Science Today

A large systematic review published in the  British Journal of Sports Medicine  pooled data from 85 studies and found that adults who consistently maintain physical activity are about 30–40 % less likely to die from any cause than those who remain inactive. Even people who increase their activity from below recommended levels enjoy a 20–25 % reduction in mortality risk, and switching from a sedentary lifestyle to an active one at any point in adulthood still offers meaningful benefits. The protective effect is more pronounced for cardiovascular disease than for cancer. Researchers stress that current guidelines—150–300 minutes of moderate or 75–150 minutes of vigorous exercise per week—are evidence-based, yet even smaller amounts of movement are better than none. Beyond lowering mortality risk, physical activity protects nearly every system in the body. The World Health Organization notes that regular activity helps prevent and manage cardiovascular disease, diabetes and some ...

When cells face heat, toxins or other challenges, they temporarily shut down most protein production. Ribosomes detach from RNA, and these unprotected RNA strands condense into stress granules—tiny holding areas until conditions improve. Yet some messenger RNAs (mRNAs) must keep working to help cells survive. Researchers at the University of Michigan discovered that these “rescue” mRNAs stay out of stress granules by hanging onto ribosomes via short upstream open reading frames (uORFs), special sequences at the start of the mRNA. Even a single ribosome bound to an mRNA is enough to prevent it from becoming trapped. The team used chemical inhibitors, single-molecule imaging and engineered RNA reporters to show that removing these uORFs caused mRNAs to lose ribosome association and end up in stress granules. By acting like a molecular “on‑ramp” for ribosomes, uORFs ensure that essential proteins can still be made during a crisis. This insight may inform future strategies for diseases suc...

Researchers at Baylor College of Medicine have uncovered how your genetic makeup and what you eat work together to influence the liver’s daily rhythms. While the circadian clock is known to regulate sleep and metabolism, the new study finds that diet can reshape these rhythms by interacting with gene variants. By examining human liver samples and two strains of mice over a 24‑hour cycle and after feeding them high‑fat diets, the team discovered that genetic differences determine when certain genes turn on or off. Thousands of genes showed daily patterns only in individuals with specific variants High‑fat diets altered gene rhythms in unique ways: some genes maintained their rhythms, others lost them, and some gained new ones. The researchers explored how segments of DNA called enhancers and promoters interact over time and found that more than 80 % of these interactions depend on both genetics and nutrition. They pinpointed ESRRγ, a “noncanonical” clock regulator, as a key player; mice...

Hyperuricemia occurs when the body accumulates too much uric acid because humans lack the enzyme uricase, which normally breaks down purines. A recent review led by Weizheng Zhang explains that high uric acid can develop through a combination of genetic variations (such as differences in genes for uric‑acid transporters and enzymes) and lifestyle factors. Purine‑rich foods (organ meats, red meat, some seafood and beer), obesity, impaired kidney function and dehydration all contribute to this imbalance. When excess uric acid crystallizes, it can trigger gout and raise the risk of cardiovascular disease, metabolic syndrome and kidney problems. The review highlights that lifestyle changes are central to preventing and managing hyperuricemia. Dietary adjustments—such as reducing intake of purine‑dense foods, alcohol and sugar‑sweetened beverages—lower uric‑acid production, while a diet rich in fruits, vegetables and whole grains supports overall metabolic health. Moderate exercise helps wi...

  Researchers working with a cohort of 342 midlife women in Northern California investigated how diet quality relates to biological age at the cellular level. Each participant logged what she ate and provided a saliva sample. The samples were analyzed with an “epigenetic clock,” a molecular test that measures chemical marks on DNA associated with aging. Diets rich in fruit, vegetables, whole grains and other antioxidant‑packed foods – patterns similar to the Mediterranean and other anti‑inflammatory diets – were linked with lower epigenetic. In other words, cells looked “younger” when people followed nutrient‑dense eating habits. A key finding was the role of added sugar. Even among people with otherwise healthy diets, each extra gram of added sugar correlated with a slightly older biological age. Study co‑senior author Elissa Epel, a professor of psychiatry at the University of California, San Francisco, noted that excessive sugar intake accelerates molecular aging and undermines ...

Tiny proteins hidden in our genetic code are changing the way scientists think about cell biology. A research team from the  Salk Institute  recently reported that a newly discovered microprotein,  SLC35A4‑MP , helps maintain the structure and function of mitochondria – the energy‑producing “powerhouses” of our cells. Microproteins like SLC35A4‑MP are encoded in sections of messenger RNA that were once dismissed as non‑coding junk. As analytical techniques improved, researchers realized these regions can encode functional proteins that influence metabolism and stress responses . Why it matters Mitochondria convert nutrients into energy, regulate body temperature and help maintain metabolic balance. When mitochondrial function declines, metabolic diseases such as obesity and age‑related disorders can follow. In the Salk study, researchers focused on  brown fat —a metabolically demanding tissue that generates heat. They removed the gene encoding SLC35A4‑MP from brown f...