Browse the evidence

GLP-1 agonists like semaglutide may reduce the exposure (efficacy) of ALK tyrosine kinase inhibitors like alectinib due to delayed gastric emptying.

Be aware that taking semaglutide might reduce how much cancer medication your body absorbs. However, slow titration (starting low and going slow) may help mitigate this interaction.

Preoperative exercise training may improve walking test distance and body weight in adults undergoing bariatric surgery, but evidence is limited.

While evidence is limited, starting exercise before bariatric surgery may help improve walking test distance and body weight. Consult with your healthcare provider to determine if preoperative exercise training is appropriate for you.

For women of childbearing age, consuming 2 seafood servings per week (limiting high-mercury species) provides neurodevelopmental benefits for the fetus that outweigh the risks of low-level methylmercury exposure.

If you are pregnant or planning to be, eat up to 12 ounces (2 average meals) of a variety of fish and shellfish per week. Avoid shark, swordfish, king mackerel, and tilefish. This provides DHA for your baby's brain and eyes without exposing them to harmful levels of mercury.

High intake of saturated fat is not associated with increased risk of all-cause mortality, cardiovascular disease, coronary heart disease, ischemic stroke, or type 2 diabetes when compared to low intake.

Current observational evidence does not support the idea that eating saturated fat directly causes heart disease or death. However, the quality of this evidence is very low, meaning future research could change these conclusions. Focus on what you replace saturated fat with, as the source of replacement nutrients matters significantly.

Global sodium consumption above 2.0 g/day is attributable to 1.65 million cardiovascular deaths annually, with the majority occurring in low- and middle-income countries.

Reducing your sodium intake to below 2.0 g/day can significantly lower your risk of cardiovascular death. This is especially important if you live in a low- or middle-income country, where the burden is highest. Focus on reducing processed foods and added salt.

Intentional weight loss does not precipitate depression and may protect against emergent symptoms of depression in obese patients.

If you have a history of depression, know that weight loss is not likely to make your mental health worse. In fact, studies suggest it may help protect against new symptoms of depression. You should not avoid weight loss efforts due to fear of mood changes.

Obesity should be staged using functional and cardiometabolic risk factors (Edmonton Obesity Staging System) rather than BMI alone, as BMI alone underestimates risk and fails to capture morbidity.

Don't just look at your BMI. Your health risk is better predicted by your blood pressure, blood sugar, cholesterol, and how physically fit you are. A higher BMI doesn't automatically mean you are unhealthy, and a normal BMI doesn't guarantee health. Focus on improving your metabolic markers and fitness.

Observational studies show a positive association between NNS consumption and weight gain or obesity incidence, suggesting a complex relationship where NNS use may be a marker for existing weight issues rather than a cause.

While some long-term studies link diet drink consumption to weight gain, this is likely because people who are already gaining weight switch to diet drinks. If you are trying to lose weight, swapping sugary drinks for diet drinks is still a valid strategy to reduce calories, but you must be aware that you might be using them to justify other poor food choices.

Low-carbohydrate and ketogenic diets are not currently recommended for the treatment of Type 1 Diabetes due to lack of long-term safety data and risk of complications like DKA and growth deficits in children.

For Type 1 Diabetes, low-carb and ketogenic diets are not currently recommended by major guidelines due to safety concerns like DKA and unknown long-term effects on growth. While some patients may see short-term improvements in glucose control, the risks are significant. Consult your healthcare provider before considering any drastic dietary changes.

Targeting well-connected individuals (highly connected nodes in social networks) who are at the edge of a BMI cluster for weight management interventions is significantly more effective at halting the spread of obesity than targeting obese individuals in the center of clusters.

If you are trying to lose weight or help others do so, focus on people who have many social connections and are on the 'edge' of a group (connected to both healthy and overweight people). Encouraging these 'influencers' to maintain a healthy weight can stabilize their social circle's weight distribution more effectively than trying to convince everyone in a group of overweight friends to change at once.

Pinning the weight of a small, random fraction (≤1%) of the population to a normal BMI, combined with increased social volatility, can reverse obesity trends and convert the majority of the population to a healthier weight.

Public health campaigns that create a 'controversy' or strong social discussion around weight loss, combined with visible support for a small group maintaining healthy weights, can trigger a broader shift in social norms toward healthier weights.

Selenium may protect against the toxic effects of mercury and reduce cardiovascular risk through antioxidant mechanisms, but current human evidence for selenium supplementation preventing CHD is inconsistent and insufficient to draw firm conclusions.

Do not take selenium supplements specifically for heart disease prevention based on current evidence. Instead, include selenium-rich foods (like fish, eggs, or meat) in your diet, as they may offer protective benefits against mercury and support antioxidant systems, though the exact CVD benefit is not yet proven.

Deep brain stimulation (DBS) of the lateral hypothalamic area (LHA) using metabolically optimized settings (specifically Contact 1) increases resting metabolic rate (RMR) and promotes weight loss in patients with refractory obesity, whereas standard movement disorder settings do not.

This finding applies to a very specific subset of individuals: those with severe, refractory obesity who have already undergone bariatric surgery without success. For the general population, this is not a practical intervention. However, for these patients, standard stimulation settings fail, but optimizing the stimulation to target the lateral hypothalamic area (specifically Contact 1) can significantly boost metabolic rate and aid weight loss. This suggests that metabolic rate suppression is a key barrier in refractory obesity that can be mechanically overridden.

GLP-1 analogs are widely used in Saudi Arabia for diabetes management and show some weight loss efficacy, but there is no trial data for their use in obesity-only patients in the country.

GLP-1 analogs are used in Saudi Arabia for diabetes, but there is no specific trial data for obesity-only patients. Use with caution and monitor weight loss.

For upper extremity musculature, there is insufficient evidence to recommend full or partial ROM over the other, as results are conflicting.

For upper body muscles, you can use either full or partial ROMs without significant disadvantage. Focus on consistency, volume, and progressive overload rather than obsessing over the specific range of motion.

Combining plyometric and resistance training does not produce additive effects on muscle hypertrophy or anabolic signaling compared to resistance training alone.

Do not expect to build muscle faster by mixing jumping exercises with weightlifting compared to just lifting weights. The current evidence suggests you get the same muscle growth from resistance training alone, so you can save time by focusing on one modality if your goal is purely hypertrophy.

Obesity in IBD patients is associated with altered pharmacokinetics of biological therapies, leading to faster drug clearance, lower trough concentrations, and potentially reduced treatment efficacy.

If you take biological injections for IBD and are obese, your body might process the drug faster than a lean person's, making it less effective. You should discuss this with your doctor. They might monitor your drug levels more closely or adjust your dose to ensure you get the full benefit of the treatment.

Sarcopenic obesity (high fat mass combined with low muscle mass and function) is a distinct and high-risk phenotype in chronic liver disease (CLD) and IBD, associated with worse prognosis, higher mortality, and increased surgical complications compared to obesity alone or sarcopenia alone.

For people with liver disease or IBD, being obese is risky, but losing muscle makes it much worse. This combination, called 'sarcopenic obesity,' leads to higher death rates and surgery complications. You need to check your muscle mass, not just your weight. If you are losing weight, make sure it's fat, not muscle.

Semaglutide (2.4 mg once weekly) promotes adipose tissue browning and mitochondrial biogenesis via the AMPK/SIRT1/PGC1α/UCP1 axis, enhancing energy expenditure and thermogenesis, although this mechanism is primarily established in preclinical rodent models rather than confirmed in humans.

Semaglutide 2.4mg weekly leads to ~15% weight loss. While it likely works partly by boosting metabolism (browning fat) via complex hormonal pathways seen in animals, the primary driver for you is reduced appetite. Do not rely on the 'browning' mechanism to explain your results; focus on the proven appetite suppression.

GLP-1 receptor agonists (GLP-1RAs) may reduce the severity of Obstructive Sleep Apnoea (OSA) as measured by the Apnoea-Hypopnoea Index (AHI), primarily through weight loss mechanisms, though evidence quality is currently low and results are conflicting.

If you have OSA and are considering GLP-1RAs (like semaglutide or liraglutide), expect a modest improvement in sleep breathing (AHI) rather than a cure. The benefit is largely tied to weight loss. Do not stop using your CPAP machine unless your doctor advises it, as CPAP is currently more effective. Be prepared for potential stomach side effects, which are common but often subside. The evidence is not yet strong enough to make this a standard first-line treatment for OSA alone.

Current evidence does not support a definitive superiority of pre- versus post-exercise creatine timing for muscle creatine loading or performance gains, as existing studies suffer from methodological limitations and conflicting results.

Do not stress about whether you take creatine before or after your workout. The current scientific consensus is that there is no definitive advantage to either timing. Focus on taking your daily dose (e.g., 3-5g) consistently every day to saturate muscle stores, rather than trying to optimize the timing relative to your exercise session.

Dual and triple incretin receptor agonists (e.g., tirzepatide, retatrutide) show potential for greater cardiovascular risk factor reduction than single GLP-1RAs, though definitive cardiovascular outcome trial results are pending.

Newer multi-incretin agonists (like tirzepatide) are showing superior improvements in blood sugar, weight, and blood pressure compared to single GLP-1RAs. While their specific impact on heart attacks and strokes is still being studied, they represent a promising next step for cardiovascular risk reduction in diabetes.

Sleeve gastrectomy (SG) combined with a left ventricular assist device (LVAD) serves as a feasible and effective pathway to cardiac transplantation in morbidly obese patients with end-stage heart failure.

If you have severe heart failure and are too heavy for a heart transplant, getting an LVAD (heart pump) and sleeve gastrectomy (stomach reduction) together is a viable medical pathway. This combination can significantly reduce your weight and make you eligible for a transplant, which was previously impossible due to your size. This requires specialized surgical care.

Resistance exercise-induced lactate accumulation may promote skeletal muscle hypertrophy through multiple mechanisms including lactate-stimulated testosterone production, histone lactylation, and activation of satellite cell pathways via GPR81/ERK1/2 signaling, although direct evidence in humans is currently insufficient.

While mechanical tension is king, incorporating training styles that generate high lactate (e.g., higher reps, shorter rest) may offer additional hypertrophic benefits via metabolic signaling. However, do not rely on this as a primary driver, as human evidence is currently weak compared to mechanical load.