Inflammation is often described as something that should be reduced. But biologically, inflammation is not inherently pathological. It is part of how the body responds to infection, injury, metabolic disturbance, and other forms of stress. The more important question may be: Can the inflammatory response finish its job and resolve? A recent review by Melo-Florián and Melo-Ramírez reframes inflammaging—the chronic, low-grade inflammatory state associated with aging—as much mor

For decades, lactate was treated mainly as a waste product of strenuous exercise. That view has changed dramatically. Lactate is now understood as an energy substrate, a signaling molecule, a regulator of blood flow and inflammation, and potentially even an epigenetic messenger. A new 2026 review by Ablitip and colleagues brings these ideas together in an intriguing framework they call the “Lactate Nexus.” Their central proposal is that lactate may provide a molecular bridge

For decades, aging research has largely focused on what goes wrong with time: DNA damage accumulates, mitochondria become less efficient, proteins lose quality control, inflammation becomes persistent, stem cells lose regenerative capacity, and senescent cells accumulate. The hallmarks of aging framework helped organize these changes into a coherent biological map. But a deeper question is now becoming increasingly important: Why do these changes persist? Perhaps aging is not

Stress is not automatically harmful. In fact, much of biology depends on the ability to detect a challenge, temporarily redirect resources, and then return toward normal function. The problem begins when that return never fully happens. Two recent reviews—one on the integrated stress response (ISR) and another on PERK and endoplasmic reticulum (ER) stress in aging—help explain how this transition may occur at the cellular level. Together, they describe a remarkably coherent s

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