Browse the evidence

Muscle typology (determined by muscle carnosine levels) does not explain inter-individual variability in resistance training-induced increases in muscle volume, maximal dynamic strength, or fiber cross-sectional area when training is performed to failure at 60% 1RM.

If you are new to resistance training, your muscle fiber type (whether you are naturally 'fast' or 'slow') does not determine how much muscle or strength you will gain. As long as you train to failure with a moderate load (around 60% of your max), you will see similar improvements regardless of your genetics. Focus on consistency and effort rather than trying to tailor your program to your fiber type.

In healthy adults, total energy expenditure (TEE) is a repeatable, durable trait that is not associated with short-term changes in body weight or body composition, meaning low TEE is not a risk factor for weight gain and high TEE is not protective against fat gain.

Stop blaming your weight on a 'slow metabolism.' This study shows that in healthy adults, metabolic rate is a stable trait and does not predict who gains weight or fat. Whether you burn calories fast or slow, it doesn't inherently protect you from or cause you to gain fat. Focus on the net energy balance (what you eat vs. what you move) rather than trying to 'boost' your metabolism, as your baseline expenditure is likely fixed and repeatable.

Chronic inflammation in adipose tissue, driven by macrophage infiltration (M1 phenotype) and pro-inflammatory cytokine release (TNFα, IL-6), directly causes insulin resistance and contributes to the development of obesity and metabolic syndrome.

Obesity involves a biological feedback loop where excess fat tissue triggers chronic inflammation, which worsens insulin resistance and makes weight loss harder. Reducing fat mass is the most effective way to lower this inflammation and improve metabolic health, rather than just focusing on calorie counting alone.

Hypothalamic inflammation, characterized by microglial activation and increased SOCS3 expression, leads to leptin and insulin resistance in the central nervous system, promoting orexigenic signaling and weight gain.

High-fat, high-calorie diets can cause inflammation in the brain's appetite control center, blunting the 'fullness' signal. Reducing dietary quality and caloric intake can reduce this central inflammation and restore sensitivity to satiety hormones.

Metabolic surgery (specifically Roux-en-Y gastric bypass) yields higher remission rates than adjustable gastric banding, independent of the amount of weight lost.

For obese patients considering surgery, Roux-en-Y gastric bypass offers significantly higher remission rates than adjustable gastric banding, even if the weight loss is similar. This is due to hormonal changes in the gut, not just calorie restriction.

Following unaccustomed eccentric exercise, females exhibit a blunted satellite cell expansion and inflammatory gene expression (Pax7, CCL2) compared to males, suggesting a delayed or reduced myogenic response.

If you are female, your muscle may not expand its satellite cell pool as aggressively as a male's after intense eccentric exercise (like heavy downhill running or heavy eccentrics). This doesn't mean you can't build muscle, but your initial repair signaling might be different. Focus on consistent training and adequate protein intake, as your body may rely on different mechanisms for repair than males.

Exenatide does not demonstrate superior weight loss compared to placebo in adults with craniopharyngioma-related obesity when both groups receive intensive lifestyle interventions.

For adults with obesity caused by brain tumor treatment (craniopharyngioma), adding exenatide to a strict diet and exercise plan does not lead to significantly more weight loss than the diet and exercise alone. The medication may reduce hunger scores, but it does not translate to superior weight loss outcomes in this specific population.

Exenatide reduces hunger scores in adults with craniopharyngioma-related obesity, although this does not translate to significant weight loss.

Exenatide may help reduce the subjective feeling of hunger in patients with craniopharyngioma-related obesity, but this reduction in hunger does not necessarily lead to greater weight loss compared to lifestyle interventions alone.

GLP-1 receptor agonists (GLP-1RAs) induce pre-ingestive, cognitive satiation by activating dorsomedial hypothalamus (DMH) GLP-1R neurons, which inhibit arcuate nucleus AgRP neurons to terminate meals before ingestion begins.

GLP-1 medications work partly by changing how your brain processes food cues before you even eat. By activating specific brain regions (DMH), they signal 'stop' based on anticipation, not just stomach fullness. This cognitive effect helps reduce meal size and frequency, contributing to weight loss beyond just slowing digestion.

GLP-2 receptor activation improves intestinal barrier function and reduces systemic low-grade inflammation in obesity, but does not directly reduce appetite or body weight in humans.

GLP-2 receptor agonists (like teduglutide) are not currently recommended for weight loss in humans because they do not reduce appetite or food intake. However, they may help reduce systemic inflammation by improving gut barrier function, which is a key driver of obesity-related complications. This strategy is best used in combination with other weight-loss interventions (like GLP-1 agonists) rather than as a standalone treatment.

Obesity acts as an independent risk factor for chronic kidney disease progression through direct mechanisms (pro-inflammatory adipocytokines, renal hemodynamic alterations causing glomerular hyperfiltration) and indirect mechanisms (hypertension, type 2 diabetes).

Maintain a healthy weight to protect kidney function. Obesity directly stresses the kidneys through hormonal and blood flow changes, leading to protein leakage and reduced filtration. Weight loss interventions can slow this progression.

Social media promotion and celebrity endorsements of semaglutide (specifically Ozempic/Wegovy) for off-label weight loss directly drive global search interest and subsequent supply shortages, overriding regulatory approval timelines.

Search interest in weight loss drugs like semaglutide is currently driven more by social media trends and celebrity endorsements than by official medical approvals. If you are seeing a surge in interest or shortages, it is likely due to viral media content rather than a change in medical guidelines.

The same mHealth intervention does NOT produce statistically significant reductions in systolic or diastolic blood pressure four years after completion, nor does it significantly reduce the incidence of hypertension, although a non-significant trend toward reduced hypertension risk was observed in high-adherence subgroups.

Do not expect this mobile health program to significantly lower your blood pressure, even if it helps you lose weight. The study showed no significant change in systolic or diastolic blood pressure four years after the intervention. However, the weight loss achieved is still a valuable health outcome, and you should continue to monitor your blood pressure with your healthcare provider.

Co-ingesting protein with carbohydrate during endurance exercise does not improve performance or glycogen resynthesis when carbohydrate recommendations are met.

Do not rely on adding protein to your in-exercise nutrition for performance or glycogen storage. Stick to recommended carbohydrate intakes. Save protein for post-exercise recovery.

Timing of creatine ingestion (pre- vs. post-exercise) does not significantly influence gains in muscle mass or strength compared to resistance training alone.

Take your creatine whenever is most convenient for you. Whether you take it before or after your workout makes no measurable difference to your muscle growth or strength gains. Focus on taking it consistently every day rather than stressing about the exact timing.

SGLT2 inhibitors reduce cardiovascular disease risk and mortality in Type 2 Diabetes patients, but are associated with increased risks of urogenital infections, dehydration, hypotension, osteoporotic fractures, and limb amputation.

SGLT2 inhibitors offer significant cardiovascular benefits but require caution in elderly patients and those with kidney disease due to risks of dehydration, hypotension, and infections. Monitor for signs of these side effects.

Acute exposure to moderate terrestrial altitude (2320 m) does not enhance metabolic stress or anabolic hormonal responses compared to normoxia during hypertrophy-oriented resistance training.

If you are training at moderate altitude (around 2300m), do not expect your muscles to grow faster or your hormones to spike more than they would at sea level, provided you are doing the same resistance training routine. The acute stress response is not enhanced by the altitude itself in this context.

Using velocity loss (VL) thresholds to prescribe or monitor resistance training volume for free-weight back squats is flawed and should not be used because the relationship between velocity loss and repetitions completed to failure lacks stability and predictive validity across sessions.

Do not use velocity loss thresholds to determine how many reps to perform in free-weight back squats. The relationship between how fast you move and how many reps you can do is too unstable from session to session to be useful for programming. Stick to traditional methods like RPE or fixed rep ranges.

Inhibition of HIF1α signaling allows regenerating skeletal muscle myofibers to bypass a neonatal maturation checkpoint, thereby accelerating muscle repair and growth following injury.

This research identifies a biological 'brake' on muscle repair: if HIF1α signaling stays high after an injury, the muscle gets stuck in an immature, small state. Pharmacologically lowering HIF1α (e.g., with PX-478 in mice) or genetically removing it allows the muscle to mature faster and grow larger. For humans, this suggests that strategies to modulate hypoxia signaling or mitochondrial fusion (Mfn2) might accelerate recovery from severe muscle trauma, though no such therapy is currently available for general use.

Current precision nutrition tools based on Polygenic Risk Scores (PRS) have limited predictive power because they often fail to account for gene-environment interactions.

Do not rely solely on genetic testing for dietary advice. Current genetic risk scores are incomplete because they ignore your lifestyle. For accurate precision nutrition, genetic data must be combined with environmental factors like diet and activity.

Caloric restriction alone in older adults with sarcopenic obesity leads to significant loss of lean muscle mass and grip strength, worsening sarcopenia.

If you are an older adult with obesity, simply eating less (caloric restriction) without exercise can cause you to lose muscle, not just fat. This makes you weaker and more frail. To avoid this, you must combine dietary changes with resistance exercise and ensure you are eating enough protein.

Short-chain fatty acids (SCFAs) such as acetate and propionate regulate glucose homeostasis primarily by activating the GPCR FFAR2 on enteroendocrine L-cells, stimulating the release of GLP-1, which in turn promotes insulin secretion and improves glucose tolerance.

To leverage the glucose-lowering benefits of short-chain fatty acids, focus on consuming fermentable dietary fibers (like those in oats, legumes, and resistant starches) to feed gut bacteria. These bacteria produce SCFAs (acetate, propionate, butyrate) which activate FFAR2 receptors in your gut. This triggers the release of GLP-1, a hormone that signals your pancreas to release insulin more effectively, thereby improving blood sugar control. This is particularly beneficial if you have insulin resistance or type 2 diabetes.

Resmetirom, a liver-targeted thyroid hormone receptor beta agonist, significantly improves both NASH resolution and fibrosis in patients with stage 2-3 fibrosis.

Resmetirom is a prescription medication for NASH with significant fibrosis that has shown the ability to improve both liver inflammation and scarring in clinical trials. It is not an over-the-counter supplement and requires medical supervision.

Obeticholic acid (OCA) reduces hepatic fibrosis without worsening NASH, but its efficacy is modest and it carries safety concerns leading to FDA rejection.

Obeticholic acid can reduce liver scarring in pre-cirrhotic NASH, but its modest benefits and side effects (itching, liver toxicity) led to FDA rejection, making it a less favorable option.