A study by researchers at the Federal University of São Carlos (UFSCar) in Brazil, in partnership with University College London (UCL) in the United Kingdom, concluded that the combination of abdominal fat and muscle loss increases the risk of death by 83%, compared to people without these conditions.

This combination is so dangerous that it identifies an even greater problem: sarcopenic obesity. This condition is characterized by loss of muscle mass while gaining fat throughout the body. It is a difficult condition to diagnose, and it is related to loss of autonomy and a worsening quality of life in older adults. It is also known as frailty syndrome and is associated with an increased risk of falls and other comorbidities.

“In addition to assessing the risk of death associated with abdominal obesity and low muscle mass, we were able to prove that simple methods can be used to detect sarcopenic obesity. This is important because the lack of consensus on diagnostic criteria for this disease makes it difficult to detect and treat,” says Tiago da Silva Alexandre, a professor in the Department of Gerontology at UFSCar and one of the authors of the study.

Frequent tanning bed users may have up to an eight times greater risk for melanoma than people considered at high risk for melanoma who don’t use tanning beds, according to a new study that also showed how tanning beds alter melanoma-linked DNA on the molecular level and damage areas of skin not usually exposed to the sun.

A case-control cohort study of patients considered at high risk for melanoma finds that tanning bed users have higher rates of melanoma and disease with significantly more mutations.

Scientists have uncovered new evidence showing how type 2 diabetes directly reshapes the human heart, altering both its energy production and physical structure.

Zhan et al. show that blood vessels serve as a migratory scaffold directing retinal microglial precursor infiltration into the developing retina. Vascular Lamb1 signaling orchestrates this precise migration, indicating a key mechanism guiding retinal microglial colonization during development.

Why do certain immune cells remain permanently active in allergic asthma – even in an environment that should actually damage them? A research team has discovered that these cells only survive because they activate a special antioxidant protection mechanism. When this mechanism is blocked, allergic inflammation in mouse models decreases significantly. The results have now been published in the scientific journal Immunity.

In allergic asthma, so-called ILC2 and Th2 cells are key drivers of inflammation. They produce messenger substances that increase mucus formation and the influx of immune cells. At the same time, the inflamed lung tissue is rich in free fatty acids and oxidative molecules — conditions that normally endanger cells.

The study shows that pathogenic ILC2s absorb large amounts of these fats and incorporate them into their membranes. In order to avoid dying from ferroptosis, an iron-dependent form of cell death caused by oxidized lipids, they activate their antioxidant systems. The enzymes GPX4 and TXNRD1 play a central role in this process. They neutralize harmful lipid peroxides and enable the cells to survive and multiply despite the stressful environment.

To test this approach, the Bonn team inhibited the thioredoxin metabolic pathway using a drug that blocks the enzyme TXNRD1. In mouse models, this led to significantly less ILC2 accumulating in the lungs. As a result, both the production of the typical type 2 cytokines IL-5 and IL-13 and the number of eosinophils and mucus production decreased. Overall, the allergic reaction was significantly less severe.