Browse the evidence

Carbohydrate loading (supercompensation) provides no performance benefit for trained runners during a 20.9-km run, as performance times were statistically identical regardless of initial muscle glycogen levels.

For a 13-mile run, you do not need to perform extreme carbohydrate loading (like eating 500+ grams of carbs for 3 days). Your performance will be the same whether you have 'supercompensated' glycogen or normal levels. Focus on maintaining adequate daily carbohydrate intake rather than trying to maximize stores through extreme diets.

Higher initial muscle glycogen levels lead to a greater rate of glycogen utilization during exercise, but this does not improve performance in a 20.9-km run.

If you have high glycogen, your body will burn more of it during your run compared to if you have low glycogen. However, for a 13-mile run, this extra burn doesn't make you faster. Don't stress about maximizing glycogen.

Reducing dietary protein intake (specifically BCAAs) improves insulin sensitivity in obese mice, whereas increasing BCAA intake exacerbates insulin resistance.

For obese individuals, reducing the intake of branched-chain amino acids (found in high-protein foods like meat, eggs, and dairy) may improve insulin sensitivity. Conversely, high BCAA intake can worsen insulin resistance. This suggests that the quality of protein (BCAA content) is as important as the quantity.

The protein content of microalgae varies significantly (6-71% of dry matter) and is heavily influenced by environmental factors such as light intensity, temperature, CO2 concentration, and nutrient availability.

When choosing microalgal products, be aware that protein content can vary widely depending on how the algae were grown. Look for products that specify their protein content, as this can range from 6% to over 70% of dry weight depending on cultivation conditions.

The delayed recovery associated with early nutrition is driven primarily by protein/amino acid intake rather than glucose intake.

Current guidelines recommending high protein intake early in critical illness may need revision. This analysis suggests that high protein/amino acid doses, rather than glucose, are the primary drivers of delayed recovery in early parenteral nutrition. Clinicians should be cautious about high-protein parenteral formulas in the first week of ICU stay.

High-protein diets and protein supplements are not essential for athletes, as a varied diet meeting energy needs provides sufficient protein for muscle maintenance and growth.

You do not need to buy protein powder or follow a high-protein diet to build muscle. Focus on eating enough total calories and a variety of foods to meet your energy needs. Your body will adapt to the protein you get from food. Supplements are only useful if you cannot meet your protein needs through food alone or for convenience.

Age-related insulin resistance in older adults is primarily driven by increased visceral adiposity and central fat distribution rather than aging itself, as accounting for body fat and distribution eliminates age as a predictor of insulin action.

Focus on maintaining a healthy body weight and minimizing visceral fat through diet and exercise. This is more critical for metabolic health in older age than simply accepting 'aging' as the cause of metabolic issues.

Replacing saturated fat with polyunsaturated fat to lower serum cholesterol does not reduce the incidence of cardiovascular events, sudden death, or all-cause mortality in institutionalized populations.

This large, long-term study of institutionalized patients found that while a diet high in polyunsaturated fats successfully lowered blood cholesterol levels, it did not reduce the risk of heart attacks, sudden death, or overall mortality compared to a standard diet. This suggests that simply lowering cholesterol through fat substitution may not be sufficient to prevent cardiovascular death in all populations, particularly those with lower baseline cholesterol or shorter life expectancies.

In humans, severe calorie restriction does not reduce serum IGF-1 levels unless protein intake is also reduced, whereas in rodents, CR reduces IGF-1 without protein restriction.

If you are practicing calorie restriction and want to potentially lower IGF-1 (which may reduce cancer risk), consider moderately reducing your protein intake to around 0.75 g/kg body weight, rather than consuming high amounts of protein. This is a nuanced strategy that differs from standard fitness advice.

Higher plasma concentrations of odd-chain fatty acids (specifically pentadecanoic and heptadecanoic acid) are significantly inversely associated with the risk of incident coronary heart disease.

Odd-chain fatty acids, which are biomarkers for dairy intake, are associated with a lower risk of heart disease. This suggests that not all saturated fats are harmful and that moderate dairy consumption may be part of a heart-healthy diet.

Increasing dietary alpha-linolenic acid (aLNA) intake results in negligible conversion to long-chain n-3 fatty acids (EPA and DHA) in humans, rendering it significantly less effective than direct EPA/DHA consumption for improving cardiovascular or inflammatory health markers.

Eating flaxseed, walnuts, or canola oil (high in aLNA) is healthy, but it will not significantly raise your levels of EPA and DHA, the long-chain fats critical for brain and heart health. If your goal is to increase EPA/DHA status, you should consume fatty fish or fish oil supplements directly, as your body cannot efficiently convert plant oils into these specific fats.

Dietary interventions that substitute n-6 PUFA for trans-fatty acids (TFA) and saturated fatty acids (SFA) without simultaneously increasing n-3 PUFA produce a non-significant trend toward increased all-cause mortality.

Replacing trans and saturated fats with n-6 oils alone may slightly increase the risk of death from any cause, although this specific finding was not statistically significant. It reinforces the need to balance n-6 intake with n-3 sources.

Women do not experience the significant increase in muscle glycogen or performance time-to-fatigue that men experience in response to a high-carbohydrate loading diet (75% of energy).

If you are a female endurance athlete, simply increasing your carbohydrate intake to 75% of your calories for 4 days before an event may not increase your muscle glycogen or extend your time to fatigue as it does for men. Your body naturally relies more on fat oxidation during submaximal exercise, sparing glycogen. You may not need to carb-load as aggressively as male athletes to achieve similar metabolic efficiency, and forcing high carb intake might not provide the expected performance boost.

Consuming low glycemic index (LGI) meals prior to high-intensity exercise does not increase fat oxidation and instead increases carbohydrate oxidation compared to high glycemic index (HGI) meals.

If you are eating before intense exercise, do not assume that 'low glycemic' or 'stable blood sugar' meals will help you burn more fat. This study shows that LGI meals actually increased carbohydrate burning and decreased fat burning compared to high glycemic meals. Focus on total carbohydrate availability and timing rather than just the glycemic index if your goal is optimizing substrate oxidation for high-intensity efforts.

Increasing carbohydrate availability (via glucose ingestion or high glycogen stores) reciprocally downregulates fat oxidation in skeletal muscle during exercise through insulin-mediated suppression of adipose lipolysis and direct inhibition of fatty acid transport proteins.

When you eat carbohydrates before or during exercise, your body prioritizes burning those carbs and burns less fat. This happens because insulin rises (blocking fat release from storage) and transport proteins for fat are inhibited. To maximize fat oxidation during exercise, you would need to exercise in a fasted state or avoid carbohydrate intake, but this comes at the cost of performance and glycogen sparing.

Increasing exercise intensity above approximately 75% VO2max downregulates fat oxidation due to decreased adipose blood flow, reduced FFA delivery, and intramuscular inhibition of fatty acid transport and oxidation.

If your goal is to maximize the amount of fat you burn *during* your workout, keep your intensity moderate (around 60-65% of your max oxygen uptake). If you exercise at very high intensities (above 75% VO2max), your body switches to burning mostly carbohydrates because it can't deliver and process fat fast enough to meet the energy demand.

Increasing fat availability (via elevated plasma free fatty acids) downregulates carbohydrate oxidation in skeletal muscle during exercise, primarily by inhibiting glycogen phosphorylase (PHOS) activity through reduced accumulation of ADP and AMP.

If you consume a high-fat meal or supplement before exercise, your body will burn more fat and less glycogen. However, this 'fat sparing' effect does not necessarily improve performance. For optimal performance, especially at high intensities, relying on carbohydrates is still superior.

Fructose ingestion acutely and robustly increases FGF21 blood levels in both mice and humans, whereas glucose causes only a modest and delayed increase, establishing a liver-brain feedback loop for sugar consumption regulation.

Eating fructose triggers a rapid spike in FGF21, a hormone that helps regulate sugar intake, while glucose has a much weaker effect. This suggests your body uses FGF21 to specifically manage fructose consumption.

Probiotic supplementation does not significantly reduce fat mass in overweight or obese subjects, despite reducing body weight and fat percentage.

Do not expect probiotics to reduce your body fat. While they might lower your total body weight slightly, the specific reduction in fat mass was not statistically significant in this review.

Commercial determinants of health (CDoH), including corporate political activity and marketing of unhealthy commodities, are primary structural drivers of non-communicable diseases (NCDs) and health inequalities, overriding individual behavioral factors.

To improve public health, focus on regulating corporate practices (marketing, lobbying, product formulation) rather than solely educating individuals. Support policies that limit the power of industries selling unhealthy commodities like ultra-processed foods, alcohol, and tobacco.

Replacing saturated fat from dairy with carbohydrates does not improve cardiovascular risk profiles and may worsen them by lowering HDL and increasing small dense LDL.

Do not simply swap high-fat dairy for high-carb low-fat alternatives expecting heart health benefits. This substitution often fails to improve risk markers and may lower protective HDL cholesterol. Prioritize whole food sources and polyunsaturated fats if modifying fat intake.

Adherence to a low carbohydrate-high protein diet is associated with a statistically significant increase in the incidence of overall cardiovascular disease in women.

If you are a woman following a low-carb, high-protein diet for weight loss, be aware that this study links this specific dietary pattern to a higher risk of heart disease and stroke over the long term. The risk appears to increase as you decrease carbs and increase protein. Consider reviewing the sources of your protein (animal vs. plant) and carbohydrates (refined vs. complex), as the study suggests these factors may modify the risk.

FAT/CD36 (CD36) facilitates long-chain fatty acid (LCFA) uptake into skeletal muscle mitochondria, a process distinct from and potentially upstream of the Carnitine Palmitoyltransferase I (CPTI) system.

Your muscles use a protein called CD36 to move fatty acids into the mitochondria to be burned for energy. This process is crucial for endurance and metabolic health. While you cannot directly 'dose' CD36 like a supplement, regular exercise (both acute and chronic) increases the amount of CD36 in your mitochondria, thereby enhancing your muscle's ability to oxidize fat. This suggests that training improves your body's efficiency in using fat as fuel.

Overexpression of the transcriptional coactivator PGC-1α in skeletal muscle increases glucose uptake and glycogen storage while suppressing glycolytic flux, thereby preventing glycogen depletion during exercise.

PGC-1α is a key protein induced by exercise that helps muscles store more glycogen and take up more glucose. This mechanism helps prevent glycogen depletion during exercise and aids in recovery. While you cannot directly 'dose' PGC-1α, engaging in exercise that induces PGC-1α (like endurance or high-intensity training) supports this metabolic adaptation.