls or sending pictures from a phone or tablet.

That’s why we need to do more. If Washington wants to make sure everyone has a fair shot at getting skin care, we need to invest in a few key things:

Better internet in rural areas so more people can use telehealth tools.
Fair insurance rules that cover online dermatology visits just like in-person ones.
Community telehealth hubs in places like libraries or clinics, where people can go for private, internet-connected appointments—even if they don’t have the technology at home.
Help for patients who aren’t used to using apps or video calls, so they feel comfortable getting the care they need.

This isn’t just about convenience—it’s about fairness. Everyone deserves to get medical help, whether they live in downtown Seattle or a small farming town. Skin health affects our comfort, our confidence, and sometimes even our lives. No one should have to wait months, drive hours, or skip care because the system makes it too hard.

Teledermatology won’t replace every in-person visit. Sometimes a mole needs to be biopsied, or a condition needs to be seen under special lighting. But for many common issues, remote care can be just as good—and a lot more accessible.

Washington has the chance to lead the way in making teledermatology part of our normal healthcare system. The technology is here. The doctors are willing. The only question is whether we’ll make the changes needed to connect more people to care.

Where you live shouldn’t determine whether you get timely, potentially life-saving care. Washington has the tools to close this gap—starting with teledermatology. Now we just need the will to use them.

Sources:

Serra-García, Marta, et al. Urban versus Rural Utilization of Teledermoscopy in Self‑Skin Examinations: A Cohort Study in Oregon and Washington. Dermatology Reports, vol. 15, 2023. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10327663/

Rise of Teledermatology in the COVID‑19 Era: A Pan‑World Perspective. Digital Health, 2022. https://pubmed.ncbi.nlm.nih.gov/35154805/

Centers for Disease Control and Prevention. Melanoma of the Skin Statistics. Updated June 10, 2025. https://www.cdc.gov/skin-cancer/statistics/index.html

Featured

Do Hormones Actually Cause Acne? A Look at the Biochemistry

Acne is one of the most common skin conditions in the world—yet also one of the most misunderstood. You’ve probably heard people casually blame it on “hormones” or reassure you that it’ll just go away with time. But what does that actually mean? What role do hormones really play in acne—and why doesn’t it always disappear on its own? In this post, we’ll break down the biochemistry behind hormonal acne and explore how your skin responds to shifts inside your body.

Hormones are chemical messengers that help regulate everything from growth to mood to skin health. During puberty or hormonal shifts, the body produces more androgens—a group of hormones that includes testosterone. Androgens are central during puberty, driving physical changes like hair growth and voice development.

In the skin, androgens stimulate sebaceous (oil) glands, telling them to produce more sebum—the oily substance that moisturizes skin. But too much sebum can clog pores, especially when mixed with dead skin cells and bacteria.

Once a pore becomes clogged, it creates the perfect environment for a normally harmless skin bacterium called Cutibacterium acnes to multiply. As the bacteria break down the trapped sebum, they release byproducts that irritate the surrounding skin. This triggers an immune response—your body sends white blood cells to the area, leading to inflammation, redness, and the formation of pimples.

In short, androgens kickstart a chain reaction: more androgens → more sebum → clogged pores → bacterial overgrowth → inflammation.

This explains why acne often appears during puberty and flares up during hormonal changes like menstrual cycles and pregnancy.

But it also explains why acne doesn’t always “just go away.” If your hormone levels remain imbalanced or your skin is particularly sensitive to even normal levels of androgens, breakouts can persist well into adulthood.

Since hormonal acne starts beneath the skin, surface-level treatments (like cleansers) often aren’t enough. Here’s how treatments target the root cause:

1. Regulating Androgens

Oral contraceptives (birth control pills): Medications that contain synthetic versions of estrogen and progesterone, which help balance hormone levels and reduce excess androgens that trigger oil production.
Spironolactone: A medication that blocks androgen receptors in the skin, reducing oil production.

2. Clearing Clogged Pores & Killing Bacteria

Topical retinoids: Vitamin A derivatives that unclog pores and normalize skin turnover.
Benzoyl peroxide: A topical antibacterial that kills C. acnes bacteria and reduces inflammation.

3. Controlling Inflammation

Niacinamide: A gentler anti-inflammatory that can reduce redness and oil production.
Azelaic acid: Fights bacteria and calms post-acne hyperpigmentation, especially useful for sensitive or darker skin types.

Why Everyone’s Acne Looks Different

Not everyone’s skin reacts to hormones the same way—and that’s where genetics, skin type, and even lifestyle come into play. Some people have sebaceous glands that are more sensitive to androgens, while others may produce stickier sebum or shed dead skin cells irregularly, making it easier for pores to get clogged.

Additionally, stress can worsen hormonal acne by increasing cortisol levels, which may indirectly boost androgen activity. Diet, while not a root cause, can also influence acne for some people—high glycemic foods and dairy have been shown in some studies to aggravate breakouts, potentially by affecting insulin and IGF-1 (insulin-like growth factor) levels, which can increase sebum production.

Treating Acne Isn’t One-Size-Fits-All

Because hormonal acne stems from a complex interaction of internal and external factors, what works for one person may not work for another. Dermatologists often take a layered approach—combining hormone-regulating medications with topical treatments and lifestyle changes tailored to each individual’s skin biology.

Takeaway:

Acne isn’t just a cosmetic issue—it’s a visible signal of underlying biochemical activity. Understanding the hormonal science of acne can empower you to seek targeted, science-backed treatments rather than relying on myths or quick fixes. Whether you’re a teen navigating puberty or an adult dealing with stubborn breakouts, knowing the “why” behind your acne is the first step toward long-term, effective solutions.

Sources:

“Androgens.” Cleveland Clinic, 28 Feb. 2023, https://my.clevelandclinic.org/health/articles/22002-androgens. Accessed 4 June 2025.

“Hormonal Acne.” Cleveland Clinic, 9 May 2022, https://my.clevelandclinic.org/health/diseases/21792-hormonal-acne. Accessed 4 June 2025.

Progesterone. ScienceDirect, https://www.sciencedirect.com/topics/psychology/progesterone. Accessed 4 June 2025.

“What Is Hormonal Acne and Why Does It Happen?” Columbia Skin Clinic, 18 July 2022, https://columbiaskinclinic.com/medical-dermatology/hormonal-acne-what-it-is-and-why-it-happens/. Accessed 4 June 2025.

Featured

The Cost of Being Unheard in Washington’s Healthcare System

Racism in healthcare is “Undeniable, irrefutable—the data is there.” Those were the words of Dr. Benjamin Danielson, one of Seattle’s most respected pediatricians. In 2020, he resigned from Seattle Children’s Hospital, citing years of systemic racism and prejudice against healthcare workers and patients. Last December, a jury awarded him $21 million in non-economic damages. But his victory is not just personal—it’s a wake-up call for Washington’s healthcare system and a reminder that for many patients of color, being unheard can be fatal.

Dr. Benjamin Danielson: 'Profound trauma and joy can coexist ... — Dr. Ben Danielson

Seattle Children’s delayed the release of its internal racism investigation for over a year—an act that deeply undermined public trust. That investigation reportedly confirmed the very patterns of racial harm that Dr. Danielson and others had long described. During the trial, the jury was presented with evidence of racial discrimination directed not only at Dr. Danielson but also at his colleagues and the hospital’s patients and families. This reveals a critical truth: racism in healthcare is systemic, institutional, and impacts both providers and patients. When hospitals allow these patterns to persist, they not only fail their staff but also endanger the very communities they are meant to serve.

16-year-old Sahana Ramesh’s tragic story reinforces the implicit racial biases embedded in our healthcare institutions. Sahana was a bright and healthy teenager living in Bothell, Washington, when she developed painful rashes and swelling on her face, hands, and feet. Her family urgently took her to the ER at Seattle Children’s Hospital, where she was diagnosed with DRESS—a rare and severe drug reaction.

Discrimination and negligence at Seattle Children's hospital led to teen's death, family alleges in lawsuit | CNN — Sahana and her mother

As her symptoms worsened, her parents desperately called the hospital 16 times and sent 22 emails in search of answers. Yet despite Sahana’s exacerbating health and her family’s urgent pleas, they were repeatedly downplayed by clinicians. By the time she and her family were taken seriously, it was too late. Sahana’s death is not an isolated incident—it is part of a pattern in which the concerns of patients of color are too often dismissed or deprioritized. “Evidence shows that if Sahana and her parents had been white, they would have had a better chance of getting admitted to the hospital,” as the Rameshs’ attorney, Martin McLean, asserted. Her story, like Dr. Danielson’s, reveals the life-threatening consequences of implicit bias and institutional neglect.

These disparities extend beyond emergency care and into specialized fields like dermatology, where racial bias begins in medical training. “Physicians must identify conditions from photos of skin in textbooks or shared in the classroom. But most of the patients in those images are white, and only 4.5% of the images show dark skin,” states dermatologist Jasmine Onyeka Obioha, MD. As a result, clinicians often struggle to diagnose conditions in patients whose appearances and symptoms fall outside of the narrow standards they were taught, leading to higher rates of misdiagnosis among patients of color. In fact, “Women and racial and ethnic minorities are 20% to 30% more likely than white men to experience a misdiagnosis,” said Johns Hopkins professor David Newman-Toker. This becomes especially dangerous in communities like South Seattle, where many families of color reside and access to dermatologists familiar with diverse skin tones remains limited.

To begin addressing these failures, Washington’s healthcare institutions must change structurally. Hospitals like Seattle Children’s must promote an ethnically inclusive workforce and improve patient advocacy systems—so that when families like Sahana’s speak up, they are heard, regardless of their background or race. Medical schools—including the University of Washington—must diversify their curricula by incorporating diagnostic imagery that equitably represents all skin tones—not just white skin.

Beyond a legal reckoning, the Seattle Children’s verdict was a stark reflection of the failures embedded in our healthcare institutions. If we don’t respond with urgency and structural reform, we risk repeating the same harm to the patients, families, and communities who need care the most.

Bibliography

Recht, Hannah. “Misdiagnosed: Women and People of Color Face Widespread Medical Diagnostic Errors.” KFF Health News, 26 Feb. 2024, https://kffhealthnews.org/news/article/medical-misdiagnosis-women-minorities-health-care-bias/.

Cedars-Sinai. “Why Skin Issues in Patients of Color Are Neglected, Mistreated.” Cedars-Sinai Newsroom, 1 Mar. 2023, https://www.cedars-sinai.org/newsroom/why-skin-issues-in-patients-of-color-are-neglected-mistreated/.

Crowder, Madison Wade. “Bothell Family Alleges Racism at Seattle Children’s Hospital in Daughter’s Death.” KING 5 News, 12 Dec. 2023, https://www.king5.com/article/news/investigations/investigators/bothell-family-alleges-racism-seattle-childrens-hospital-daughters-death/281-50d708b3-3b06-422b-a19a-cc3b766d82b6.
Schroeter Goldmark & Bender. “Jury Awards Former Seattle Children’s Doctor $21M in Race Discrimination Lawsuit.” SGB Law, 19 Dec. 2024, https://sgb-law.com/news/jury-awards-former-seattle-childrens-doctor-21m-in-race-discrimination-lawsuit.

Williams, Race and Justice Reporter Erica. “Dr. Ben Danielson Speaks out on Systemic Racism in Health Care.” KING 5 News, 18 Dec. 2020, https://www.king5.com/article/news/community/facing-race/doctor-ben-danielson-seattle-childrens-hospital-systemic-racism-health-care/281-94b16198-3c41-4db8-96d1-1dfc257d98e5.

Featured

Botox Explained: How a Neurotoxin Became a Beauty Staple

In 2022, over 9 million Botox injections were given worldwide, making it one of the most popular cosmetic treatments today. Known for its ability to reduce wrinkles and give skin a smoother, younger appearance, Botox is particularly popular among celebrities looking to maintain a youthful appearance. But what exactly is Botox, and how does it work?

What is Botox?

Botulinum toxin, or Botox, is a neurotoxic protein derived from a bacteria known as bacterium Clostridium botulinum. Neurotoxic proteins are substances that disrupt the function of the nervous system. Botulinum toxin works by blocking the release of acetylcholine, a neurotransmitter that plays a critical role in muscle contraction, by interfering with the vesicles responsible for releasing acetylcholine. Located in neurons, vesicles are small sacs that store neurotransmitters, like acetylcholine. Botox targets and breaks down the proteins that help these vesicles release acetylcholine, preventing it from being released into the space between the nerve and the muscle.

This prevention of muscle contraction ultimately leads to reduced wrinkles, fine lines, improved skin texture, and overall a more youthful appearance.

While Botox is best known for its cosmetic benefits, it also provides several other medical benefits. This versatile procedure can also mitigate neck spasms and chronic migraines under the same mechanism. Additionally, Botox is effective in treating excessive sweating (hyperhidrosis). Not only is acetylcholine responsible for muscle contraction, but it also plays a key role in triggering sweat production in sweat glands. Botox can be injected in the affected areas, preventing them from producing excess sweat. Botox injections can also treat lazy eye by relaxing the overactive muscle in the eye—specifically, the extraocular muscle, which controls eye movement.

Different muscles vary in size and strength, so they require varying amounts of Botox to effectively relax the target muscle. Botox injections are administered in units, with 1 unit being a standardized measure of biological potency.

Where is Botox injected?

Botox can be used wherever facial muscles are creating lines. Here are the most common injection sites:

Forehead – to relax those horizontal lines that show up when you raise your eyebrows. 10-30 units of Botox.

Between eyebrows (glabella) – to soften the vertical lines caused by frowning. 5-15 units of Botox on each side.

Outer corners of eyes (crow’s feet) – to soften the orbicularis oculi muscles at the outer corners of the eyes. 10-15 units of Botox per side.

Around the mouth – to reduce smile lines (nasalabial folds) by pulling the corners of the mouth down. 3-6 units of Botox on each side.

How long does Botox last?

Botox injections generally last 3 to 4 months, depending on the dosage and site of injection. In areas with more muscle activity, like around the eyes or mouth, the effects of Botox will wear off faster compared to areas with less movement, like the forehead.

Side effects of Botox

As we’ve learned, Botox prevents the release of acetylcholine and ultimately muscle contraction. After injection, the targeted muscle remains entirely inactive for the treatment’s duration—typically 3 to 4 months. This prolonged inactivity can cause muscle atrophy, meaning that the muscle will reduce in mass, size, and strength. Some studies have shown that if a patient continues to undergo Botox injections in the long term, their skin might experience increased susceptibility to sun damage, premature aging, and dehydration. Granted, the current research on the long-term effects of Botox remains inconclusive.

Takeaway:

Known for its effective ability to smooth wrinkles by temporarily paralyzing facial muscles, Botox continues to reign as one of the most popular cosmetic treatments. Beyond aesthetics, Botox also treats medical conditions like migraines, excessive sweating, and muscle spasms. However, while generally safe, long-term use may lead to muscle atrophy and potential skin changes. As with any procedure, it’s important to weigh the benefits against possible risks and consult a healthcare provider for personalized care.

Bibliography

“Botox.” MedlinePlus, U.S. National Library of Medicine, 2 Aug. 2023, https://medlineplus.gov/botox.html.

“Vesicle.” NCI Dictionary of Cancer Terms, National Cancer Institute, https://www.cancer.gov/publications/dictionaries/cancer-terms/def/vesicle.

“What Areas Can Be Treated with Botox?” Westlake Dermatology & Cosmetic Surgery, https://www.westlakedermatology.com/blog/what-areas-can-be-treated-with-botox/.

“The Long-Term Effects of Botox: What Research Says.” Your Laser Skin Care, https://www.yourlaserskincare.com/blog/the-long-term-effects-of-botox-what-research-says.

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Why Skin of Color Still Gets Misdiagnosed — and How We Can Fix It

13,400+ Black Man At Doctors Office Stock Photos, Pictures & Royalty-Free Images - iStock

In 2012, Lauryn Taylor—a Black woman—was misdiagnosed with eczema. Another doctor thought it might be vitiligo. Then came guesses like pityriasis alba or macular hypomelanosis. But none of them were right. In reality, Lauryn had skin cancer—and it took nearly 10 years to get the correct diagnosis.

I'm a Black Woman and My Skin Cancer Was Misdiagnosed for Years — Lauryn Taylor

Let that sink in — for nearly a decade, Lauryn lived with a misdiagnosis while her skin cancer went untreated, simply because her condition wasn’t recognized on darker skin.

Misdiagnosis isn’t just a medical error—it’s a public health crisis with endangering consequences. Diagnosis of the wrong condition can delay the proper treatment, allowing the condition to worsen over time. Dermatologists may prescribe particular creams or medications that can cause irreversible damage.

It’s also emotionally draining. Patients may feel frustrated or anxious when their ‘treatments’ are not working, leaving them feeling hopeless and dismayed. In desperation, patients will keep paying and returning for medical consultations and buying the wrong products/treatments. This becomes a heavy financial burden.

These are licensed physicians, right? Why are so many of them misdiagnosing patients?

“Probably no doctor is intending to do worse on any type of person, but it might be the fact that you don’t have all the knowledge and the experience, and therefore on certain groups of people, you might do worse,” says Northwestern University professor Matt Groh. In fact, it’s not the dermatologists’ fault — it’s the education system.

“A large part of dermatology education involves visual recognition,” states dermatologist Jasmine Onyeka Obioha, MD. “Physicians must identify conditions from photos of skin in textbooks or shared in the classroom. But most of the patients in those images are white and only 4.5% of the images show dark skin.” As a result, most medical students don’t know how to identify the skin conditions of patients of color, leading to a disparity in misdiagnosis among racially and ethnically diverse populations.

However, the misrepresentation of racially/ethnically diverse populations extends beyond dermatology textbooks, reflecting a broader, systemic issue within clinical education and diagnostic training. “Women and racial and ethnic minorities are 20% to 30% more likely than white men to experience a misdiagnosis,” said Johns Hopkins professor of neurology David Newman-Toker. This astounding statistic reveals the racial/ethnic disparities embedded in the foundations of medical training.

It’s no wonder why physicians often struggle to diagnose conditions in patients whose appearances and symptoms fall outside of the narrow standards they were taught.

What can we do?
In order for us to promote racial equality in dermatology/health care and prevent misdiagnoses, we must:

Reform medical education:
As only ~4.5% of dermatology images feature darker skin, we need to bring that number up to at least 30%. This number ensures equitable inclusion and representation of racially and ethnically diverse populations.

We need to incorporate modules tailored to diagnosing and treating conditions presented by racially and ethnically diverse populations into the medical curriculum.

Advocate for change:
Acknowledging the issue and the devastating statistics is the first step. Now, to turn awareness into action, we must collectively raise our voices, educate others, and advocate for meaningful change. People of color deserve to be treated with dignity and equity in the healthcare system.

Available resources:
https://guides.ucsf.edu/c.php?g=1081119&p=9159811

https://skinofcolorsociety.org/

https://www.aad.org/member/career/diversity

Bibliography:

1. UCSF Library. Health Disparities and Skin of Color in Dermatology. University of California San Francisco, 2022, https://guides.ucsf.edu/c.php?g=1081119&p=9159811.

2 Skin of Color Society. Home. https://skinofcolorsociety.org/.

3. American Academy of Dermatology. Diversity, Equity, and Inclusion in Dermatology. https://www.aad.org/member/career/diversity.

4. Miller, Korin. “Doctors Told Me My Skin Cancer Was Eczema for Almost a Decade.” Prevention, 28 May 2021, https://www.prevention.com/health/health-conditions/a36230501/mycosis-fungoides-misdiagnosis/.

5. Kim, Sophia, et al. “Diagnostic Performance of Dermatologists and General Practitioners in Skin Diseases on Diverse Skin Tones.” Nature Medicine, vol. 29, 2023, pp. 1941–1948. https://www.nature.com/articles/s41591-023-02728-3.

6. Loftus, Peter. “Misdiagnosed: Women and Minorities Face Higher Risk of Harm from Medical Errors.” KFF Health News, 15 Dec. 2023, https://kffhealthnews.org/news/article/medical-misdiagnosis-women-minorities-health-care-bias/.

7. Cedars-Sinai. “Why Skin Issues in Patients of Color Are Neglected, Mistreated.” Cedars-Sinai Newsroom, https://www.cedars-sinai.org/newsroom/why-skin-issues-in-patients-of-color-are-neglected-mistreated/.

8. Pew Research Center. Facts About the U.S. Black Population. 9 Feb. 2023, https://www.pewresearch.org/race-and-ethnicity/fact-sheet/facts-about-the-us-black-population/.

9. Massachusetts General Hospital. Skin Assessment in Patients with Dark Skin Tone. Munn Center, Apr. 2023, https://www.mghpcs.org/MunnCenter/Documents/weekly/apr-23/Skin-Assessment-in-Patients-with-Dark-Skin-Tone.pdf.

10. Trafton, Anne. “Doctors Struggle to Diagnose Diseases in Patients with Darker Skin.” MIT News, 5 Feb. 2024, https://news.mit.edu/2024/doctors-more-difficulty-diagnosing-diseases-images-darker-skin-0205.

11. TEDx Talks. “Why Doctors Misdiagnose Skin Conditions on Darker Skin.” YouTube, uploaded by TEDx, 7 Oct. 2022, https://www.youtube.com/watch?v=2JUQo-PnY2g.

Why You Still Burn with SPF 50: The Truth About Sunscreens for Darker Skin Tones

“Why do I keep sunburning with SPF 50 on?” If you’ve said this before, you’re not losing it — and you’re certainly not alone. Dozens of consumers, especially those with medium to dark skin, burn, itch, or develop chronic discoloration after using high-SPF sunscreen. It doesn’t make sense, and it’s infuriating, especially when you’re doing all the right things for sun safety. The truth is that SPF 50 doesn’t offer the absolute protection most believe.

SPF, or Sun Protection Factor, is an index of a sunscreen’s ability to block UVB rays, the kind that creates the sunburn you see. So SPF 50 would, theoretically, allow you to stay out 50 times longer than unprotected skin before burning — if you’d burn in 10 minutes, SPF 50 would last around 500 minutes. SPF, on the other hand, checks for only UVB protection, but not UVA, a critical flaw. UVA rays penetrate deeper into the dermis and induce long-term photodamage in the form of photoaging (wrinkles, loss of elasticity), suppression of the immune system, chronic hyperpigmentation, and skin cancer. Whereas UVB occurs in greatest intensity at noon, UVA occurs all day long, even on cloudy days, and through glass — and represents about 95% of ultraviolet radiation that strikes the Earth’s surface.

As for individuals with darker skin, who may not get sunburned as readily since melanin inherently absorbs UVB radiation, are at increased risk for post-inflammatory hyperpigmentation (PIH). PIH is a common consequence of acne, eczema, or any cutaneous injury, and UVA radiation tans such spots and impairs healing. Since SPF does not indicate UVA protection, someone applying SPF 50 may still experience flare-ups, discoloration, or stinging because their sunscreen is doing little to stop the UVA rays quietly damaging their skin.

Worse yet, in the United States, the FDA’s “broad-spectrum” labeling standards are relatively lenient. As long as a sunscreen has low levels of UVA protection relative to UVB, it qualifies — but that UVA protection may not be enough to prevent PIH or aging. This is unlike the standards in Europe and Asia. In Europe, UVA protection is quantified by the PPD (Persistent Pigment Darkening) system — an excellence designation for a PPD rating of 10–20+. In Japan and Korea, the PA system is used, with PA++++ being the maximum UVA protection.

To protect against both UVA and UVB, more than SPF is needed. Choose sunscreens that contain broad-spectrum filters like zinc oxide or titanium dioxide (physical blockers), or premium chemical filters like Tinosorb S, Tinosorb M, or Mexoryl SX/XL, which are photostable and give efficient coverage for both UVA and UVB spectrums. These ingredients are often present in more European and Asian products, which more clearly disclose UVA protection. For white cast-wary users — a problem on melanin-dense skin — tinted mineral sunscreens provide a more natural-looking blend with continued full-spectrum protection.

Takeaway

If SPF 50 hasn’t been cutting it, perhaps it’s because it wasn’t protecting you from what truly matters in the long term: UVA. For darker skin tones especially, the goal isn’t just to keep sunburn at bay — it’s to keep hyperpigmentation, flare-ups, and aggregated UV damage at bay. Next time you’re on a mission to shop for sunscreen, read past the number on the SPF. Your skin deserves protection that’s in tune with its needs — both on the surface and beneath.

References

“Sunscreen: How to Help Protect Your Skin from the Sun.” U.S. Food and Drug Administration, 10 Oct. 2023, www.fda.gov/drugs/understanding-over-counter-medicines/sunscreen-how-help-protect-your-skin-sun.

“What’s the Difference Between UVA and UVB Rays?” Skin Cancer Foundation, 27 June 2023, www.skincancer.org/blog/whats-the-difference-between-uva-and-uvb-rays.

“How to Apply Sunscreen.” American Academy of Dermatology Association, www.aad.org/public/everyday-care/sun-protection/sunscreen/how-to-apply-sunscreen.

Williams, Kiyanna, MD. “Why Sunscreen Is an Important Tool for People of Color.” Cleveland Clinic Health Library, Cleveland Clinic, 23 May 2024, health.clevelandclinic.org/sunscreen-for-black-people.

“What’s the Difference Between UVA and UVB Rays?” Focused on Health, MD Anderson Cancer Center, n.d., www.mdanderson.org/publications/focused-on-health/what-s-the-difference‑between‑uva‑and‑uvb‑rays‑.h15‑1592991.html.

Moyal, D., A. Chardon, and N. Kollias. “UVA Protection Efficacy of Sunscreens Can Be Determined by the Persistent Pigment Darkening (PPD) Method. (Part 2).” Photodermatology, Photoimmunology & Photomedicine, vol. 16, no. 6, Dec. 2000, pp. 250–255. PubMed, PMID 11132127.“PA ++++ in Sunscreen: What It Means & Why It Matters.” Colorescience Learn, Colorescience, [no date], www.colorescience.com/blogs/learn/what-is-pa?srsltid=AfmBOooy7s7avHhFFs7v6z0hd09als6YQVhIvzcy2beQ1Sl0jrTZlKap

Why Vitiligo Looks So Different on Dark Skin—And Why Doctors Keep Missing It

Vitiligo is a chronic skin condition where the immune system of the body attacks and kills the melanocytes, the pigment cells of the skin. It causes the formation of white patches of pale skin that may appear anywhere on the body. Vitiligo occurs in all races more or less equally but can be more conspicuous—and sometimes more difficult to treat—in darker skin due to the strong color contrast with normal skin. Unfortunately, medical cosmetics and dermatological literature have most often dealt with lighter skin types, leaving both patients and practitioners poorly informed. This article discusses the biology of vitiligo, the way color functions in the skin, and why vitiligo differs in people with darker skin.

What is vitiligo?

Vitiligo is believed to be an autoimmune disease. In other words, the body’s immune system incorrectly attacks the body’s own cells, in this instance called melanocytes. These are cells with a special function in the skin’s lower layer. They produce melanin!

Melanin colors the skin, hair, and eyes. Where melanocytes are lost or are not functioning, the areas involved lose their pigment and turn milky white.

Vitiligo is one of two types: non-segmental (more common and occurs on both sides of the body symmetrically) or segmental (less common and is typically on one side of the body). The disease is neither painful nor contagious but can be devastating to one’s self-esteem.

How Skin Pigmentation Is Formed

In order to find out why vitiligo appears more on darker skin, we have to examine how the skin color is created. Melanocytes produce melanin and package it into small organelles known as melanosomes, which are transported to the surrounding skin cells. We all have roughly the same number of melanocytes, but in darker-skinned individuals, the cells effort more and produce more melanin.

When people with darker skin lose pigment, the contrast between the light spots and the rest of the skin is so much more pronounced. In light skin, the spots may be quite light or pink.

Why Vitiligo Appears So Different on Dark Skin

Dark-skin vitiligo patches tend to be very noticeable and snow white, attracting more attention than they would if they were located on light skin. In fact, most dermatology textbooks and instructional photos of skin diseases show vitiligo in light skin. This contributes to delayed or erroneous diagnosis of the disease in darker patients.

Inequalities in Skin of Color Diagnosis and Treatment

Vitiligo may be misdiagnosed in dark-skinned patients as another skin condition such as tinea versicolor, post-inflammatory hypopigmentation, or chemical leukoderma. This is particularly so for physicians who are not used to dealing with dark skin. After proper diagnosis, treatment may involve creams with corticosteroids, calcineurin inhibitors (such as tacrolimus), and narrowband UVB phototherapy. Depigmentation therapy may be considered for severe cases. But not everyone chooses to get treated. Most individuals would prefer to accept the way they appear and search for makeup products that will enable them to hide their imperfections. Even then, very few makeup or concealer products are suitable for dark skin.

Closing Comments

Vitiligo is not riskier on darker skin but can be readily noticeable, less understood more frequently, and under-treated or mistreated more frequently. Diversity role models, more medical training, and education are the solutions to all of these problems. If you or your relative have vitiligo on darker skin, you need to know that help is growing—and your skin’s narrative needs to be told accurately, sensitively, and with pride.

References

Pietrangelo, Ann. “Vitiligo on Black Skin: What You Should Know.” Medical News Today, Healthline Media, 28 Oct. 2022, https://www.medicalnewstoday.com/articles/vitiligo-black-skin.

Cleveland Clinic. “Vitiligo.” Cleveland Clinic, 13 Oct. 2023, https://my.clevelandclinic.org/health/diseases/12419-vitiligo.

Hitti, Miranda. “What People of Color Should Know about Vitiligo.” WebMD, 6 June 2023, https://www.webmd.com/skin-problems-and-treatments/features/vitiligo-darker-skin-tones.

NHS. “Vitiligo.” NHS, National Health Service UK, 13 Feb. 2024, https://www.nhs.uk/conditions/vitiligo/.

Goldman, Lisa Zamosky. “Vitiligo and People of Color: The Nuances of a Visible Condition.” WebMD, 6 June 2023, https://www.webmd.com/skin-problems-and-treatments/features/vitiligo-poc-nuance.

Biochemical Markers of Psoriasis: What’s Happening Beneath the Skin?

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Often confused with atopic dermatitis, psoriasis is also an incurable chronic skin condition that is characterized by itchy/inflamed and scaly patches of skin. As psoriasis affects ~2% of the United States population, the demand for treatment continues to soar. Unfortunately, psoriasis is a complex autoimmune condition that entails various factors. In this post, we’ll learn about the causes of psoriasis, the role of the immune system in psoriasis, remedies, as well as how it differs from other inflammatory skin conditions like eczema.

What causes psoriasis?

The root causes of psoriasis start with genetics and environmental triggers. This combination is integral for psoriasis, with genetic predispositions endangering the host to an overreactive immune response, which can be provoked by an environmental trigger. Triggers include skin injuries, infections, stress, alcohol, and more.

What happens during a psoriasis flare-up?

Once triggered, the immune system begins to malfunction. Crucial immune cells known as t cells—responsible for fighting off pathogens—become overactive. They begin to mistakenly orchestrate an attack on skin cells, assuming them to be pathogens. First, T cells release cytokines (typically IL-17 and IL-23)—proteins that regulate immune responses and contribute to inflammation. These cytokines then stimulate the overproduction of keratinocytes (skin cells) to try to repair the damage. The basal layer of the epidermis (where keratinocytes are produced) then goes overdrive, resulting in rapid cell division. This manifests as flaky, inflamed, and itchy lesions of the skin of psoriasis.

Here is a flowchart to help demonstrate the process:

Genetic predisposition and environmental triggers

T cells become overactive

T cells release cytokines

Cytokines stimulate keratinocyte overproduction

Visible symptoms of psoriasis (Scaly, itchy plaques)

Psoriasis vs. atopic dermatitis

Psoriasis and atopic dermatitis are both chronic skin conditions that manifest as flaky, inflamed, and itchy patches of skin. However, the difference between these two comes down to their underlying cause. As we’ve learned, psoriasis is an autoimmune condition that involves the immune system mistakenly attacking the body. In contrast, atopic dermatitis is an inflammatory condition involving a defective/hypersensitive skin barrier due to genetic mutation. Although psoriasis can also be triggered by environmental triggers, think of atopic dermatitis as being the direct, inflammatory response to a trigger. Psoriasis, on the other hand, happens because the immune system is already defective and attacking the body’s own skin cells, and outside triggers just make it worse.

Types of psoriasis

Psoriasis can take on several forms, depending on the types of cytokines involved. Accounting for 80-90% of psoriasis cases, plaque psoriasis is the most common form. Primary cytokines involved: IL-17 and IL-23. Manifests as raised, silver-colored, scaly patches of skin. Most commonly forms on the elbows and knees. Psoriasis can also take several other forms, affecting different parts of the body. These include: guttate psoriasis (torso, upper arms, and legs), pustular psoriasis (palms of hands or soles of feet), inverse psoriasis (skin folds), and many more.

Plaque psoriasis

Treatments:

Luckily, scientists have developed various treatment options for psoriasis that work by reducing inflammation and slowing the overproduction of skin cells. Treatments include topical therapies (creams and ointments), light therapy, and oral or injected medications. The best option for each patient depends on the severity of the condition, medical history, and lifestyle.

Conclusion:

Understanding the biochemistry and immunology behind psoriasis reveals the complexity of this abstract, chronic, autoimmune condition. Although there isn’t currently a direct cure for psoriasis, several treatments have been developed to mitigate symptoms, reduce inflammation, and prevent flare-ups. The more we understand the underlying cause of psoriasis, the closer we get to hopefully curing this chronic condition.

Bibliography

American Academy of Dermatology Association. “What Causes Psoriasis?” AAD, https://www.aad.org/public/diseases/psoriasis/what/causes. Accessed 13 Apr. 2025.

Rendon, Adriana, and Benjamin Schäkel. “Psoriasis Pathogenesis and Treatment.” International Journal of Molecular Sciences, vol. 19, no. 5, 2019, p. 1475, https://pmc.ncbi.nlm.nih.gov/articles/PMC5751129/. Accessed 13 Apr. 2025.

National Institute of Arthritis and Musculoskeletal and Skin Diseases. “Psoriasis.” NIAMS, U.S. Department of Health and Human Services, https://www.niams.nih.gov/health-topics/psoriasis. Accessed 13 Apr. 2025.

“Psoriasis.” TeachMe Paediatrics, https://teachmepaediatrics.com/dermatology/dermatology/psoriasis/. Accessed 13 Apr. 2025.

Greb, Jennifer E., et al. “Psoriasis.” International Journal of Molecular Sciences, vol. 20, no. 10, 2019, p. 2558, https://www.mdpi.com/1422-0067/20/10/2558. Accessed 13 Apr. 2025.

Radiant Dermatology. “Psoriasis.” Radiant Dermatology & Skin Cancer Center, https://www.radiantdermtx.com/view-medical-dermatology/psoriasis. Accessed 13 Apr. 2025.

Thomas, Liji. “What Are T Cells?” News Medical, 27 Feb. 2019, https://www.news-medical.net/health/What-are-T-Cells.aspx. Accessed 13 Apr. 2025.

Di Meglio, Paola, et al. “The Role of APCs in Psoriasis Pathogenesis.” Frontiers in Immunology, vol. 6, 2015, https://pmc.ncbi.nlm.nih.gov/articles/PMC4437803/. Accessed 13 Apr. 2025.

WebMD. “Cytokines and Psoriasis.” WebMD, https://www.webmd.com/skin-problems-and-treatments/psoriasis/cytokines-psoriasis. Accessed 13 Apr. 2025.

Parisi, Rosalind, et al. “Psoriasis Vulgaris: A Comprehensive Overview.” Dermatology and Therapy, vol. 10, no. 2, 2020, pp. 261–273, https://pmc.ncbi.nlm.nih.gov/articles/PMC7122924/. Accessed 13 Apr. 2025.

Laser Resurfacing vs. Pigmentation Lasers: Which Treatment Suits Your Skin?

Which is better? Erbium YAG Laser vs CO2 Laser | The Ferguson Clinic

Providing a diverse plethora of skin benefits, laser treatments have revolutionized dermatology and have skyrocketed in popularity, with roughly 4 million laser skin treatments being performed annually. This surge in demand can be attributed to their ability to effectively address a variety of skin concerns: acne scars, wrinkles, hyperpigmentation, and unwanted hair. Offering precision and long-lasting results, laser treatments work in a very fascinating and non-invasive manner.

The significance of collagen

Before exploring the various types of laser treatments for the skin, it’s essential to understand why they’re effective: they stimulate collagen production — a key factor in maintaining youthful, healthy skin. Collagen is the most abundant protein in the human body and forms the structural framework of the skin. It interacts with other molecules like hyaluronic acid to provide firmness, elasticity, and hydration. As we age, natural collagen production declines, leading to wrinkles, sagging, and thinning skin. To combat this, laser treatments can be used to trigger fibroblasts to produce more collagen, consequently rebuilding smoother skin.

Laser resurfacing:

One of the more popular laser treatments, laser resurfacing is a technique that uses ablative lasers, non-ablative lasers, or fractional lasers. Ablative lasers (eg: CO₂) cast a beam of light that destroys the protective keratin on the epidermis—the outer layer of the skin—and heats the underlying skin—dermis. Ablative lasers emit energy at a wavelength of around 10,600 nm. In response, the body stimulates collagen growth to regrow the targeted wound. Once fully healed, the treated area returns smoother—free of sun damage and wrinkles. Ablative lasers are the most effective/intense laser option, requiring longer recovery time while providing the most drastic results.

Types of ablative lasers

CO₂ and Er:YAG lasers are the most commonly used ablative lasers, each with distinct advantages and applications. CO₂ lasers, operating at a high wavelength of ~10,600 nm, penetrate deeply into the skin, making them highly effective for severe sun damage, deep wrinkles, acne scars, and skin tightening. In contrast, Er:YAG lasers, with a moderate wavelength of ~2940 nm, offer more precise and controlled resurfacing, making them ideal for treating mild to moderate wrinkles, fine lines, and sun damage while minimizing heat damage.

Non-ablative lasers

If you seek a more gentle procedure with a shorter recovery time, non-ablative lasers would be a more suitable option. Unlike ablative lasers that both vaporize the epidermis and heat the dermis, non-ablative lasers do not create a wound on the surface, only heating the dermis. Non-ablative lasers operate at a marginally lower wavelength, typically between 1320 nm – 1927 nm. This still stimulates collagen production, but more gradually/gently.

Both ablative and non-ablative lasers can alternatively be offered fractionally instead of full-field. Fractional ablative/non-ablative lasers create microscopic wounds on the skin, leaving the surrounding skin intact. It should be noted that this fractional approach maintains the same wavelength as its full-field counterpart, but the delivery of the laser energy is different. Fractional lasers allow for reduced downtime and faster healing. It still effectively stimulates collagen production, though the results tend to be more gradual compared to full-field treatments.

Pigmentation & spot removal lasers

Similarly to laser resurfacing, pigmentation lasers also target and treat sun spots and pigmentation; however, they are a targeted treatment specifically designed to break down melanin without affecting the surrounding skin. The significantly low wavelength of pigmentation lasers—between 532 nm and 1064 nm—enables pinpoint accuracy for melanin to more effectively absorb laser energy. Unlike resurfacing lasers, which also improve skin texture, wrinkles, and scars, pigmentation lasers focus solely on degrading pigmentation, making them ideal for treating sunspots, freckles, melasma, and hyperpigmentation. It’s important to note that pigmentation lasers do not strongly stimulate collagen production, as they do not heat the dermis and trigger fibroblasts to produce new collagen.

Laser Pigmentation Removal in Portland, Oregon — Process of Laser Pigmentation Removal

Takeaway:

Ultimately, if your skin concern is solely moderate pigmentation and sun damage, pigmentation & spot removal lasers would be a better choice. These lasers operate at a low wavelength, ensuring minimal downtime, targeted melanin degradation, and reducing damage to surrounding tissue. If you wish to also treat scarring/texture or severe sun damage, resurfacing lasers (ablative/non-ablative) would be more suitable, as their potency stimulates collagen production and promotes new and smoother skin.

Bibliography

Cambridge Laser Clinic. “Detailed Explanation of Pigment Laser Treatments.” Cambridge Laser Clinic, https://cambridgelaserclinic.com/laser-treatments/pigment/detailed-explanation/#:~:text=Several%20different%20laser%20wavelengths%20can,(Nd%20Yag%201064nm%20laser). Accessed 2024.

“Laser Resurfacing.” Mayo Clinic, https://www.mayoclinic.org/tests-procedures/laser-resurfacing/about/pac-20385114#:~:text=Results%20after%20nonablative%20laser%20resurfacing,treatments%20to%20get%20noticeable%20results. Accessed 2024.

“Laser Light Energy-Based Procedures in the U.S. by Type.” Statista, https://www.statista.com/statistics/319224/distribution-of-laser-light-energy-based-procedures-in-the-us-by-type/. Accessed 2024.

RCSB Protein Data Bank. “Collagen Structure.” Protein Data Bank, https://pdb101.rcsb.org/motm/4. Accessed 2024.

“Lasers in Dermatology and Medicine.” National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/books/NBK557474/. Accessed 2024.

Rokhsar, C. K., and Fitzpatrick, R. E. “The Treatment of Wrinkles and Skin Laxity Using a Fractional Ablative CO₂ Laser: A Retrospective Study.” National Center for Biotechnology Information, https://pmc.ncbi.nlm.nih.gov/articles/PMC3580982/. Accessed 2024.

The Ferguson Clinic. “Which Is Better? Erbium YAG Laser vs. CO₂ Laser.” The Ferguson Clinic, https://www.thefergusonclinic.com/which-is-better-erbium-yag-laser-vs-co2-laser/. Accessed 2024.

Full Potential Men. “Laser Pigmentation Removal.” Full Potential Men, https://www.fullpotentialmen.com/laser-pigmentation-removal/. Accessed 2024.

Tyrosinase Inhibitors vs. Melanogenesis Inhibitors: Which is Better for Treating Pigmentation?

What causes pigmentation?

Responsible for providing color to our skin, hair, and eyes, melanin is an essential, naturally produced pigment that our body–and most organisms— is constantly producing. Our natural skin tone is largely accredited to our genetically determined melanin production rate, which vastly varies across ethnicities. Inhabitants of regions with more intense UV radiation have evolved to develop genetic mutations that increase their melanin production and thus have darker skin tones, whereas people in lower UV regions have lighter skin tones. The process of melanin production—otherwise known as melanogenesis—entails the conversion of tyrosinase—a natural enzyme—into melanin.

Simplified pathways of tyrosine-derived melanin synthesis showing... | Download Scientific Diagram — Process of Melanin Synthesis
(ResearchGate)

How does UV radiation influence melanin production?

As a defense mechanism against UV radiation, the skin initiates melanogenesis. Melanin then transfers to keratinocytes—the cell that produces keratin, an essential protein in the epidermis—where the melanin internally absorbs UV rays and reduces DNA damage. However, if the skin receives excessive exposure to UV radiation—without sun protection—the melanin will eventually fail to provide skin protection, leading to sun damage and, soon enough, hyperpigmentation. Although tyrosinase production is also largely influenced by genetics and exposure to UV radiation, tyrosinase, and melanin production can be reduced by tyrosinase inhibitors.

What are tyrosinase inhibitors?

Whether found synthetically in ingredients like azelaic acid or naturally in ingredients like aloe vera, tyrosinase inhibitors are widely used to even out skin tone by blocking tyrosinase activity during catalytic reaction, thereby reducing melanin production and, in some cases, breaking down and degrading pre-existing melanin. Their versatility makes them a key component in the treatment of hyperpigmentation, melasma, and age spots. While different tyrosinase inhibitors function differently, they ultimately yield the same results—reduced melanin synthesis and a more even complexion. Here are some examples of tyrosinase inhibitors with varying potency.

Niacinamide: Although not technically a tyrosinase inhibitor, niacinamide Inhibits melanosome transfer—the process of turning melanin into a visible pigment. Niacinamide does not alter tyrosinase production, making it a more gentle alternative to typical tyrosinase inhibitors. It can be applied up to twice daily.

Azelaic acid: Inhibits tyrosinase and gently reduces pigmentation by targeting hyperactive melanocytes—cells that produce melanin. Azelaic acid is slightly more potent than niacinamide. It can be applied up to twice daily.

Hydroquinone: Directly inhibits tyrosinase and melanin synthesis. It can be used up to twice a day for 3-6 months as treatment for intense hyperpigmentation or melasma; to avoid irritation, it should not be used any longer, as it is highly potent.

Melanogenesis inhibitors are often confused with tyrosinase inhibitors, and although they yield similar results—reducing pigmentation—tyrosinase inhibitors are a subset of melanogenesis inhibitors, which differ in that they affect melanin synthesis as a whole rather than directly targeting tyrosinase. Alongside just targeting tyrosinase production, melanogenesis inhibitors also promote melanin degradation and target melanogenesis pathways, blocking melanin from transferring to keratinocytes.

Which inhibitor is better?

Although melanogenesis inhibitors target several steps in melanogenesis as opposed to directly targeting tyrosinase activity—as seen with tyrosinase inhibitors—that doesn’t necessarily mean that one is stronger or more effective than the other. In general, melanogenesis inhibitors are preferred for more gradual and long-term treatment for pigmentation, whereas tyrosinase inhibitors are stronger for more rapid pigmentation treatment and results. While both are effective in their own ways, combining these treatments with sun protection, exfoliants, and antioxidants ensures the best results for maintaining an even skin tone and treating hyperpigmentation.

Bibliography

Boissy, R. E. “Melanosome Transfer to and Translocation in the Keratinocyte.” Experimental Dermatology, vol. 7, no. 3, 1998, pp. 143-150. PubMed.

National Cancer Institute. “Melanocyte.” NCI Dictionary of Cancer Terms, n.d., [https://www.cancer.gov/publications/dictionaries/cancer-terms/def/melanocyte](https://www.cancer.gov/publications/dictionaries/cancer-terms/def/melanocyte#:~:text=(meh%2DLAN%2Doh%2D,contains%20the%20pigment%20called%20melanin.).

University of Rochester Medical Center. “What Is Skin Pigmentation?” Health Encyclopedia, n.d., https://www.urmc.rochester.edu/encyclopedia/content?contenttypeid=85&contentid=p01359.

Costin, G. E., and V. J. Hearing. “Human Skin Pigmentation: Melanocytes Modulate Skin Color in Response to Stress.” The FASEB Journal, vol. 21, no. 4, 2007, pp. 976-994. PMC.

Burkhart, C. G., and H. R. Burkhart. “Hydroquinone.” StatPearls, StatPearls Publishing, 2019. NCBI.

Pillaiyar, T., M. Manickam, and V. Namasivayam. “Skin Whitening Agents: Medicinal Chemistry Perspective of Tyrosinase Inhibitors.” Journal of Enzyme Inhibition and Medicinal Chemistry, vol. 32, no. 1, 2017, pp. 403-425. PMC.

Chang, T. S. “Natural Melanogenesis Inhibitors Acting Through the Down-Regulation of Tyrosinase Activity.” International Journal of Molecular Sciences, vol. 10, no. 6, 2009, pp. 2440-2475. PMC.

Sasaki, M., K. Hasegawa, and Y. Takahashi. “Recent Advances in Skin Lightening Agents: A Comprehensive Review.” Journal of Dermatological Science, vol. 110, no. 1, 2023, pp. 12-24. PMC.