Browse evidence-based analysis of health-related claims and assertions
Increased carbohydrate intake enhances intramuscular glycogen storage, thereby improving resistance training performance and volume capacity.
Assertion
Untrained individuals undergoing resistance training with a significant caloric surplus achieve high rates of muscle hypertrophy with relatively low concomitant fat accumulation.
Quantitative
Progressive increases in strength within the 6–12 repetition range under consistent training conditions are a reliable proxy for skeletal muscle hypertrophy.
Endogenous adipose tissue serves as a metabolic substrate that can support muscle protein synthesis during periods of caloric restriction or maintenance.
The efficiency of muscle gain during a caloric surplus is significantly higher in untrained individuals compared to trained individuals, with the latter accumulating proportionally more adipose tissue under the same surplus conditions.
Comparison
In individuals with elevated body fat stores, resistance training during a caloric deficit can sustain muscle hypertrophy while promoting net fat loss.
Protein intake at 0.7 grams per pound of body weight is sufficient to maximize muscle protein synthesis in non-elite, non-lean individuals undergoing resistance training.
A caloric maintenance state combined with resistance training can result in simultaneous fat loss and muscle gain by mobilizing endogenous fat stores to support muscle protein synthesis.
Chronic elevation of cortisol preferentially promotes central adiposity due to the higher density of glucocorticoid receptors in visceral adipose tissue compared to subcutaneous depots.
Ethanol metabolism prioritizes hepatic clearance over fatty acid oxidation, leading to de novo lipogenesis, hepatic triglyceride accumulation, and elevated serum triglycerides.
Skeletal muscle mass is a primary determinant of whole-body glucose disposal capacity, and higher muscle mass is inversely associated with visceral adipose accumulation via reduced insulin demand.
Chronic hyperinsulinemia promotes preferential accumulation of visceral adipose tissue, while insulin reduction triggers selective mobilization of visceral fat over subcutaneous fat.
Waist circumference demonstrates superior predictive validity for metabolic disease and all-cause mortality compared to body mass index in adult human populations.
Visceral adiposity is an independent predictor of cardiovascular disease morbidity and mortality, irrespective of total body mass index.
Chronic exposure of the liver to visceral adipose-derived free fatty acids and cytokines induces hepatic steatosis, elevates serum triglycerides, increases blood pressure, and promotes systemic insulin resistance.
Visceral adipose tissue releases bioactive molecules directly into the portal venous system, exposing the liver to elevated concentrations of free fatty acids and inflammatory cytokines.
An increase in waist circumference is quantitatively associated with increased all-cause mortality risk in adult humans.
When people eat red meat, their bodies make certain chemicals called N-nitroso compounds, but these are not the same dangerous ones that damage DNA and cause cancer.
Mechanistic
Some mouse studies that link heme to colon cancer feed the mice way too much red meat and not enough calcium, so those results don’t tell us what happens when people eat normal amounts of red meat.
Scientists think the iron in red meat might cause colon cancer, but the lab tests that suggest this use way more iron than people normally eat, so we can't say eating red meat like usual actually causes cancer.
When scientists turned on the 'stop eating' signal in mice’s brains and then gave a drug to block nicotine-like signals, the mice still ate less — meaning something else besides nicotine-like signals is also helping to suppress hunger.
Scientists found that the brain cells that use acetylcholine in mice send wires directly to the part of the brain that tells you when you're full — and those wires touch the 'full' cells.
Descriptive
When scientists removed the ability of certain brain cells in mice to make acetylcholine, the mice started eating way more and gained weight — but they didn’t move less or burn fewer calories at first.
When scientists turned on certain brain cells in mice, it made other cells that tell the body 'I'm full' fire more — and this only partly stopped when they gave a drug that blocks nicotine-like signals.