It’s possible that I shall make an ass of myself. But in that case one can always get out of it with a little dialectic. I have, of course, so worded my proposition as to be right either way (K.Marx, Letter to F.Engels on the Indian Mutiny)
Friday, December 12, 2025
Indoor tanning makes youthful skin much older on a genetic level
Tanning bed users are known to have a higher risk of skin cancer, but for the first time researchers have found that young indoor tanners undergo genetic changes that can lead to more mutations in their skin cells than people twice their age.
The study, which was led by UC San Francisco and Northwestern University, appears Dec. 12 in Science Advances.
“We found that tanning bed users in their 30s and 40s had even more mutations than people in the general population who were in their 70s and 80s,” said Bishal Tandukar, PhD, a UCSF postdoctoral scholar in Dermatology who is the co-first author of the study. “In other words, the skin of tanning bed users appeared decades older at the genetic level.”
Such mutations can lead to skin cancer, which is the most common cancer in the U.S., according to the American Cancer Society. Among those skin cancers is melanoma, which accounts for only about 1% of skin cancers but causes most of the deaths. About 11,000 Americans die annually from melanoma, primarily from exposure to ultraviolet radiation.
UV radiation occurs naturally in sunlight, as well as in artificial light sources like tanning beds. Rates of melanoma have risen along with the use of tanning beds in recent years, disproportionately affecting young women, who are the main clients of the tanning industry.
Numerous countries effectively ban tanning beds, and the World Health Organization classifies them as a group 1 carcinogen, the same category as tobacco smoke and asbestos, but tanning beds remain legal and popular in the U.S.
In their study, the authors looked at the medical records of more than 32,000 dermatology patients including their tanning bed usage, history of sunburn, and family history of melanoma. They also obtained skin samples from 26 donors and sequenced 182 cells.
The young tanning bed users had more skin mutations than people twice their age, especially in their lower backs, an area that does not get much damage from sunlight but has a great deal of exposure from tanning beds.
“The skin of tanning bed users was riddled with the seeds of cancer — cells with mutations known to lead to melanoma,” said senior author A. Hunter Shain, PhD, associate professor in the UCSF Department of Dermatology.
“We cannot reverse a mutation once it occurs, so it is essential to limit how many mutations accumulate in the first place,” said Shain, whose laboratory focuses on the biology of skin cancer. “One of the simplest ways to do that is to avoid exposure to artificial UV radiation.”
Authors: From UCSF, authors include Delahny Deivendran; Limin Chen, PhD; Jessica Tang, PhD; Tuyet Tan; Harsh Sharma, PhD; Aravind K. Bandari, PhD; Noel Cruz-Pacheco, MS; Darwin Chang; Annika L. Marty, MS; Adam Olshen, PhD; Natalia Faraj Murad, PhD; and Iwei Yeh, MD, PhD. Co-first author Pedram Gerami, MD, is with Northwestern University, Chicago.
Funding: The study was supported by the National Cancer Institute (R01 CA265786); the National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR080626); the Department of Defense Melanoma Research Program (ME210014); and the Melanoma Research Alliance. Please see the paper for additionalfunders.
Disclosures: None reported.
About UCSF: The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF’s primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area. UCSF School of Medicine also has a regional campus in Fresno. Learn more at https://ucsf.edu or see our Fact Sheet.
Study analyzed thousands of medical records to compare melanoma rates in tanning bed users vs. non-users, and sequenced 182 skin biopsies from tanning bed users and controls
Tanning bed users carried double the mutation burden of controls
In users, mutations appeared even in body areas that don’t get much sun exposure
CHICAGO ---Tanning bed use is tied to almost a threefold increase in melanoma risk, and for the first time, scientists have shown how these devices cause melanoma-linked DNA damage across nearly the entire skin surface, reports a new study led by Northwestern Medicine and University of California, San Francisco.
Melanoma, the deadliest skin cancer, kills about 11,000 in the U.S. each year. Despite decades of warnings, the precise biological mechanism behind tanning beds’ cancer risk remained unclear. The indoor tanning industry, which is making a comeback, has used that uncertainty to argue that tanning beds are no more harmful than sunlight.
This new study “irrefutably” challenges those claims by showing how tanning beds, at a molecular level, mutate skin cells far beyond the reach of ordinary sunlight, according to the authors.
“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 with histories of tanning bed use, who donated their biopsies for this study, are available for interviews upon request.
The findings will publish Dec. 12 in Science Advances.
A clinical mystery
Gerami, who also directs the melanoma program in dermatology at Northwestern, has been treating melanoma patients for 20 years. Over the years, he noticed an unusually high number of women under 50 with a history of multiple melanomas, and suspected the linking factor was tanning bed usage. So, along with his research team, he designed the epidemiologic part of the study and compared the medical records of roughly 3,000 tanning bed users with 3,000 age-matched controls with no history of indoor tanning.
The team found that melanoma was diagnosed in 5.1% of tanning bed users compared with 2.1% of non-users. After adjusting for age, sex, sunburn history and family history, tanning bed use remained associated with a 2.85-fold increase in melanoma risk.
Tanning bed users were also more likely to develop melanoma on sun-shielded body sites, such as the lower back and buttocks. These findings supported the idea that tanning beds may cause broader DNA injury than sun exposure.
DNA sequencing
To test that hypothesis, the scientists used new genomic technologies to perform single-cell DNA sequencing on melanocytes (the pigment-producing skin cells where melanoma begins) from three skin donor groups.
The first group included 11 patients from Gerami with long histories of indoor tanning. The second group consisted of nine patients who had never used tanning beds but were otherwise matched for age, sex and cancer risk profiles. A third group of six cadaver donors supplied additional skin tissue to round out the control samples.
The scientists sequenced 182 individual melanocytes and found skin cells from tanning bed users carried nearly twice as many mutations as those from controls and were more likely to contain melanoma-linked mutations. In indoor tanners, the mutations also appeared in body areas that typically remain protected from the sun, confirming that tanning beds create a broader field of DNA injury.
“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 donates skin biopsy
The study would not have been possible without the generosity of Gerami’s patients who donated their biopsies. One of them, 49-year-old Heidi Tarr from the Chicago area, used tanning beds heavily during 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.”
Decades later, as a mother in her thirties, she noticed a mole on her back and immediately feared the worst. Her melanoma diagnosis led to surgery, years of frequent follow-up visits 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.”
When Gerami explained the study, she volunteered more biopsies without hesitation. “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’
After seeing the biological and clinical evidence side by side, Gerami said the need for policy change is clear. “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 said tanning beds should carry warnings similar to those on cigarettes. “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.”
Gerami suggests that anyone who frequently tanned earlier in life should have a total-body skin exam by a dermatologist and be evaluated for whether they need routine skin checks.
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.
Credit: Western oak mistletoe in northern red oak. Photo by Dave Shaw, Oregon State University College of Forestry/OSU Extension Service.
CORVALLIS, Ore. – If mistletoe’s status as a nutrient-stealing freeloader has been cooling your holiday ardor, new research led by an Oregon State University scientist may help relight the fire.
A survey of urban forests in seven western Oregon cities found no observable connection between mistletoe infestation and negative health outcomes for the trees it was parasitizing.
So worry not: Your yuletide kissing tradition probably does not involve a tree killer. And as you’re setting concern aside, you might want to head outside.
“This is the best time of year to look for mistletoe because there are no leaves on the trees,” said College of Forestry professor emeritus Dave Shaw, an OSU Extension Service forest health specialist. “Also, chances are it will be found in an oak tree – most other trees don’t get infested. So if you are looking for a kiss, keep an eye out for oaks.”
Shaw and collaborators at OSU, the U.S. Forest Service and the Oregon Department of Forestry examined the occurrence of western oak mistletoe in city forests to learn about mistletoe hosts and gain insight into mistletoe management.
Common from Baja California to the northern Willamette Valley, western oak mistletoe is one of more than 1,400 species of mistletoe, a type of flowering plant that attaches to the branches of trees and shrubs around the globe.
Western oak mistletoe berries (on the female plants only, and toxic to humans) ripen in late fall or early winter and are eaten by western bluebirds and other birds, who disperse the seeds, most commonly on larger trees.
Mistletoe seeds are covered in a sticky substance that allows them to cling to branches. Mistletoes siphon food and water from their hosts via a bark-penetrating, root-like structure, sometimes to the detriment of the host tree.
“Western oak mistletoe is probably a benefit to wildlife in urban forests,” Shaw said. “On the other hand, there is the potential for negative impacts on amenity trees, which is why it’s important for urban forest managers to have assessments of mistletoe host range, both for future tree planting decisions and managing current tree populations.”
Western oak mistletoe occurs on native oaks and a collection of other hosts – including acacia, alder, aspen, birch, chestnut, locust, pear, poplar, walnut and willow – so vast that no definitive host list exists.
Shaw notes that urban forests often include a variety of non-native trees, planted historically for reasons that include aesthetics, adaptability, and rapid growth of shade-producing canopy. For this study, the researchers focused on introduced tree species in Salem, Corvallis, Eugene, Medford, Central Point, Rogue River and Ashland.
The scientists conducted their surveys by driving, walking and biking city streets, parks, university campuses and arboreta, with the goal of visually examining all non-native tree crowns for the presence of mistletoe plants.
“Urban forests are unique settings that allow for a wide assortment of potential hosts to be exposed to mistletoe seed,” Shaw said. “We observed western oak mistletoe in 227 non-native trees, of which 85% were pin oak or northern red oak.”
Among the rest, 12% were other oak species, meaning just 3% were not some kind of oak tree – even though non-oaks were in the majority.
Western oak mistletoe infested trees of all size classes, but only six of the 227 infested trees were less than 10 centimeters in diameter and just nine were less than 10 meters tall. Only one infested tree looked to be in poor condition, 14 were in moderate condition, and 212 appeared to be in good condition.
“That suggests mistletoe, at the levels of infestation we saw, is not adversely impacting tree health,” Shaw said. “Of the 42 trees with greater than 20 mistletoe plants in their crowns, none was in poor condition, one was moderate and 41 were in apparently good condition.”
Mistletoe has been a symbol of health, love, vitality and fertility in multiple cultures since ancient times, and the tradition of kissing under mistletoe has its roots in 18th century England.
“The word ‘parasite’ can carry negative connotations, but mistletoe is a remarkable and beautiful plant with centuries of cultural importance behind it,” Shaw said. “It was nice that our survey showed that it wasn’t causing appreciable harm to its hosts.”
OSU professor emeritus Max Bennett also participated in the study, which was published in Northwest Science. The other collaborators were retired Forest Service researcher Don Goheen, retired Oregon Department of Forestry scientist Alan Kanaskie, and current ODF scientist Scott Altenhoff.
Journal
Northwest Science
Method of Research
Observational study
Subject of Research
Not applicable
Article Title
Western Oak Mistletoe (Phoradendron villosum subsp. villosum) on Non-native Urban Trees of Western Oregon
Article Publication Date
12-Dec-2025
Mysterious X-ray variability of the strongly magnetized neutron star NGC 7793 P13
Credit: X-ray（NASA/CXC/Univ of Strasbourg/M.Pakull et al）； Optical（ESO/VLT/Univ of Strasbourg/M.Pakull et al）；H-alpha（NOAO/AURA/NSF/CTIO 1.5m）
When gas falls onto a compact object, such as a neutron star or black hole, due to its strong gravity (a process called accretion), it emits electromagnetic waves. High-sensitivity observations have discovered objects with extremely high X-ray luminosities. One possible explanation for the ultraluminosity is that an extraordinary amount of gas falls onto a compact object through a process called supercritical accretion. However, the mechanism of supercritical accretion remains unclear.
The research team focused on NGC 7793 P13 (hereafter, P13), which is a neutron star in supercritical accretion, located in the galaxy NGC 7793 (about 10 million light-years from the Earth; Figure 1). As gas falls onto a neutron star, it forms a column structure (called an accretion column) on magnetic poles, from which intense X-ray is thought to be emitted. Then, coherent X-ray pulsation accompanied by the rotation of a neutron star can be detected. According to previous studies, P13 rotates with a period of 0.4 s with a constant acceleration rate. Moreover, the luminosity changed by more than two orders of magnitude in about 10 years. Both rotation velocity and luminosity are effective parameters to estimate the amount of gas accreted. However, the relation between them was not found for P13.
The research team investigated the long-term evolution of the X-ray luminosity and rotation period of P13 from 2011 to 2024, using the archival data of XMM-Newton, Chandra, NuSTAR, and NICER. It was found that P13 was in a faint phase in 2021 and started to be bright again in 2022. By 2024, it reached a high luminosity, more than two orders of magnitude higher than in 2021 (Figure 2). Moreover, in the rebrightening phase in 2022, the acceleration rate of the rotation velocity was increased by a factor of 2, and it was maintained until 2024. This result suggests a relationship between X-ray luminosity and rotation velocity, and that the accretion system changed during the faint phase. The research team then focused on the pulsation and performed detailed analyses. It was suggested that the height of the accretion column was changed with the 10-year flux modulation (Figure 3). Those results are expected to be clues to reveal the mechanism of supercritical accretion.
The luminosity and rotation speed changed significantly. There is an inverse relationship between rotational speed and period; a shorter period indicates faster rotation. The acceleration rate of rotational speed is represented by the slope.
During the bright phase, the accretion column is tall, while during the faint phase, it becomes shorter.
Distinct psychiatric disorders have more in common biologically than previously believed, according to the largest and most detailed analysis to date of how genes influence mental illness.
The study, led by University of Colorado Boulder and Mass General Brigham researchers, could inform efforts to improve the way psychological disorders are diagnosed and provide insight for developing novel treatments that address multiple disorders at once.
The findings were published Dec. 10 in the journal Nature.
“Right now, we diagnose psychiatric disorders based on what we see in the room, and many people will be diagnosed with multiple disorders. That can be hard to treat and disheartening for patients,” said corresponding author, Andrew Grotzinger, PhD, assistant professor of psychology and neuroscience at CU Boulder. “This work provides the best evidence yet that there may be things that we are currently giving different names to that are actually driven by the same biological processes.”
Co-corresponding author Jordan Smoller, MD, director of the Center for Precision Psychiatry at Mass General Brigham in Boston, said the findings also provide key insight into the biological pathways and gene expression in brain cell types that may underly certain conditions.
“These findings provide valuable clues for advancing our understanding and treatment of mental illness with greater precision,” said Smoller.
Five categories
The researchers, in collaboration with the international Psychiatric Genomics Consortium Cross-Disorder Working Group, examined DNA data from more than 1 million individuals diagnosed with at least one of 14 psychiatric disorders and 5 million individuals with no diagnoses.
They found that five underlying “genomic factors” involving 238 genetic variants made up the majority of the genetic differences between those with a particular disorder and those without it. The paper groups disorders into five categories, each with a shared genetic architecture, including: disorders with compulsive features such as anorexia nervosa, Tourette disorder and obsessive-compulsive disorder (OCD); “internalizing conditions” including depression, anxiety and post-traumatic stress disorder; substance use disorders; and neurodevelopmental conditions, including autism and attention-deficit/hyperactivity disorder (ADHD).
Notably, the paper groups bipolar disorder and schizophrenia in a fifth category, reporting that 70% of the genetic signal associated with schizophrenia is also associated with bipolar disorder. The field of psychology has historically viewed bipolar disorder and schizophrenia as very different, and clinicians typically will not diagnose an individual with both.
“Genetically, we saw that they are more similar than they are unique,” said Grotzinger.
Pinpointing biological pathways
The paper also points to specific biological pathways that may underlie the individual groupings.
For instance, genes that influence excitatory neurons, which are involved in transmitting signals across other neurons, tend to be over-expressed in both bipolar disorder and schizophrenia, the research suggests.
In internalizing disorders like depression and anxiety, variants in genes that control non-neuronal cells called oligodendrocytes, were common. These specialized cells help maintain and protect the brain’s wiring infrastructure.
The findings suggest that some shared genetic factors play a role very early in brain development during the fetal stages of life, while others could have a greater influence later in adult life. This insight could help to create a more biological way of understanding psychiatric conditions and lead to new treatment strategies, the authors said.
According to one 2018 review, more than half of people diagnosed with one psychiatric disorder will be diagnosed with a second or third in their lifetime. About 41% will meet the criteria for four or more.
Grotzinger said it is too early to begin combining diagnoses based on the findings. But as researchers work to update the Diagnostic and Statistical Manual of Mental Disorders (DSM), the guiding handbook for the field of psychology, he hopes the new study will be considered.
“By identifying what is shared across these disorders, we can hopefully come up with strategies to target them in a different way that doesn’t require four separate pills or four separate psychotherapy interventions.”
