The Rise of Dry Eye Disease in Young Adults: A Growing Concern

Researchers at Aston University have sounded the alarm about the increasing prevalence of dry eye disease among young adults. A recent study conducted in collaboration with Oslo University Hospital and Sørlandet Hospital Trust in Norway has found that a staggering 90% of participants exhibited at least one sign of the condition, with 56% meeting the criteria for dry eye disease.

Dry eye disease occurs when the eyes do not produce enough tears or create poor-quality tears, leading to instability and rapid evaporation of the tear film. This can cause a range of symptoms, including gritty feeling eyes, itching or stinging sensations, redness, sensitivity to light, and blurry vision.

The study, led by Dr. Rachel Casemore at Aston University School of Optometry, followed 50 young adults aged 18-25 over time, assessing their lifestyle factors, screen use habits, and tear quality. The results showed a significant correlation between prolonged screen use and signs of dryness on the eye surface, with participants averaging eight hours per day of screen time.

The researchers found that around half of the participants had lost at least 25% of the meibomian gland, which produces the outer lipid layer of the tear film responsible for preventing evaporation. This loss can contribute to the progression of dry eye disease.

Dr. Casemore emphasized the need for early detection and prevention of dry eye disease in young adults, as it can lead to significant discomfort and vision problems if left unchecked. She recommends simple measures such as taking regular screen breaks, performing blink exercises to release oils from the meibomian glands, staying hydrated, and maintaining a healthy diet rich in omega-3 fatty acids.

The study’s findings highlight the importance of eye care practitioners identifying clinical indicators of dry eye disease and counseling young adults on modifiable risk factors, such as screen use habits, sleeping patterns, contact lens use, diet, blinking patterns, and stress management.

As Dr. Casemore noted, “It is concerning to note the increasing prevalence of dry eye disease signs and symptoms in young adults, which has been referred to as a ‘lifestyle epidemic’ by some researchers.” Further research aims to explore the potential tear and meibomian gland oil biomarkers identified during the study and examine the effect of diet on dry eye disease development.

The field of exposomics is revolutionizing health science by unlocking the power of advanced technologies to study the complex interactions between environmental, social, and psychological factors that shape our biology. By analyzing the molecular fingerprints left in our bodies from every breath we take, every meal we eat, and every environment we encounter, researchers are uncovering new insights into disease prevention and personalized medicine.

Led by the Banbury Exposomics Consortium, an interdisciplinary group of scientists gathered at Cold Spring Harbor’s Banbury Center to define the core principles of this rapidly evolving field. Gary Miller, PhD, a foremost expert in exposomics and faculty member at Columbia University Mailman School of Public Health, was the lead organizer of the Consortium.

Exposomics explores how environmental factors such as pollutants in our water and food, social stressors, and psychological factors shape our biology. By studying these combined exposures, researchers can uncover how they collectively influence health, from metabolism and heart function to brain health and disease risk.

The young field is already proving its transformative potential. Researchers analyzing molecular evidence identified a specific industrial solvent as the culprit behind kidney disease clusters among factory workers. In another study, scientists merged satellite pollution mapping with residential location information to reveal how airborne particulates prematurely age the brain.

These discoveries are made possible by cutting-edge technologies and tools such as wearable sensors that track chemical exposures in real-time, satellite imagery that maps pollution down to city blocks, and ultra-sensitive mass spectrometers that detect compounds present at just one part per trillion.

While genetics provides our biological blueprint, it explains only a fraction of chronic disease risk. The exposome captures everything that happens to us, from industrial chemicals to social stressors. Unlike traditional studies examining single exposures in isolation, exposomics integrates advanced tools to understand how environmental, social, and psychological factors collectively interact with our biology.

Systematically analyzing these complex interactions can improve drug development, uncover hidden drivers of disease, and address health disparities. The approach bridges precision medicine and population health.

Miller and colleagues outline critical priorities for advancing exposomics, including the development of more sensitive technologies, creating a human exposome reference to enable analysis and contextualization at the population scale, and implementing standardized protocols to enable AI-driven analysis of complex datasets.

Newly launched U.S. and European exposomics hubs now provide the infrastructure for worldwide collaboration, standardizing methods, harmonizing data, and training researchers in the cross-disciplinary skills needed to advance this field.

“We’re now building the first systematic framework to measure how all exposures — from chemical to social — interact with biology across the lifespan,” says Miller. “Our goal is to create actionable strategies for healthier lives.”

For years, doctors have been puzzled by the mysterious case of post-treatment Lyme disease syndrome (PTLD), where patients who have received treatment for Lyme disease still experience severe fatigue, cognitive challenges, body pain, and arthritis. A recent study found that 14% of patients who were diagnosed and treated early with antibiotic therapy would still develop PTLD.

Now, Northwestern University scientists believe they have cracked the code to understanding the causes behind this condition. According to Brandon L. Jutras, a bacteriologist leading the research, the body may be responding to remnants of the Borrelia burgdorferi cell wall, which breaks down during treatment yet lingers in the liver.

The key lies in peptidoglycan, a structural feature of virtually all bacterial cells and a common target of antibiotics. Jutras’ team found that while peptidoglycan from other bacteria is rapidly shed after treatment, Lyme disease’s peptidoglycan persists for weeks to months. In humans, pieces of this peptidoglycan were omnipresent in the fluid of patients with Lyme arthritis, even after treatment.

The research suggests that the maladaptive response to these lingering molecules may be behind PTLD. Jutras explained that some patients have a more robust immune response, which could result in a worse disease outcome, while others’ immune systems largely ignore the molecule. This individualized response is likely influenced by genetic factors.

The findings open up new avenues for research and treatment options. Jutras hopes to develop more accurate tests for PTLD patients and refine treatment options when antibiotics have failed. He also proposes neutralizing the inflammatory molecule using monoclonal antibodies to target peptidoglycan for destruction.

With this breakthrough, scientists are one step closer to understanding and effectively treating PTLD, providing relief to millions of people worldwide affected by this debilitating condition.