Tattoos are more popular than ever, but a growing body of research suggests a connection between permanent ink and certain types of cancer. How concerned should the public be?

From tribal sleeves to lower-back butterflies, humans have been inking their skin for thousands of years. For most, the main concern has been the fear of future regrets. However, recent studies suggest that tattoos could carry more serious long-term health risks.

The popularity of tattoos has risen sharply in recent years. Research published in the European Journal of Public Health estimates that between 13 and 21 percent of people in Western Europe now have at least one tattoo. Despite this prevalence, relatively little is known about the potential long-term effects of permanent ink.

Previous studies have shown that tattoo pigments can accumulate in the lymph nodes, sometimes causing inflammation and, in rare cases, lymphoma—a type of blood cancer. A 2025 study by the University of Southern Denmark (SDU) expanded on this, reporting that individuals with tattoos may face higher risks of skin cancer and lymphoma. Using a cohort of randomly selected twins, the researchers found that tattooed participants had nearly four times the risk of skin cancer compared with their non-tattooed siblings.

The study also suggested that tattoo size could affect risk, with designs larger than the palm associated with higher hazard rates.

“We have evidence that there is an association [between the amount of ink and risk] for lymphoma and for skin cancer,” said Signe Bedsted Clemmensen, co-author of the study and assistant professor of biostatistics at SDU. “For lymphoma, the hazard rate is 2.7 times higher, so this is quite a lot. And for skin cancers, before it was 1.6 and now it’s 2.4. This indicates that the more ink you have, the higher the risk, the higher the hazard rate.”

Clemmensen emphasized that these findings remain preliminary, with many variables—including ink types, tattoo placement, and genetic and environmental factors—still under investigation. “The bottom line is, more research is needed,” she said. “But also, the next step I think is studying the biological mechanisms [of getting tattooed] and trying to understand what happens there.”

Experts also note other risks unrelated to cancer. Tattoo inks consist of pigments combined with a carrier fluid to deposit color into the dermis. Some inks, often imported, can contain trace amounts of heavy metals such as nickel, chromium, cobalt, and lead, which can trigger allergic reactions or immune sensitivity. In 2022, the European Union restricted more than 4,000 hazardous substances in tattoo inks under its REACH regulations.

While tattoos are generally considered safe when applied hygienically, the long-term health consequences remain uncertain. “It’s up to each of us how we choose to live our lives, right? But as a researcher, it’s also my job to inform people of these risks,” Clemmensen said. “Or, when it comes to tattooing, right now it’s more about informing people about how little we know.”

Scientists have identified a potential new approach to slow memory loss in Alzheimer’s disease, offering hope for treatments that could improve the lives of millions affected by the neurodegenerative disorder.

Researchers at Cold Spring Harbor Laboratory, a non-profit research institution in New York, found that an enzyme called PTP1B contributes to memory decline in mice with Alzheimer’s. The study reveals a previously unknown role for the enzyme in immune cell signaling and suggests it could be a promising target for therapy.

Nicholas Tonks, a professor at the laboratory and the study’s corresponding author, discovered PTP1B in 1988 and has since explored its role in health and disease. Tonks and his team found that reducing PTP1B activity improved the ability of the brain’s immune cells, known as microglia, to clear amyloid-β (Aβ) plaques. These protein accumulations are a hallmark of Alzheimer’s disease and contribute to neuronal damage. Normally, microglia remove debris in the brain, but their function declines as the disease progresses.

The researchers discovered that PTP1B interacts with a protein called spleen tyrosine kinase (SYK), which regulates microglial responses to damage and plaque clearance.

“Over the course of the disease, these cells become exhausted and less effective,” said Yuxin Cen, the study lead. “Our results suggest that PTP1B inhibition can improve microglial function, clearing up Aβ plaques.”

PTP1B is also known for its role in metabolic conditions such as obesity and type 2 diabetes, which are recognized risk factors for Alzheimer’s disease. Researchers are now working to develop PTP1B inhibitors for multiple applications, including as a potential therapy for the neurodegenerative condition.

Tonks envisions combining PTP1B inhibitors with existing approved drugs for Alzheimer’s, such as cholinesterase inhibitors like donepezil or NMDA receptor antagonists such as memantine, used for more advanced stages.

“The goal is to slow Alzheimer’s progression and improve the quality of life of the patients,” Tonks said. He added that the research is particularly personal: “It’s a slow bereavement. You lose the person piece by piece,” recalling his mother’s experience with the disease.

According to the World Health Organization, more than 55 million people live with dementia globally, with Alzheimer’s accounting for up to 70 percent of cases. Current treatments manage symptoms but do not halt disease progression, making the search for new therapies critical.

The Cold Spring Harbor Laboratory team says their findings open the door to a new pathway for treatment, targeting the immune system’s capacity to remove harmful plaques. Researchers are hopeful that continued development of PTP1B inhibitors could complement existing drugs and slow the devastating effects of Alzheimer’s, potentially transforming care for millions worldwide.