Browse the evidence

Exogenous infusion of sodium-3-hydroxybutyrate (ketone bodies) in healthy humans significantly reduces myocardial glucose uptake and increases myocardial blood flow.

For healthy individuals, raising ketone levels (e.g., through fasting, ketogenic diet, or supplementation) shifts the heart's fuel source from glucose to ketones and increases blood flow to the heart muscle. This metabolic shift may be beneficial for cardiac efficiency and health, particularly in conditions where glucose utilization is impaired or blood flow is restricted.

Human skeletal muscle contains two distinct muscle stem cell (MuSC) subpopulations: a 'quiescent' population (MuSC1) characterized by high PAX7 and EGFR expression, and an 'early-activated' population (MuSC2) characterized by inflammatory markers (TNFRSF12/FN14, CCL2) and signs of dysfunction associated with aging and wasting diseases.

This research highlights that muscle stem cells are not all the same. In healthy, young muscle, most stem cells are 'quiescent' (resting) and express EGFR, which is crucial for proper repair. However, in aging or disease states, a subset of stem cells becomes 'early-activated' and expresses inflammatory markers (like TNFRSF12/FN14) associated with muscle wasting. For fitness, this implies that maintaining muscle health through resistance training may help preserve the healthy, quiescent pool and prevent the shift toward this dysfunctional, inflammatory state seen in aging.

Obesity is metabolically heterogeneous, distinguished by metabolically unhealthy obese (MUHO) phenotypes exhibiting insulin resistance, inflammation, and altered metabolite profiles, versus metabolically healthy obese (MHO) phenotypes.

Do not assume that a high BMI automatically implies poor metabolic health or high disease risk. Metabolically Healthy Obesity (MHO) exists, but Metabolically Unhealthy Obesity (MUHO) carries specific risks like insulin resistance and inflammation. To understand your actual health risk, metabolic markers (like blood sugar, lipids, and inflammation) must be tested, as BMI alone is insufficient.

As food systems transition from rural/traditional to industrial/consolidated, the affordability of a recommended nutritious diet improves significantly, yet industrial systems fail to deliver optimal nutrition, environmental sustainability, and equity.

Do not assume that simply having the money to buy a 'healthy' diet guarantees good health outcomes. In industrialized food systems, while you can afford the recommended diet, the actual quality, environmental impact, and equity of that food supply may still be suboptimal. Focus on the quality and source of food, not just its cost.

Six weeks of supervised endurance exercise alters gut microbiome composition (increasing Akkermansia, decreasing Proteobacteria) and function in overweight women, but these changes do not translate into significant systemic metabolic improvements or major body composition changes.

If you are an overweight woman doing 6 weeks of endurance exercise, expect your gut bacteria to shift (more Akkermansia, less Proteobacteria) and your fitness to improve, but do not expect significant weight loss or major metabolic changes unless you also adjust your diet. The gut changes are real but may not immediately impact your blood work or scale weight.

Sleeve Gastrectomy (SG) is associated with higher T2DM relapse rates and less sustained glycemic control compared to Roux-en-Y Gastric Bypass (RYGB) over a 5-year period.

If you have already had Sleeve Gastrectomy (SG) and achieved diabetes remission, be aware that the risk of diabetes returning (relapse) is higher compared to those who had Gastric Bypass (RYGB). Regular monitoring of your blood sugar is crucial, as SG may not sustain remission as effectively as RYGB in the long term.

Oxidative stress, driven by excessive reactive oxygen species (ROS) from both endogenous (mitochondrial dysfunction, NOX activity) and exogenous (air pollution, UV, smoking) triggers, is a central causal mechanism in cellular senescence and the pathogenesis of aging-related diseases including neurodegeneration, cardiovascular disease, and cancer.

Aging and many chronic diseases are linked to cellular damage from oxidative stress. You can mitigate this by reducing exposure to external triggers like air pollution, UV radiation, and smoking, and by maintaining healthy lifestyle habits such as regular exercise and a balanced diet rich in antioxidants, which help manage internal ROS levels.

Dietary fiber promotes the production of beneficial tryptophan metabolites, specifically indolelactic acid (ILA) and indolepropionic acid (IPA), by making more tryptophan available for Stickland fermentation.

To support gut health and potentially reduce the production of harmful metabolites like indole, incorporate fermentable fibers (such as pectin found in apples) into your diet. This encourages beneficial bacteria to produce protective metabolites (ILA, IPA) and suppresses the production of indole, which is linked to chronic kidney disease risk.

A 76-protein plasma proteomic signature of age (PROage) and its derived measure of biological age acceleration (PROaccel) predict the accumulation of chronic diseases (multimorbidity) and all-cause mortality independent of chronological age.

Your chronological age is not your destiny. This research identifies a specific set of 76 proteins in your blood that act as a 'biological clock.' If your biological age (calculated from these proteins) is higher than your actual age, you are at significantly higher risk for developing multiple chronic diseases and dying earlier. This test can identify 'fast-agers' who may benefit from early, intensive lifestyle or medical interventions to slow down this biological acceleration, rather than waiting for symptoms to appear.

Aging is characterized by a significant decline in adaptive homeostasis capacity, specifically the inability to transiently expand or contract homeostatic ranges in response to sub-toxic stressors, leading to increased susceptibility to damage and mortality.

As you age, your body's ability to bounce back from minor stressors (like mild exercise or dietary changes) diminishes. This isn't just about damage accumulation; it's about losing the signaling capacity to adapt. To maintain healthspan, focus on avoiding chronic, repetitive stressors rather than seeking constant 'hormetic' spikes, as your adaptive reserves are likely compressed.

Early aggressive provision of full caloric and protein targets in critically ill patients provides no clinical benefit and may cause harm, whereas permissive underfeeding (restricted feeding) during the acute phase reduces ICU-acquired weakness and improves outcomes.

In the first week of critical illness, do not aim to meet full caloric or protein targets. Instead, use a 'permissive underfeeding' strategy. This approach has been shown to reduce muscle weakness and improve recovery compared to aggressive feeding. Focus on safety and tolerance rather than hitting specific calorie numbers immediately.

Strength training does not significantly affect maximal oxygen uptake (VO2max), velocity at VO2max, blood lactate levels, or body composition in middle- and long-distance runners.

Do not expect strength training to increase your VO2max or change your body weight significantly. Its primary benefit lies in improving running economy and sprint speed, not aerobic capacity or body composition.

Aging is characterized by a loss of structural and functional complexity in physiological systems, which impairs adaptability and leads to disease.

View aging not just as damage accumulation, but as a loss of system flexibility. Maintaining diverse physical and cognitive challenges may help preserve the 'complexity' that protects against sudden health failures.

The gut-microbiome derived metabolite 3-(4-hydroxyphenyl)lactate is significantly associated with hepatic fibrosis and steatosis in NAFLD, sharing a significant genetic determination with these liver conditions.

This research highlights that a specific gut-derived metabolite, 3-(4-hydroxyphenyl)lactate, is linked to liver scarring (fibrosis) and fat accumulation in NAFLD. While this is a biomarker finding rather than a direct treatment, it suggests that modulating gut microbiome composition or function could be a future therapeutic target for managing NAFLD progression. Patients should focus on general gut health through fiber-rich diets and avoiding unnecessary antibiotics, as these support a healthy microbiome, though specific 'probiotic' prescriptions for this metabolite are not yet established.

Nonalcoholic fatty liver disease (NAFLD) is a systemic condition with multifactorial pathogenesis, not merely a hepatic manifestation of metabolic syndrome, and it can precede the development of metabolic syndrome and type 2 diabetes.

NAFLD is not just a liver issue; it is a systemic metabolic disorder that can drive diabetes and heart disease risk. Even if you are lean, genetic factors or gut health issues can cause it. Focus on metabolic health markers (blood sugar, lipids) rather than just weight, and prioritize lifestyle changes that improve insulin sensitivity and gut health, as these address the root multifactorial causes.

Genetic variants, specifically PNPLA3 I148M and TM6SF2 E167K, significantly increase the risk of liver disease progression and hepatocellular carcinoma in NAFLD patients, independent of metabolic syndrome severity.

If you have a family history of liver disease or known genetic variants like PNPLA3, you are at higher risk for liver damage even if your weight is normal. This means you need stricter monitoring of liver enzymes and fibrosis markers, and you must be aggressive with lifestyle interventions to reduce liver fat and inflammation.

Wearable sleep-tracking technology introduces healthcare disparities because sensor performance is negatively impacted by person-specific factors such as skin color and obesity, leading to inaccurate data for minority and obese populations.

If you have darker skin or obesity, be aware that consumer sleep wearables may be less accurate for you. Do not use these devices for critical health decisions without verifying their accuracy against clinical standards for your specific body type.

Downregulation of genes encoding mitochondrial proteins is a highly conserved hallmark of cellular ageing across multicellular eukaryotes, correlating with reduced mitochondrial function and lifespan.

Aging is associated with a consistent drop in the genetic instructions for making mitochondrial proteins. While this is a hallmark of aging, interventions like caloric restriction or metformin can reverse this specific gene expression change, suggesting that maintaining mitochondrial gene expression levels may be beneficial for healthspan.

Downregulation of ribosomal proteins and ribosome biogenesis factors is a conserved hallmark of cellular ageing, likely serving as a protective programme rather than a cause of pathology.

Aging involves a reduction in the genetic instructions for building ribosomes. This is not a defect but a protective mechanism. Interventions that extend lifespan, such as caloric restriction and rapamycin, also reduce these levels, suggesting that this downregulation is beneficial for longevity.

Dysregulation of immune system genes, specifically the upregulation of inflammation-associated genes (inflammaging), is a conserved transcriptional hallmark of cellular ageing.

Aging is associated with a consistent upregulation of immune and inflammation-related genes. This 'inflammaging' is linked to senescent cells and immune dysfunction. Interventions like metformin can reduce this inflammation, suggesting that managing chronic low-grade inflammation is relevant to healthspan.

Poor dietary intake in low-income groups is an emergent property of a complex adaptive system that sustains a food environment increasing the accessibility, availability, affordability, and acceptability of unhealthy foods.

For policymakers and advocates: Do not rely solely on 'food desert' fixes like new supermarkets. Interventions must simultaneously address household financial strain, social/cultural norms, and the systemic drivers that make unhealthy food the rational choice for low-income households.

Dietary intake in low-income groups is driven more by demand-side factors (social, cultural, economic) than by supply-side factors (accessibility, availability).

For health educators: Nutrition education alone is ineffective if it doesn't address the economic and social realities of low-income households. Interventions must focus on making healthy choices financially viable and socially supported, not just 'known'.

Dietary nitrate supplementation does not improve performance in highly trained endurance athletes during cycling or running, likely due to higher baseline nitric oxide bioavailability.

If you are an elite endurance athlete, stop wasting money on beetroot juice for running or cycling; it won't help you. Focus on training.

Accumulation of senescent endothelial cells and vascular smooth muscle cells drives the progression of atherosclerosis and hypertension.

Cellular aging in blood vessels contributes to heart disease and high blood pressure. Managing cardiovascular risk factors may help slow this process.