Browse the evidence

Reduced muscle mass is a key phenotypic criterion for malnutrition, measurable by DXA, BIA, CT, MRI, or anthropometric proxies like calf/arm circumference.

Assess muscle mass using available tools like DXA, BIA, CT, or MRI. If these are unavailable, use anthropometric measures like calf or arm circumference, or functional assessments like grip strength.

Replacing dietary saturated fat with refined carbohydrates or sugars does not reduce cardiovascular disease risk and may be neutral or harmful.

Do not replace saturated fats with refined carbs or sugars if your goal is heart health. This substitution does not lower cardiovascular risk. Instead, replace saturated fats with unsaturated fats (polyunsaturated or monounsaturated).

Replacing animal-source foods with plant-based foods in high-income countries reduces greenhouse gas emissions by up to 84% and premature mortality by up to 12%, but may increase freshwater use by up to 16%.

In high-income countries, reducing your intake of animal-source foods and replacing them with plant-based options (especially legumes, fruits, and vegetables) can significantly lower your carbon footprint and improve your health. Be aware that this might increase your water usage, so choosing water-efficient plant foods can help mitigate this. This strategy is most effective where current meat consumption is high.

Despite improvements, US adults continue to consume disproportionately high energy from low-quality carbohydrates and saturated fat remains above recommended levels.

Do not assume that 'healthy eating' is complete. Actively monitor and reduce your intake of added sugars and saturated fats, as these remain the primary dietary challenges for the average US adult.

High dietary fructose intake promotes non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance by stimulating de novo lipogenesis via GLUT2 and GLUT5 transporters.

Limiting high-fructose corn syrup and excessive free fructose in processed foods is more effective for preventing liver fat accumulation than limiting glucose alone, as fructose uniquely drives hepatic lipogenesis.

Visceral adipose tissue (VAT) and epicardial adipose tissue (EAT) accumulation is a primary driver of cardiovascular injury in obesity and diabetes, independent of overall body mass index (BMI), through the release of pro-inflammatory factors and free fatty acids.

For individuals with obesity or Type-2 Diabetes, focusing solely on BMI is insufficient for assessing heart disease risk. Visceral and epicardial fat are more dangerous indicators. Reducing these specific fat depots through lifestyle changes or medication is crucial for preventing heart failure and other cardiovascular injuries.

Macrofungi are a source of high-quality protein, unsaturated fatty acids, and minerals, making them a low-calorie functional food suitable for general health.

Eat mushrooms regularly as a source of protein and fiber. They are low in calories but nutrient-dense, making them a good addition to a balanced diet.

Genotype-based personalization of macronutrient intake (high-fat vs. high-carbohydrate) does not result in greater weight loss compared to genotype-discordant diets in individuals with overweight or obesity.

If you are overweight or obese, matching your diet to your genetic profile (e.g., high-fat vs. high-carb) does not provide a weight loss advantage over a diet that doesn't match your profile. Focus on sustainable caloric restriction and macronutrient choices you can maintain, as genetic testing for diet response currently offers no predictive benefit for weight loss magnitude.

Higher circulating and tissue levels of arachidonic acid (AA) are not associated with an increased risk of cardiovascular disease, and may be associated with a lower risk of total CVD.

You do not need to worry about high levels of arachidonic acid (AA) in your blood as a risk factor for heart disease. This study shows that higher AA levels are not associated with increased CVD risk and may even be linked to lower risk.

Obesity can result from an intrinsic metabolic disorder that shifts fuel partitioning toward storage and sequestration in adipose tissue, causing 'internal starvation' and compensatory hyperphagia, independent of excessive energy intake.

This paper argues that for some individuals, obesity is driven by a biological defect in how the body handles fuel (partitioning), not just by eating too much. This biological defect traps energy in fat cells, causing the body to feel starved and triggering hunger. While this explains specific pathological cases in animal models, it suggests that for some humans, treating obesity requires addressing these underlying metabolic shifts rather than just focusing on calorie restriction.

Caloric restriction (CR) and dietary restriction (DR) extend lifespan and healthspan, largely by suppressing the IIS/mTOR axis, although CR may also act through mTOR-independent mechanisms.

Reducing calorie intake by 20-40% or restricting specific nutrients like protein or methionine can extend lifespan and healthspan in model organisms. This works partly by suppressing the mTOR pathway, but also through other mechanisms. For humans, this suggests that mindful eating, potentially focusing on protein quality and quantity, may offer longevity benefits.

Low-carbohydrate diets are not superior to higher-carbohydrate or low-fat diets for weight loss in adults with type 2 diabetes.

Do not expect low-carb diets to produce more weight loss than low-fat or high-carb diets if calories are matched. The choice of macronutrients should be based on preference and adherence, not expected superior weight loss results.

Atherogenesis is fundamentally driven by the accumulation of oxidatively modified LDL in the arterial intima, facilitated by endothelial dysfunction and scavenger receptor uptake by macrophages to form foam cells.

High LDL cholesterol is a primary cause of atherosclerosis. The risk is highest when LDL is oxidized and taken up by macrophages to form foam cells. Managing LDL levels and reducing oxidative stress are key to preventing plaque buildup.

Athletes should consume 1.4–2.0 g of protein per kg of body weight per day to optimize lean body mass and strength during resistance training.

If you train with weights, aim for 1.4 to 2.0 grams of protein for every kilogram of your body weight each day. This range is the scientific standard for building and keeping muscle while you train hard.

In overweight/obese adults, a low-carbohydrate diet (26% of calories) without calorie restriction produces significantly greater weight loss and BMI reduction than a calorie-restricted diet (1200-1500 kcal) with standard carbohydrate intake (55-65%).

If you are overweight or obese, try reducing your carbohydrate intake to about 26% of your total calories (roughly 50-60g of carbs per day for many adults) without worrying about counting calories. Eat more fat and protein. You do not need to restrict your total energy intake to lose weight effectively; in fact, you may eat more calories than on a standard low-calorie diet and still lose more weight. This approach was shown to be superior to standard calorie restriction over 12 weeks.

For individuals performing resistance training, muscle strength increases linearly with total protein intake up to 1.5 g/kg body weight per day, with no additional benefit from higher intakes.

If you lift weights, aim for 1.5 grams of protein per kilogram of body weight daily. This is the sweet spot for maximizing strength gains. Eating more than this does not provide additional strength benefits.

In overweight and obese adults, low-carbohydrate diets (LCD) produce greater reductions in triglycerides, diastolic blood pressure, and body weight, along with greater increases in HDL cholesterol, compared to low-fat diets (LFD) over a duration of 6 to 23 months.

If you are overweight or obese, switching to a diet with less than 40% of your calories from carbohydrates (instead of less than 30% from fat) is likely to help you lose more weight, lower your triglycerides, raise your 'good' HDL cholesterol, and lower your diastolic blood pressure over the next 6-23 months. However, this benefit disappears after 24 months, where both diets are equally effective.

Limiting consumption of sugar-sweetened beverages (SSBs) is a critical intervention for weight control and obesity prevention.

Cut out sugary sodas and sweetened juices. Replacing them with water or non-caloric beverages is one of the most effective single changes for preventing weight gain, especially in children.

Adoption of the DASH diet or similar healthy dietary patterns (high in fruits, vegetables, low-fat dairy, low in saturated fat/salt) reduces blood pressure and is recommended as a first-line intervention for hypertension management.

Adopt a DASH-style diet: eat more fruits, vegetables, and low-fat dairy, and reduce saturated fats and salt. This is a proven, first-line strategy to lower blood pressure. If cost or access is a barrier, focus on affordable staples like beans, rice, and seasonal produce, and seek guidance from healthcare providers on local resources.

High-quality protein supplementation (whey) during and after step reduction improves muscle protein synthesis recovery compared to low-quality protein (collagen) or no specific supplementation.

When recovering from a period of reduced activity, ensure you are eating high-quality protein (like whey, eggs, or meat) rather than just any protein source. In a study, older adults who took whey protein recovered their muscle-building capacity after inactivity, while those who took collagen (which lacks some essential amino acids) did not. Aim for about 1.6 grams of protein per kilogram of body weight daily, prioritizing high-quality sources.

Athletes engaged in moderate to high intensity training lasting over 12 hours per week should consume 8-10 g of carbohydrates per kg of body weight daily to maximize glycogen storage and performance.

If you train hard for more than 12 hours a week, aim for 8 to 10 grams of carbs for every kilogram of your body weight each day. If you struggle to eat that much food, switch to denser carb sources like sports drinks or gels instead of just eating large amounts of vegetables or grains.

Post-exercise carbohydrate ingestion of 1.0-1.5 g/kg/hour is sufficient to maximize muscle glycogen resynthesis rates.

After a hard workout, eat or drink 1-1.5 grams of carbs for every kg of your body weight each hour for up to 6 hours. Split this into small amounts every 30 minutes rather than eating it all at once for better absorption.

Athletes should consume 1.4-2.8 g/kg of body weight of protein daily, depending on their specific training goals and type of exercise.

Eat 1.4 to 2.8 grams of protein per kilogram of body weight every day. If you are strength training, aim for the higher end (up to 2.8 g/kg). If you are just maintaining muscle, 1.4-2.0 g/kg is sufficient.

Consuming 0.4 g/kg/meal of protein across at least four meals daily maximizes muscle protein synthesis and lean tissue accretion in resistance-trained individuals.

To build muscle, aim for 0.4 grams of protein per kilogram of body weight in each of your meals. If you weigh 70kg, eat about 28g of protein per meal. Spread this across at least four meals daily. This strategy ensures your muscles receive a steady supply of amino acids for growth, avoiding the myth that high doses per meal are wasted.