Browse the evidence

The Visceral Adiposity Index (VAI) is a superior surrogate marker for arterial stiffness compared to BMI or waist circumference, as it remains an independent predictor of increased brachial-ankle pulse wave velocity (baPWV) even after adjusting for confounding factors.

If you are concerned about heart health and obesity, relying solely on your weight (BMI) or waist size may be misleading. A more comprehensive index (VAI) that includes blood lipid levels (Triglycerides and HDL) alongside your waist and weight provides a better assessment of arterial stiffness risk, even if you appear metabolically healthy.

Individual dietary advice to reduce salt intake fails to produce clinically important reductions in cardiovascular mortality or morbidity in normotensive or hypertensive populations.

Relying solely on your own willpower to reduce salt intake through advice is unlikely to significantly lower your risk of cardiovascular death or events. The evidence suggests that individual behavioral changes are hard to sustain and have limited clinical impact on mortality. Consider that structural or environmental changes to food sources might be more effective than individual dietary advice alone.

Brown adipose tissue (BAT) is present and metabolically active in adult humans, particularly after cold exposure, challenging the historical view that adult humans lack significant brown fat.

Recent evidence confirms that adult humans possess active brown adipose tissue, which can be stimulated by cold exposure. While this does not replace the need for diet and exercise, it suggests that cold exposure may be a valid adjunct strategy to increase energy expenditure by activating this tissue.

The transcription factor PRDM16 controls the bidirectional switch between skeletal muscle and brown adipose tissue, promoting brown adipogenesis.

PRDM16 is a key regulator of brown fat development in rodents. While it offers a promising molecular target for future obesity treatments, its direct application in humans is not yet established.

The presence of markets (grocery stores) in one's local food environment is negatively associated with obesity and abdominal obesity, although this association may not be significant when accounting for city-level clustering.

Having grocery stores nearby is associated with a lower risk of obesity, although this effect might be influenced by broader city-level factors. If you have access to markets, use them to stock up on healthy foods. However, be aware that your overall city environment also plays a role.

Short-term thyroxine (T4) supplementation (200 mg/day for 3 days) in healthy euthyroid males reduces skeletal muscle mitochondrial efficiency (state 3 respiration and RCR) by approximately 30% without altering ATP demand or exercise efficiency.

Taking T4 (thyroxine) for 3 days at a dose of 200 mg/day in healthy men does not improve exercise efficiency or resting metabolic rate significantly. However, it does reduce the efficiency of skeletal muscle mitochondria, meaning the muscles become less effective at producing ATP. This suggests that T4 supplementation in healthy individuals may impair mitochondrial function without providing metabolic or performance benefits.

Among Indian women with PCOS, adherence to a vegetarian diet is associated with significantly higher pro-inflammatory markers (hs-CRP, resistin) and lower anti-inflammatory markers (adiponectin) compared to non-vegetarian counterparts.

If you have PCOS and follow an Indian vegetarian diet, your inflammatory markers (like hs-CRP) might be higher than if you ate a non-vegetarian diet with more fat and protein. This doesn't mean you should stop being vegetarian, but it suggests that the specific high-carbohydrate, low-fat composition of traditional Indian vegetarian diets might not be optimal for inflammation in this specific group. Consider discussing macronutrient balance with a dietitian.

Human milk consumption in infancy is associated with lower risk of obesity, type 2 diabetes, and cardiovascular disease in adulthood, mediated by improved glucose homeostasis, lipid metabolism, and gut microbiota modulation.

Breastfeeding offers long-term metabolic advantages, including lower risks of obesity and diabetes, likely due to unique components like oligosaccharides that shape gut health and energy regulation. If breastfeeding is not possible, focus on high-quality nutrition for the infant, as the metabolic programming benefits are significant but not exclusive to breast milk.

Weight loss interventions induce significant but small changes in DNA methylation (DNAm) across the genome, and baseline DNAm levels at specific loci (e.g., TNF-α, LEP, CLOCK, PER2) can predict the magnitude of weight loss response.

Your body's epigenetic markers (DNA methylation) change when you lose weight, and your starting levels might predict how much weight you'll lose. While these changes are small on a genome-wide scale, specific markers like TNF-α and LEP show promise as predictors. This suggests personalized medicine may eventually use these markers to tailor weight loss strategies, but for now, standard interventions (diet/exercise/surgery) remain the primary lever.

Acute moderate-intensity endurance exercise increases nuclear p53 abundance in untrained human skeletal muscle, suggesting a pro-autophagy response to clear damaged components before mitochondrial biogenesis.

For untrained individuals, a single 60-minute moderate-intensity cardio session triggers a cellular cleanup process (autophagy) mediated by p53 moving to the cell nucleus. This cleanup likely happens before the muscle builds new mitochondria. To support this natural adaptation, ensure you are recovering adequately and maintaining consistent activity levels.

PP protects against beta-cell apoptosis and may improve insulin sensitivity by enhancing the availability of insulin receptors.

PP may protect beta-cells and improve insulin sensitivity, suggesting potential anti-diabetic benefits.

Consuming raw milk does not reduce lactose malabsorption or lactose intolerance symptoms compared to pasteurized milk in adults with confirmed lactose malabsorption.

If you have confirmed lactose malabsorption, switching to raw milk will not help you digest lactose better than regular pasteurized milk. The lactose content is identical, and your body will process it similarly. You are better off sticking to pasteurized milk or lactose-free options to avoid the health risks of raw milk without gaining any digestive benefit.

Bariatric surgery is the only weight-loss treatment providing sustained weight loss and improvement of obesity-related comorbidities, yet access is inequitably distributed based on sociodemographic factors.

Bariatric surgery is the most effective treatment for morbid obesity, but access is not equal. If you meet the medical criteria (BMI ≥40 or ≥35 with comorbidities), systemic factors like income, race, or location may prevent you from receiving it. The paper calls for identifying these specific barriers to improve equity.

Weight loss in obese individuals fails to resolve visceral adipose tissue (VAT) inflammation because senescent CD153+ PD-1+ CD4+ T cells persist and continue to produce osteopontin, maintaining a chronic inflammatory loop despite fat mass reduction.

If you have been obese for a long time, simply losing weight may not fully restore your metabolic health because your body retains 'senescent' immune cells that keep you inflamed. To mitigate this, focus on strategies that reduce chronic inflammation (like exercise and anti-inflammatory diets) in addition to weight loss, as weight loss alone may not clear these persistent immune cells.

GLP-1 receptor agonists (specifically exenatide) reduce fat mass and energy intake in HO patients but do not significantly alter BMI compared to placebo in the short term, and may decrease total energy expenditure.

Exenatide may help reduce fat mass and waist size in HO, but it often fails to lower BMI significantly. It is not a magic bullet for HO and requires careful monitoring for side effects like nausea.

Setmelanotide (MC4R agonist) is effective in reducing hunger and BMI in patients with HO due to hypothalamic injury, particularly those with specific genetic defects or structural damage affecting the melanocortin pathway.

Setmelanotide is a promising new treatment for HO that targets the root cause (MC4R deficiency). It requires daily injections and may cause skin darkening, but it is one of the few treatments showing efficacy in reducing BMI in this specific population.

Post-liver transplant lifestyle interventions must prioritize psychological coping and emotional resilience before addressing physical diet and exercise prescriptions to ensure adherence and effectiveness.

If you have had a liver transplant, do not force yourself into a strict diet or exercise routine until you feel emotionally stable. Your medical team should address your anxiety and coping mechanisms first. Once you feel mentally ready, start with small, guided physical activities tailored to your specific recovery stage.

Exogenous administration of undercarboxylated osteocalcin (ucOC) improves whole-body and skeletal muscle glucose metabolism and insulin sensitivity in animal models, though human evidence remains discordant.

Current research suggests that bone-derived factors like osteocalcin may help regulate blood sugar, especially in muscle. However, because human studies are inconsistent, there is no specific protocol to manipulate osteocalcin levels for diabetes treatment yet. Focus on proven methods: exercise (which naturally increases ucOC) and maintaining healthy bone density.

Sclerostin levels are elevated in individuals with Type 2 Diabetes and insulin resistance, and blocking sclerostin signaling improves insulin sensitivity in animal models.

High levels of sclerostin are linked to insulin resistance. While drugs targeting sclerostin (like romosozumab) exist for osteoporosis, their metabolic benefits are still being studied. For now, exercise and weight management remain the best ways to improve insulin sensitivity.

GLP-1 receptor agonists (specifically exenatide) reduce body fat and waist circumference in patients with hypothalamic obesity, with greater adiposity reduction observed in those with more extensive hypothalamic damage.

For patients with hypothalamic obesity, weekly exenatide injections (2 mg) can significantly reduce body fat and waist circumference, even if BMI changes are modest. This treatment is particularly effective for those with severe hypothalamic damage, likely because it works through brain pathways outside the damaged area. Side effects are mostly gastrointestinal.

Setmelanotide, a melanocortin-4 receptor (MC4R) agonist, reduces hunger and BMI in patients with hypothalamic obesity caused by acquired hypothalamic injury, marking a potential breakthrough for this condition.

Setmelanotide is an MC4R agonist that reduces hunger and BMI in patients with hypothalamic obesity. It is FDA-approved for genetic obesity and is showing effectiveness for acquired hypothalamic injury. A large Phase 3 trial is currently underway.

A technology-based intervention combining weekly telephone counseling with WiFi scale monitoring is not effective in reducing excess gestational weight gain among women with overweight or obesity compared to treatment as usual.

For pregnant women with overweight or obesity, using a WiFi scale and weekly phone calls with a dietitian starting in the second trimester does not appear to be enough to prevent excessive weight gain compared to standard care. The intervention failed to show benefits, suggesting that more intensive or earlier-starting interventions may be required for this high-risk group.

Skeletal muscle regeneration efficiency is time-of-day dependent, with injury occurring during the active phase (when satellite cell BMAL1 expression peaks) resulting in enhanced repair compared to injury during the inactive phase.

If you sustain a muscle injury or undergo strenuous exercise that causes damage, your body repairs the tissue more effectively during your active phase (typically daytime for humans). This is driven by satellite cell clocks peaking in activity (BMAL1) during this time. While you cannot control the injury, scheduling intense training sessions during your active phase may theoretically support faster or more robust repair compared to late-night sessions, though human data is still emerging.

The molecular clock component BMAL1 is required for satellite cell proliferation and the metabolic transition from oxidative to glycolytic energy sources during early muscle regeneration.

BMAL1 acts as a metabolic switch for muscle stem cells. When muscle is damaged, these cells must switch from resting energy (oxidative) to building energy (glycolytic) to multiply. BMAL1 regulates this switch. Disrupting your circadian rhythm (e.g., chronic shift work) might impair this metabolic flexibility, potentially slowing down the initial proliferation phase of muscle repair.