What muscle biology, bioenergetics and the protein leverage hypothesis tell us about regular protein intake—and why some protein myths need updating For decades, discussions about protein have tended to fall into two extremes. One side treats protein mainly as a bodybuilding nutrient: useful if you want bigger muscles, but otherwise easy to get enough of. The other warns that eating “too much” protein may chronically activate growth pathways, accelerate ageing, increase cance

For much of modern aging research, one of the most influential ways to think about aging has been through the Hallmarks of Aging: genomic instability, telomere attrition, epigenetic alteration, loss of proteostasis, mitochondrial dysfunction, cellular senescence, altered nutrient sensing, and other processes that become increasingly disturbed with age. This framework has been enormously useful. It gave aging biology a common language and helped organize a field that was previ

Most laboratory reports are designed around a simple question: is the result inside or outside the reference interval? That distinction is clinically useful. A markedly abnormal glucose level, inflammatory marker, liver enzyme, or renal marker deserves attention. But biology does not suddenly change at the exact boundary printed beside a laboratory result. Physiological function exists on a continuum. A new study in GeroScience provides an unusually clear example of why this

For decades, nutrition has been framed as a competition between macronutrients. First, fat was blamed for obesity and cardiovascular disease. Then carbohydrate became the problem, particularly through its effects on insulin. More recently, protein has increasingly been promoted as the solution: more satiety, better muscle maintenance, improved body composition and easier weight control. At the same time, another camp warns that too much protein could activate growth pathways

For decades, major depressive disorder has often been explained to the public through a simple story: neurotransmitters such as serotonin or dopamine become imbalanced, and antidepressants help restore them. That explanation was always incomplete. A growing body of research now places depression within a much broader physiological landscape involving metabolism, insulin signaling, inflammation, stress physiology, mitochondrial function, and neural plasticity. Neurotransmitter

When we think about mitochondrial dysfunction, we usually think about fuel. Is enough glucose reaching the cell? Are fatty acids being oxidized efficiently? Is oxygen delivery adequate? Can electrons move through the respiratory chain fast enough to maintain ATP production? These questions are important. But they may describe only part of the problem. A detailed review by Song, Herrmann, and Becker in Nature Reviews Molecular Cell Biology, “Quality control of the mitochondria

Why can two people face similar physiological stress yet recover so differently? One may experience temporary fatigue, adapt, recover, and return to baseline. Another may remain exhausted for days, become increasingly intolerant of exertion, develop pain or cognitive symptoms, and gradually lose resilience. We often explain this difference by looking for a disease, a mitochondrial defect, or a nutrient deficiency. But there may be another way to think about it: What if health

Why does one person remain cognitively resilient into old age while another develops accelerated decline? We often look for the answer in individual factors: omega-3 fatty acids, vitamin D, exercise, sleep, the gut microbiome, glucose control, or perhaps a particular supplement. But a new review in Ageing Research Reviews suggests that this fragmented way of thinking may be too narrow. Shin and colleagues bring together evidence across nutrition, metabolism, physical activity

When we think about recovery, we often imagine something passive: stop the stress, wait long enough, and the body returns to normal. Biology is more demanding than that. Recovery is an active process. It requires time, but it also requires sufficient physiological resources to restore homeostasis, repair structures, replenish reserves, and prepare the system for the next challenge. A remarkable 2026 study in Science provides a vivid example of this principle in the nervous sy

For decades, cholesterol—especially LDL cholesterol (LDL-C)—has been framed primarily as something to lower. The logic is understandable: sustained exposure to ApoB-containing lipoproteins contributes to atherosclerosis, and lowering LDL-C in people at cardiovascular risk reduces cardiovascular events. But biology is rarely captured by a single direction or a single number. A new 2026 study in Cell Reports provides a striking reminder that cholesterol is not merely a cardiova

A new review in Cell Metabolism challenges one of the most familiar assumptions in metabolic medicine: that insulin resistance, reduced insulin secretion, mild hyperglycemia, and even glucosuria are simply signs that glucose regulation is failing. Prentki and colleagues propose something more nuanced. In obesity-related prediabetes and early type 2 diabetes, these changes may initially represent allostatic responses to chronic nutrient excess—coordinated adaptations that help

Why can the same person think clearly, exercise well, tolerate stress, and remain motivated on one day, yet struggle with concentration, effort, or emotional regulation on another? The conventional explanation often focuses on individual neurotransmitters, hormones, or psychological states. A major new review in Nature Reviews Neuroscience offers a broader perspective: the ability of neural circuits to function depends partly on the energetic capacity available to support the

Aging is often described as a gradual decline in immune function. Older adults respond less effectively to infections and vaccines, recover more slowly from tissue injury, and carry a greater burden of chronic low-grade inflammation. At the same time, immune tolerance becomes less reliable: the immune system may fail to restrain unnecessary inflammation while also becoming less effective at eliminating damaged, infected, or abnormal cells. A recent study in Nature Aging offer

Protein restriction, rapamycin, and the missing biology of rhythm A provocative new review, The hallmarks of protein and amino acid restriction in aging and longevity, argues that eating less protein—or restricting particular amino acids—may improve metabolic health, reduce cellular senescence, and extend healthy lifespan. The review brings together an impressive body of evidence. It highlights methionine, isoleucine, and valine as especially influential amino acids and propo

Grey hair is usually treated as a one-way sign of aging: pigment is lost, the follicle has become “old,” and the change is permanent. A study led by Ayelet Rosenberg and Martin Picard challenges that simple picture. By analysing pigmentation patterns along individual human hairs, the researchers documented something unusual but biologically important: some hairs that had turned grey later regained their original colour. The study does not show that stress reduction will relia

The lining of the respiratory tract is often described as a barrier. That description is incomplete. The airway epithelium is a living, metabolically active tissue that detects microbes, communicates with immune cells, produces mucus and antimicrobial molecules, regulates inflammation, and repairs itself after injury. It also appears capable of remembering what it has encountered. A recent review in Cell Reports, “Microbial imprinting of the airway epithelium,” proposes that

When we think about the immune system, we usually picture its defensive side: detecting danger, attacking pathogens, and generating inflammation. But an effective immune response is not complete when the threat is contained. The body must also stop the response, clear the damage, rebuild tissue, and restore tolerance. That final stage is recovery—and recovery requires work. A major 2026 review by Jeffrey Bluestone and colleagues places regulatory T cells, or Tregs, at the cen

Cellular senescence is often described as the end result of accumulated damage. DNA breaks, oxidative stress, telomere shortening, inflammation, and oncogenic signals eventually persuade a cell to stop dividing. That explanation is important, but incomplete. A growing body of research suggests that metabolism is not merely damaged after a cell becomes senescent. The cell’s capacity to transform nutrients into usable energy, maintain redox balance, and support biosynthesis may

Anabolism is the biology of building. Cells build proteins, membranes, nucleotides, organelles and extracellular matrix. Tissues rebuild muscle after exercise, replace damaged cells, expand immune populations during infection and regenerate after injury. These processes require nutrients, hormonal signals and growth pathways—but they also require something more fundamental: sufficient metabolic throughput to convert those signals and raw materials into functional new structur

Senescent cells have become one of the most recognizable targets in longevity science. These are damaged or stressed cells that enter a persistent state in which they no longer function normally and may release inflammatory and tissue-remodeling signals collectively known as the senescence-associated secretory phenotype, or SASP. Because senescent cells accumulate with age and can contribute to chronic inflammation, fibrosis and impaired tissue repair, a seemingly straightfor