Indoor tanning drastically increases melanoma risk, and scientists have now mapped the sweeping DNA damage tanning beds inflict across nearly the entire skin surface -- damage far beyond what sunlight causes.

  • Researchers examined thousands of medical records to compare melanoma rates in people who used tanning beds and those who did not, then performed genomic analysis on 182 skin biopsies from both groups to track mutation patterns.
  • People who used tanning beds showed nearly twice as many DNA mutations as individuals in the control group.
  • These mutations were found not only on commonly exposed skin, but also in body areas that rarely see sunlight, revealing how far tanning bed damage can spread.

Indoor tanning, melanoma risk and DNA damage

Using tanning beds is linked to nearly a threefold increase in the risk of melanoma, and for the first time, researchers have shown how these devices create melanoma-related DNA damage across almost the entire surface of the skin, according to a new study led by Northwestern Medicine and the University of California, San Francisco.

Melanoma is the most lethal form of skin cancer and is responsible for about 11,000 deaths in the U.S. each year. For years, health experts have warned about the dangers of indoor tanning, yet the exact biological pathway connecting tanning beds to cancer had not been fully mapped. The indoor tanning industry, which has been experiencing a resurgence in popularity, has pointed to that gap in knowledge to claim that tanning beds are no more dangerous than natural sunlight.

The new research, the authors say, "irrefutably" counters those arguments by demonstrating that tanning beds, at the molecular level, change skin cells in ways that go far beyond the impact of everyday sun exposure.

"Even in normal skin from indoor tanning patients, areas where there are no moles, we found DNA changes that are precursor mutations that predispose to melanoma," said study first author Dr. Pedram Gerami, professor of skin cancer research at Northwestern University Feinberg School of Medicine. "That has never been shown before."

Melanoma survivors who previously used tanning beds and donated their skin biopsies for this work are available for interviews upon request.

The findings were published Dec. 12 in the journal Science Advances.

Clinical mystery in younger melanoma patients

Gerami, who also directs the melanoma program in dermatology at Northwestern, has treated people with melanoma for two decades. During that time, he began to notice a striking pattern: an unusually high number of women under age 50 who had experienced multiple melanomas and reported using tanning beds. He suspected that frequent indoor tanning was the shared factor tying these cases together.

To investigate, Gerami and his team designed the epidemiologic portion of the study. They analyzed medical records for about 3,000 people with a history of tanning bed use and compared them with roughly 3,000 age-matched individuals who had never used indoor tanning devices.

In this comparison, melanoma was diagnosed in 5.1% of people who used tanning beds, versus 2.1% of those who did not. Even after the researchers accounted for age, sex, history of sunburn, and family history of melanoma, indoor tanning was still associated with a 2.85-fold increase in melanoma risk.

The study also found that people who used tanning beds were more likely to develop melanoma on body areas that are usually shielded from the sun, such as the lower back and buttocks. These observations supported the idea that tanning beds may inflict more widespread DNA damage than ordinary sun exposure.

DNA sequencing reveals widespread mutations

To explore that possibility further, the scientists turned to advanced genomic tools. They used newer technologies to perform single-cell DNA sequencing on melanocytes (the pigment-producing skin cells where melanoma begins) from three different groups of skin donors.

The first group consisted of 11 patients from Gerami's clinic who had long histories of indoor tanning. The second group included nine individuals who had never used tanning beds but were otherwise similar in age, sex and overall cancer risk. A third group of six cadaver donors provided additional skin samples to strengthen the control group.

In total, the team sequenced 182 individual melanocytes. They discovered that melanocytes from tanning bed users carried nearly twice as many genetic mutations as those from the control groups and were more likely to harbor mutations associated with melanoma. In people who tanned indoors, these mutations also showed up in areas of the body that typically stay covered and are not regularly exposed to the sun, reinforcing the conclusion that tanning beds cause a broad field of DNA damage.

"In outdoor sun exposure, maybe 20% of your skin gets the most damage," Gerami said. "In tanning bed users, we saw those same dangerous mutations across almost the entire skin surface."

Cancer survivor shares the toll of tanning beds

The study depended on the willingness of Gerami's patients to donate skin biopsies. One participant, 49-year-old Heidi Tarr from the Chicago area, used tanning beds frequently as a teenager in high school -- two to three sessions a week -- because friends and celebrities at the time were also doing it and "it felt like that's what made you beautiful."

Years later, in her thirties and now a mother, she spotted a mole on her back and immediately feared it might be something serious. The spot turned out to be melanoma, leading to surgery, years of regular follow-up appointments and more than 15 additional biopsies as new moles appeared. "The biopsies can be painful, but the mental anxiety is worse," she said. "You're always waiting for the call that it's melanoma again."

After Gerami described the new research project, Tarr readily agreed to provide additional biopsies. "I value science, and I wanted to help," she said. "If what happened to my skin can help others understand the real risks of tanning beds, then it matters."

'Wronged by the industry'

Seeing the genetic data and the clinical trends together convinced Gerami that stronger safeguards are needed. "At the very least, indoor tanning should be illegal for minors," he said.

"Most of my patients started tanning when they were young, vulnerable and didn't have the same level of knowledge and education they have as adults," he said. "They feel wronged by the industry and regret the mistakes of their youth."

Gerami also believes tanning beds should carry warnings comparable to those on cigarette packages. "When you buy a pack of cigarettes, it says this may result in lung cancer," he said. "We should have a similar campaign with tanning bed usage. The World Health Organization has deemed tanning beds to be the same level of carcinogen as smoking and asbestos. It's a class one carcinogen."

He recommends that anyone who frequently used tanning beds earlier in life schedule a total-body skin examination with a dermatologist and talk with their doctor about whether they should have ongoing, routine skin checks.

Gerami is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

The study, titled "Molecular effects of indoor tanning," was funded by the National Institutes of Health (grants R01 CA265786 and AR080626), the Department of Defense Melanoma Research Program (grant ME210014), the Melanoma Research Alliance Team Science Award, the Melanoma Research Alliance Dermatology Fellows Award, the LEO Foundation Region Americas Award, Cancer Center Support (grant P30CA082103), the IDP Foundation Award and the Greg and Anna Brown Family Foundation Award.

One potential strategy for treating a wide range of illnesses involves targeting senescent cells. These cells -- also known as "zombie cells" -- stop multiplying but fail to clear themselves from the body as healthy cells normally do. They appear in many conditions, including cancer, Alzheimer's disease, and throughout the aging process. Although scientists are working on ways to eliminate or repair these cells, a major challenge has been detecting them within living tissue without disturbing nearby healthy cells.

Researchers at Mayo Clinic, writing in the journal Aging Cell, describe a new method for labeling senescent cells. Their approach uses "aptamers" -- short pieces of synthetic DNA that fold into three-dimensional structures. These structures can attach to proteins found on the outer surfaces of cells. In experiments with mouse cells, the team identified several rare aptamers, selected from more than 100 trillion random DNA sequences, that were able to recognize specific surface proteins and mark senescent cells.

"This approach established the principle that aptamers are a technology that can be used to distinguish senescent cells from healthy ones," says biochemist and molecular biologist Jim Maher, III, Ph.D., a principal investigator of the study. "Though this study is a first step, the results suggest the approach could eventually apply to human cells."

How a Chance Conversation Sparked a Collaboration

The idea that led to this project began when a Mayo Clinic graduate student shared an offbeat thought during a casual discussion with a classmate.

Keenan Pearson, Ph.D. -- who recently received his degree from Mayo Clinic Graduate School of Biomedical Sciences -- had been working with Dr. Maher on how aptamers might be used for neurodegenerative diseases or brain cancer.

Meanwhile, several floors above, fellow graduate student Sarah Jachim, Ph.D., was studying senescent cells and aging in the lab of researcher Nathan LeBrasseur, Ph.D.

Their paths crossed at a scientific gathering, where they exchanged ideas about their thesis projects. Dr. Pearson wondered if aptamers could be adapted to detect senescent cells. "I thought the idea was a good one, but I didn't know about the process of preparing senescent cells to test them, and that was Sarah's expertise," says Dr. Pearson, who became lead author of the publication.

Mentors Back a Bold Student Idea

The students brought their concept to their advisors and to researcher Darren Baker, Ph.D., whose work centers on senescent cell therapies. Dr. Maher recalls that the idea initially struck him as "crazy" but worth exploring. All three mentors supported the proposal. "We frankly loved that it was the students' idea and a real synergy of two research areas," says Dr. Maher.

As early experiments produced promising results, the pair enlisted more students from their labs. Then-graduate students Brandon Wilbanks, Ph.D., Luis Prieto, Ph.D., and M.D.-Ph.D. student Caroline Doherty added new techniques, including advanced microscopy and additional tissue types. "It became encouraging to expend more effort," Dr. Jachim says, "because we could tell it was a project that was going to succeed."

Revealing New Clues About Senescent Cells

Beyond providing a tagging method, the research offered insight into the biology of senescent cells. "To date, there aren't universal markers that characterize senescent cells," says Dr. Maher. "Our study was set up to be open-ended about the target surface molecules on senescent cells. The beauty of this approach is that we let the aptamers choose the molecules to bind to."

The team found that several aptamers attached to a variant of a protein called fibronectin on the surface of mouse cells. Scientists do not yet know how this fibronectin variant relates to senescence. However, its discovery suggests that aptamers may help identify features unique to senescent cells.

Potential Applications for Human Health

More work will be needed to find aptamers that can reliably detect senescent cells in human tissue. If aptamers can be adapted for this purpose, they could eventually be used to deliver treatments directly to these cells. Dr. Pearson notes that aptamers are less costly and more flexible than traditional antibodies, which are commonly used to distinguish one cell type from another.

"This project demonstrated a novel concept," says Dr. Maher. "Future studies may extend the approach to applications related to senescent cells in human disease."

Researchers have used a deep learning artificial intelligence model to identify what they describe as the first biomarker of chronic stress that can be directly seen on standard medical images. The findings are being presented next week at the annual meeting of the Radiological Society of North America (RSNA).

Chronic stress does not just affect mood. It can influence both physical and mental health, contributing to problems such as anxiety, trouble sleeping, muscle pain, high blood pressure and a less effective immune system, according to the American Psychological Association. Studies have also linked ongoing stress to major conditions including heart disease, depression and obesity.

AI measures adrenal glands on routine CT scans

The study's lead author, Elena Ghotbi, M.D., a postdoctoral research fellow at Johns Hopkins University School of Medicine in Baltimore, Maryland, created and trained a deep learning tool designed to calculate the size of the adrenal glands using CT scans that had already been performed.

Each year, tens of millions of chest CT scans are performed in the United States alone.

"Our approach leverages widely available imaging data and opens the door to large-scale evaluations of the biological impact of chronic stress across a range of conditions using existing chest CT scans," Dr. Ghotbi said. "This AI-driven biomarker has the potential to enhance cardiovascular risk stratification and guide preventive care without additional testing or radiation."

Making the burden of stress visible in the body

Senior author Shadpour Demehri, M.D., professor of radiology at Johns Hopkins, noted that chronic stress is extremely common and is something many adults experience every day.

"For the first time, we can 'see' the long-term burden of stress inside the body, using a scan that patients already get every day in hospitals across the country. Until now, we haven't had a way to measure and quantify the cumulative effects of chronic stress, other than questionnaires, surrogate serum markers like chronic inflammation, and cortisol measurement, which is very cumbersome to obtain." Dr. Demehri said.

Unlike a single cortisol test, which reflects stress at just one point in time, the size of the adrenal glands functions more like a long-term gauge of chronic stress.

Large multi-ethnic cohort links imaging, hormones and stress load

In this research, the team analyzed information from 2,842 participants (mean age 69.3; 51% women) enrolled in the Multi-Ethnic Study of Atherosclerosis, a large study that combines chest CT imaging, validated stress questionnaires, cortisol measurements and indicators of allostatic load -- the cumulative physiological and psychological effects of chronic stress on the body. Because it integrates imaging, biochemical data and psychosocial assessments in the same individuals, this cohort was uniquely suited, and likely the only one available, for creating an imaging-based marker of chronic stress.

The investigators applied their deep learning model to the CT scans to automatically outline and measure adrenal gland volume. They defined Adrenal Volume Index (AVI) as adrenal volume (cm3) divided by height2 (m2). To capture hormonal patterns, participants provided salivary cortisol eight times per day over the course of two days. Allostatic load was calculated using body mass index, creatinine, hemoglobin, albumin, glucose, white blood count, heart rate and blood pressure.

Adrenal Volume Index tracks stress, hormones and heart risk

The team then examined how AVI related to cortisol, allostatic load and a range of psychosocial stress indicators, such as depression scores and perceived stress questionnaires. They discovered that AVI generated by the AI model aligned with established stress questionnaires, with circulating cortisol levels and with future adverse cardiovascular events.

Higher AVI values were linked with greater overall cortisol exposure, higher peak cortisol levels and increased allostatic load. People who reported high levels of perceived stress had higher AVI compared with those who reported low stress. AVI was also connected to a higher left ventricular mass index, a measure related to heart structure. For every 1 cm3/m2 increase in AVI, the risk of heart failure and death increased.

"With up to 10-year follow-up data on our participants, we were able to correlate AI-derived AVI with clinically meaningful and relevant outcomes," Dr. Ghotbi said. "This is the very first imaging marker of chronic stress that has been validated and shown to have an independent impact on a cardiovascular outcome, namely, heart failure."

A new way to quantify the cumulative impact of stress

"For over three decades, we've known that chronic stress can wear down the body across multiple systems," said Teresa E. Seeman, Ph.D., study co-author and professor of epidemiology at UCLA and a pioneering researcher in stress and health. "What makes this work so exciting is that it links a routinely obtained imaging feature, adrenal volume, with validated biological and psychological measures of stress and shows that it independently predicts a major clinical outcome. It's a true step forward in operationalizing the cumulative impact of stress on health."

Dr. Demehri explained that connecting a simple imaging measure with several well-established markers of stress and disease outcomes creates a new, practical approach to measuring chronic stress in everyday clinical practice.

"The key significance of this work is that this biomarker is obtainable from CTs that are performed widely in United States for various reasons," Dr. Demehri said. "Secondly, it is a physiologically sound measure of adrenal volume, which is part of the chronic stress physiologic cascade."

The researchers noted that this imaging biomarker could potentially be applied to many stress-related diseases that commonly affect middle-aged and older adults.

Other co-authors are Roham Hadidchi, Seyedhouman Seyedekrami, Quincy A. Hathaway, M.D., Ph.D., Michael Bancks, Nikhil Subhas, Matthew J. Budoff, M.D., David A. Bluemke, M.D., Ph.D., R. Graham Barr and Joao A.C. Lima, M.D.

A recent investigation from Flinders University sheds new light on how two widely consumed drinks, coffee and tea, could play a role in bone health for women later in life.

The study, published in the journal Nutrients, monitored nearly 10,000 women aged 65 and older for ten years to examine whether regularly drinking coffee or tea was connected to changes in bone mineral density (BMD). BMD is a central marker used to assess osteoporosis risk.

Osteoporosis affects one in three women over 50 and leads to millions of fractures every year, making bone health an important global issue. Because coffee and tea are part of daily routines for billions of people, researchers note that understanding their long-term effects on bones is essential. Previous findings have often been inconsistent, and few studies have followed such a large group across an entire decade.

Study Design and Long-Term Tracking

Researchers at Flinders University used information from the Study of Osteoporotic Fractures, drawing on repeated measures of beverage intake and BMD at the hip and femoral neck. These areas are closely tied to fracture risk.

Throughout the ten-year period, participants regularly reported how much coffee and tea they consumed. At the same time, bone density was assessed using advanced imaging tools.

Tea's Modest but Meaningful Bone Benefits

Results showed that women who drank tea had slightly higher total hip BMD than those who did not. Although the improvement was small, it was statistically significant and may matter when considering the health of a large population.

"Even small improvements in bone density can translate into fewer fractures across large groups," says Adjunct Associate Professor Enwu Liu from the College of Medicine and Public Health.

Coffee Consumption and Bone Density Risks

Findings for coffee were more varied. Moderate intake, roughly two to three cups a day, was not associated with harm. However, consuming more than five cups per day was linked to lower BMD, indicating that very high levels of coffee could negatively affect bone strength.

Women with higher lifetime alcohol intake appeared particularly vulnerable to coffee's negative effects, whereas tea showed stronger benefits in women with obesity.

Ryan Liu, co-author of the study, explains that tea is rich in catechins, compounds that may encourage bone formation and help slow bone loss.

"Coffee's caffeine content, by contrast, has been shown in laboratory studies to interfere with calcium absorption and bone metabolism, though these effects are small and can be offset by adding milk," says Ryan Liu from Flinders University.

Practical Implications for Aging Women

Adjunct Associate Professor Enwu Liu notes that the research suggests drinking tea daily may be an easy way to support bone health as people grow older.

"While moderate coffee drinking appears safe, very high consumption may not be ideal, especially for women who drink alcohol," he says.

The researchers emphasize that while the results are statistically meaningful, the differences are not dramatic enough to require sweeping lifestyle changes.

"Our results don't mean you need to give up coffee or start drinking tea by the gallon," says Associate Professor Liu.

"But they do suggest that moderate tea consumption could be one simple way to support bone health, and that very high coffee intake might not be ideal, especially for women who drink alcohol.

"While calcium and vitamin D remain cornerstones of bone health, what's in your cup could play a role too. For older women, enjoying a daily cup of tea may be more than a comforting ritual, it could be a small step toward stronger bones," he concludes.

Study Funding

The SOF study received support from the National Institute on Aging (NIA) and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), with funding provided through grants (AG05407, AR35582, AG05394, AR35584, and AR35583).

More Articles …