🎯 Today's Nutrition Pulse
Precision nutrition poised to reshape chronic liver disease management
A new narrative review outlines how integrating genomics, metabolomics, gut‑microbiome data and lifestyle factors can personalize nutrition across the lifecycle of chronic liver disease. The authors propose stage‑specific diets, from Mediterranean‑style low‑energy plans in early disease to protein‑rich, micronutrient‑supplemented regimens in advanced stages.
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Valorization of Wine Industry By-Products as a Flavoring Agent in Water Kefir: Microbiological Viability and Functional Properties
IntroductionThis study developed a functional water kefir beverage flavored with grape pomace (Vitis labrusca.) and evaluated its physicochemical, microbiological, and sensory properties, alongside its functional effects in a Caenorhabditis elegans model.MethodsFour treatments were tested: 0% (KC), 25% (K25), 37.5% (K37.5), and 50% (K50) pomace addition.ResultsAnthocyanin and phenolic contents were dose-dependent, peaking in K50 (33.56 mg L−1 and 4.31 mg g−1, respectively). During 21 days of refrigerated storage, a decrease in reducing sugars, pH (4.3 to 3.5), and a concomitant increase in acidity (up to 6.60%) were observed, reflecting continuous microbial metabolic activity. Due to excessive acidity and residual taste, K37.5 and K50 were deemed unfeasible. Consequently, K25 was selected for biological and sensory validation. In K25, yeast and acetic acid bacteria (AAB) maintained high viability (107 CFU mL−1), whereas lactic acid bacteria (LAB) remained below 105 CFU mL−1 due to the selective pressure of the grape pomace. K25 achieved a sensory acceptance index of 76.11% and a 65% purchase intention.DiscussionThese results indicate that water kefir flavored with 25% grape pomace is a viable probiotic carrier rich in bioactive compounds with promising sensory appeal.
Frontiers in Nutrition
Time-Restricted Eating and Metabolic Health: Implications for Nutritional Strategies and Weight Loss
Time-restricted eating (TRE) has emerged as a promising dietary strategy within the field of chrononutrition, focusing on the temporal organization of food intake rather than caloric restriction alone. This mini review summarizes current evidence on the effects of TRE on body weight, metabolic health, and circadian regulation. Experimental and clinical studies suggest that TRE, typically involving daily eating windows of 6–10 h, may promote modest weight loss and improvements in glycemic control, insulin sensitivity, and lipid profile. Some effects have been observed even in the absence of significant weight loss, supporting a potential role of meal timing in cardiometabolic regulation, although findings are still inconsistent. Data indicates that many of the identified advantages appear to be largely driven by spontaneous caloric restriction, with several randomized controlled trials showing no additional benefits of TRE compared to conventional hypocaloric diets. The timing and duration of the eating window might influence outcomes, with early TRE and moderate eating windows having more favorable results than delayed or extreme protocols. Circadian biology provides a mechanistic framework for understanding these effects, as alignment between feeding-fasting cycles and endogenous rhythms can enhance metabolic efficiency. Most studies do not account for individual chronotype, and evidence on circadian, inflammatory, and behavioral outcomes remains limited. TRE represents a feasible and non-invasive dietary approach with potential health benefits, particularly when compared to unrestricted eating patterns, although its superiority over caloric restriction alone has not been fully elucidated. Future research should prioritize long-term interventions, standardized protocols, and the integration of circadian factors, particularly chronotype, to better elucidate the role of TRE in metabolic health and clinical practice.
Frontiers in Nutrition
Precision Nutrition in Gastric Cancer: Current Advances and Future Directions
Patients with gastric cancer frequently experience malnutrition, weight loss, and sarcopenia from diagnosis through treatment and follow-up. These conditions are not solely attributable to inadequate intake but are closely related to systemic inflammation, metabolic reprogramming, treatment-related toxicities, and altered digestion and absorption after gastrectomy. This review summarizes the theoretical basis, assessment approaches, stage-specific intervention strategies, and current evidence limitations of precision nutrition in gastric cancer. It focuses on nutritional risk screening, diagnosis of malnutrition based on the Global Leadership Initiative on Malnutrition (GLIM) criteria, computed tomography (CT)-based body composition analysis, energy and protein provision, support pathways including oral nutritional supplements, enteral nutrition, and parenteral nutrition, as well as emerging areas such as immunonutrition, microbiota-targeted interventions, AI-assisted body composition analysis, and multi-omics integration. Current evidence suggests that precision nutrition in gastric cancer should remain grounded in standardized nutritional assessment and guideline-recommended supportive strategies. Prospective, multicenter studies are needed to clarify the benefits and scope of nutritional interventions across different nutritional phenotypes.
Frontiers in Nutrition
The Skinny-Fat Paradox: Why a "Normal" BMI Leaves Millions of Women Critically Vulnerable to Metabolic Decay
Body Mass Index (BMI) has long served as the clinical gold standard for obesity screening, yet its reliance on crude height-to-weight ratios obscures a dangerous physiological reality. A growing body of medical literature identifies a highly prevalent, underdiagnosed cohort: individuals who possess a perfectly “normal” BMI (18.5–24.9 kg/m2) but exhibit a pathologically high body fat percentage (>25% for men, >30% for women). This condition, termed Normal Weight Obesity (NWO), represents a hidden public health crisis that disproportionately targets women, who face a two- to six-fold higher risk of developing the phenotype compared to men. The clinical hazard of NWO lies in its ability to evade traditional anthropometric screenings while quietly driving systemic deterioration. Because these individuals appear outwardly lean, underlying hormonal, metabolic, and musculoskeletal dysregulation accumulates unchecked. Throughout the female lifespan, this phenotype interacts destructively with natural endocrine shifts. During the reproductive years, high total and visceral adipose tissue (VAT) promotes chronic low-grade inflammation, insulin resistance, and ovulatory disorders—frequently masked by widespread use of hormonal contraceptives. As women transition into perimenopause and postmenopause, the rapid decline in estrogen amplifies central fat accumulation, triggering a cascading failure in tissue quality. Adipose tissue infiltrates the skeletal muscle architecture (myosteatosis), causing localized lipotoxicity, structural fiber misalignment, and a dramatic drop in muscular force production. Simultaneously, the protective structural adaptations that typically defend bone mineral density in standard obesity are absent in NWO due to a severe deficit in lean mass, leaving women uniquely vulnerable to silent microarchitectural bone decay and catastrophic fracture risks. Actionable Insights To counteract the insidious progression of NWO, individuals and clinicians must shift focus from total body mass to precise tissue composition and metabolic quality. Mandatory Advanced Screening: Relying on BMI is insufficient, as it misclassifies over 50% of individuals with excess adiposity. Individuals must utilize advanced body composition tracking, such as Dual-Energy X-ray Absorptiometry (DXA) or Bioelectrical Impedance Analysis (BIA), to establish precise lean mass and visceral fat metrics. High-Frequency Resistance Training: To reverse the metabolic and structural damage of NWO, regular resistance exercise is non-negotiable. Data from young female cohorts indicates an exceptional preventive effect size: women are 48% less likely to have NWO if they are physically active more than 3 times per week. Resistance training directly targets the hallmark SMM deficits (NWO women carry an average 4 kg less skeletal muscle mass than lean controls) while restoring peripheral leptin sensitivity and mitigating myosteatosis. Nutritional Optimization: Diets must be engineered to optimize protein intake to actively support muscle protein synthesis and prevent the preferential differentiation of mesenchymal stem cells into adipocytes rather than bone-forming osteoblasts. Routine Endocrine Tracking: Longevity protocols must include proactive blood biomarker panels tracking lipid profiles, fasting glucose, and sex hormone variations to capture subclinical metabolic syndrome before clinical symptoms manifest. This is critical for postmenopausal women with NWO, who suffer a massive 200% increase in odds (double the odds) of presenting with at least two metabolic syndrome risk factors compared to lower-adiposity peers. Source: Open Access Paper: Beyond BMI: The musculoskeletal and metabolic consequences of normal weight obesity across the female lifespan Lead Institution: University of Idaho, USA Collaborating Countries: United States, Canada, South Africa Journal Name: Women’s Health Impact Evaluation: The impact score of this journal is not explicitly stated in the source text. Related Reading: Amount of Central Fat Predicts Mortality Risk in Non-Obese Individuals The Kyoto Cocktail: Can a High-Carotenoid "Salad in a Glass" Melt Visceral Fat? Greater visceral fat mass accumulation with high alcohol consumption Sustained visceral fat loss is associated with attenuated brain atrophy and improved cognitive function in late midlife (paper March 26) Rapamycin and Visceral Fat Reduction Mike Lustgarten Video Series - #7 by RapAdmin
Rapamycin News
Why Tiny Amounts of Vitamin B12 Matter More as We Age
Berna Namoglu/Shutterstock Two micrograms is an almost unimaginably small amount. It weighs less than a tiny fragment of a grain of table salt. Yet adults need only around this amount of vitamin B12 each day, depending on the guideline used, to support red blood cells, nerves and DNA production. In 2026, it is 100 years since George Minot and William Murphy reported that a liver-rich diet could treat pernicious anaemia, then a frequently fatal disease. Their work transformed medicine and eventually led scientists to identify vitamin B12 as the substance in liver that treated the disease. But the route to that breakthrough began with an unexpected clue from animal experiments. The American physician and pathologist George Whipple had shown that liver helped dogs recover from anaemia caused by blood loss. Blood-loss anaemia happens when the body loses red blood cells through bleeding. Pernicious anaemia is different: the problem is not bleeding, but poor absorption of vitamin B12. Even so, Whipple’s experiments pointed researchers towards liver as a source of a powerful blood-forming factor. Patients with pernicious anaemia who had been close to death often improved dramatically within weeks of eating liver-rich diets. The success of liver treatment eventually led scientists to isolate the deep red compound now known as vitamin B12, or cobalamin. Often mistaken Despite decades of research, vitamin B12 deficiency remains common, particularly among older adults, vegans, vegetarians and people with conditions that affect absorption. Some people do not consume enough B12 because it is naturally found mainly in foods from animals, including meat, fish, eggs and dairy products. Others struggle to absorb it properly. This becomes more common with age. Some older people produce less stomach acid, which is needed to release B12 from food. Others develop autoimmune gastritis, in which the immune system damages stomach cells involved in producing acid and intrinsic factor, the protein needed for vitamin B12 absorption. Weight-loss surgery and some medicines used for diabetes or acid reflux can also reduce absorption. The symptoms of deficiency can develop slowly and are often mistaken for normal ageing. People may feel exhausted, weak or short of breath. Some develop numbness or tingling in their hands and feet, poor balance, memory problems or what many describe as “brain fog”. These symptoms are not specific to B12 deficiency, so persistent tiredness, tingling or balance problems should be checked rather than assumed to be a simple vitamin problem. People at higher risk, including vegans, vegetarians, older adults and those taking medicines that affect stomach acid or diabetes treatment, may need testing or supplementation advice from a health professional. Vegan and vegetarian diets may lack certain nutrients – here’s how to get more of them Doctors have traditionally linked tiredness in B12 deficiency to anaemia. Without enough vitamin B12, the bone marrow cannot produce healthy red blood cells. Instead, it releases unusually large and immature cells that carry oxygen less effectively around the body. But anaemia may not be the only reason people with low B12 feel exhausted. Low energy In humans, vitamin B12 is directly needed by only two enzymes, the proteins that help chemical reactions happen in the body. One helps the body make DNA, which cells need when they divide. The other helps mitochondria process certain fats and protein building blocks. Mitochondria are the tiny structures inside cells that help turn food into usable energy. This mitochondrial role has attracted growing interest from researchers studying ageing, muscle function and vitamin B12 status. A 2026 study explored what happens when cells do not have enough B12. Researchers found that low B12 could interfere with the DNA inside mitochondria and reduce energy production in laboratory models of skeletal muscle (muscle cells studied outside the human body). A related study in aged female mice found that B12 supplementation improved several signs of mitochondrial health in muscle, including the number and structure of mitochondria. Together, this work points to one possible reason why some people with low B12 report fatigue before obvious anaemia is detected. These findings do not mean vitamin B12 supplements can reverse ageing or act as an energy booster for people whose B12 levels are already normal. Scientists have suspected a link between B12 and mitochondrial function for many years, because one of the two B12-dependent enzymes works inside mitochondria. Earlier research has also suggested that low B12 status may be linked with poorer muscle function in older adults, although much of this work is observational and cannot prove cause and effect. So if you’re feeling persistently tired, is it worth paying for vitamin B12 injections at a wellness clinic or medispa? For most people, no. B12 injections are an established treatment for diagnosed deficiency, particularly when absorption is impaired, and the NHS uses hydroxocobalamin injections for vitamin B12 deficiency anaemia. But there is little evidence that B12 shots boost energy, weight loss or performance in people whose B12 levels are already normal. The more useful first step is to find out what is causing the tiredness. The story of vitamin B12 is unusual because the body needs so little of it, yet the consequences of deficiency can be profound. Long before scientists understood its chemistry, doctors recognised that something in liver could restore strength, appetite and vitality to desperately ill patients. A century later, researchers are still finding that this tiny cobalt-containing molecule does more than prevent anaemia. It may also help explain how cells maintain energy and function as the body ages. Martin Warren receives funding from the Biotechnology and Biological Sciences Research Council (BBSRC) as well as the Advanced Research and Invention Agency (ARIA).
The Conversation – Fashion (global)
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A daily multivitamin can reduce brain aging and modestly slow down epigenetic aging clocks. In the COSMOS trial, older adults who took a standard Centrum Silver multivitamin daily for about 4 years performed better on cognitive tests and showed the equivalent of ~2 years less brain aging compared with those taking a placebo. The multivitamin also slowed epigenetic aging clocks, with an effect equivalent to about 2.7 to 5 months of slowed biological aging. That may sound modest, but I don’t think it’s trivial, and @prof_horvath says that effects from safe, low-cost interventions can matter if they’re sustained over years to decades—2 months of slower biological aging could translate to 2.5 years if a good habit is maintained. These data push back on the idea that multivitamins are “completely useless.” If you’re filling nutritional gaps consistently over time, even a small benefit to cognition and biological aging could become meaningful. From the latest episode of the FoundMyFitness podcast.