Browse the evidence

Dietary fat intake (both long-chain and medium-chain triglycerides) does not increase postprandial fat oxidation rates, leading to positive fat balance and net fat storage when consumed with carbohydrates.

Eating dietary fat does not trigger your body to burn that fat for energy. Instead, when you eat fat alongside carbohydrates, your body stores the fat. To lose body fat, you must create an overall energy deficit, as simply changing the fat content of your meals does not increase fat burning.

In patients with diabetes, LDL cholesterol concentration is a poor indicator of cardiovascular risk because it masks an increased number of atherogenic lipoprotein particles (high apoB) and the presence of small, dense LDL particles.

Do not rely solely on your LDL cholesterol number to assess your heart health. In diabetes, your blood may contain many more small, dangerous cholesterol particles than a standard test shows. Ask your doctor about measuring ApoB or Non-HDL cholesterol for a more accurate risk assessment, and follow their advice on statin therapy even if your LDL looks 'normal'.

Type 2 diabetes negates the natural cardiovascular protection typically afforded to premenopausal women, resulting in a 25–50% greater excess risk of incident cardiovascular disease in women compared to men with diabetes.

If you have type 2 diabetes, your risk of heart disease is not lower than a man's, even if you are a woman. Diabetes removes the natural heart protection women usually have. You need to manage blood pressure, lipids, and blood sugar as aggressively as a man would to protect your heart.

Females have higher rates of insulin resistance than males from early childhood through mid-puberty, whereas males exhibit greater insulin resistance during late puberty and adulthood.

Insulin resistance changes differently for boys and girls as they grow. Girls tend to be more insulin resistant during early puberty, while boys become more resistant later. This biological difference contributes to why girls are more prone to type 2 diabetes in youth, while men are more prone in midlife.

Increased intake of starchy vegetables, specifically potatoes, corn, and peas, is positively associated with weight gain, contrasting with non-starchy vegetables.

Be mindful of starchy vegetables like potatoes, corn, and peas. Unlike leafy greens or broccoli, increasing your intake of these specific vegetables is linked to weight gain, likely due to their higher glycemic load. Balance your plate with non-starchy vegetables and moderate portions of starchy ones.

A high Triglyceride-Glucose (TyG) index is positively associated with a higher prevalence of symptomatic coronary artery disease (CAD) in secondary care patients, independent of social, clinical, and behavioral risk factors.

If you are in secondary cardiac care, ask your doctor about your Triglyceride-Glucose (TyG) index. It is a calculated marker of insulin resistance derived from your fasting triglycerides and glucose levels. A high TyG index is a strong predictor of symptomatic heart disease, even if your standard cholesterol numbers look acceptable. Managing this index through lifestyle changes (diet and activity) is crucial for reducing cardiac risk.

Systematic reviews on sugar-sweetened beverages (SSBs) and weight gain that disclose financial conflicts of interest with food or beverage industries are five times more likely to conclude there is no positive association between SSB consumption and weight gain compared to reviews without such conflicts.

When evaluating health advice about sugary drinks, check who funded the research. If the study or review was funded by a beverage or food company, be skeptical of conclusions that claim these drinks do not contribute to weight gain. Independent research is more likely to find a link between SSB consumption and weight gain.

In nondiabetic Pima Indians, higher insulin resistance (lower glucose disposal) is associated with a significantly lower rate of weight gain over time compared to insulin-sensitive individuals.

For individuals with high insulin resistance, standard weight loss advice might need to account for metabolic adaptations. This study suggests that insulin resistance might naturally slow down weight gain in some populations, acting as a protective feedback mechanism against extreme obesity, rather than solely driving it. This does not mean insulin resistance is healthy, but it complicates the simple 'high insulin = fat gain' narrative.

Low fasting muscle sympathetic nerve activity (MSNA) predisposes individuals to body weight gain by reducing resting metabolic rate and energy expenditure.

Your body's 'idle speed' (metabolic rate) is partly controlled by your sympathetic nervous system. If your baseline nerve activity to muscles is low, your body burns fewer calories at rest, making weight gain more likely even without overeating. This is a physiological predisposition, not a character flaw.

Muscle glycogen depletion following exercise increases in vivo insulin-stimulated carbohydrate storage and total glucose disposal (M-value) in glycogen-replete humans, provided no immediate carbohydrate re-feeding occurs.

If your goal is to maximize your body's ability to store glucose as glycogen (a marker of insulin sensitivity) after a workout, try not to eat carbohydrates immediately after exercising. However, if you prioritize performance or recovery, eating carbs is still beneficial and does not make the exercise 'useless'; it just means you won't get this specific metabolic boost.

Global dietary quality, measured by the Alternative Healthy Eating Index (AHEI), is modest (mean score 40.3/100) and has improved only slightly (+1.5 points) globally between 1990 and 2018, with significant regional disparities where South Asia and Sub-Saharan Africa saw no improvement or decline.

Your overall diet matters more than any single food. Globally, average diet quality is low (40/100). To improve, focus on increasing fruits, vegetables, whole grains, and healthy fats while reducing sugar-sweetened beverages, red/processed meat, and sodium. This applies to everyone, but the specific gaps vary by region and education level. In many areas, simply increasing produce intake yields the biggest health return.

Post-exercise carbohydrate co-ingestion provides no additional muscle protein synthesis (MPS) benefit over adequate protein intake alone following resistance exercise.

You do not need to consume carbohydrates with your post-workout protein to maximize muscle growth. Adequate protein (20-25g) is sufficient to stimulate muscle protein synthesis. Carbs are still recommended for replenishing glycogen stores, but they do not add to muscle building benefits beyond what protein provides.

Females have a significantly lower sedentary 24-hour energy expenditure (24EE) than males, even after adjusting for fat-free mass, fat mass, age, and spontaneous physical activity.

Women naturally burn about 100-125 fewer calories per day than men of similar size and activity levels. This is a small but real physiological difference. To manage weight, women may need to be slightly more precise with caloric intake or slightly more active than men with similar body composition, but the difference is manageable and not a barrier to health.

Beta-adrenergic receptor blockade with propranolol significantly reduces the thermic effect of glucose and the energy cost of glucose storage in healthy men, indicating that sympathetic nervous system activity drives the facultative component of diet-induced thermogenesis.

Your body burns extra calories after eating carbs partly because your nervous system gets activated by insulin. Blocking this nervous system response (as done in this study with propranolol) significantly reduces that extra calorie burn, bringing it down to the basic energy cost of storing glucose as glycogen. This suggests that the 'thermic effect' of food is not just a chemical cost of storage, but an active neural process.

Acute post-exercise myofibrillar protein synthesis (MPS) rates measured in untrained individuals are not correlated with long-term resistance training-induced muscle hypertrophy.

Do not use your acute muscle protein synthesis response (or how 'pumped' you feel) to predict your long-term muscle growth potential. High acute MPS does not guarantee high hypertrophy, and low acute MPS does not mean you won't grow. Focus on consistent progressive overload over 16+ weeks rather than optimizing for the immediate post-workout metabolic spike.

The thermic effect of food (TEF) increases linearly with caloric intake and is independent of leanness or obesity when meals are normalized to fat-free mass.

If you are obese, your body does not necessarily process food calories differently than a lean person's body. The increase in energy expenditure after eating scales directly with how much you eat, regardless of your weight. Focus on the total amount of calories consumed rather than assuming your body is uniquely efficient at storing them.

Two weeks of unilateral limb immobilization induces a coordinate down-regulation of mitochondrial bioenergetic and carbohydrate metabolism pathways in human skeletal muscle, leading to significant reductions in muscle strength and cross-sectional area.

If you must immobilize a limb (e.g., cast, brace) for two weeks, expect significant strength and size loss, driven largely by a shutdown of mitochondrial energy production. This metabolic suppression happens very early (within 48 hours). To mitigate this, active rehabilitation of the non-immobilized limb and nutritional strategies supporting mitochondrial health may be considered, though the primary intervention is minimizing immobilization time.

Protein ubiquitination and the expression of atrogenes (atrogin-1, MuRF-1) are significantly increased early (48 hours) during immobilization but return to baseline levels by 14 days, suggesting a transient role for this pathway in short-term human muscle atrophy.

Early in an injury period (first 2 days), your body may ramp up protein breakdown markers, but this does not necessarily mean muscle loss continues at the same rate or via the same mechanism after the first week. The body shifts focus to metabolic down-regulation.

Immobilization significantly reduces the phosphorylation of mTOR at 48 hours, indicating early suppression of anabolic signaling, which correlates with the down-regulation of PGC-1alpha and mitochondrial biogenesis.

Early in immobilization, your body's primary anabolic signaling (mTOR) is suppressed, which likely contributes to the shutdown of mitochondrial function. This suggests that early nutritional or pharmacological interventions targeting mTOR might be most effective in preserving metabolic health during the first few days of inactivity.

Acute post-exercise increases in systemic hormones (testosterone, GH, IGF-1) are not related to muscle hypertrophy following resistance training.

Stop worrying about how much your hormones spike after a workout. The acute rise in testosterone or growth hormone does not predict how much muscle you will gain. Focus on consistent training and recovery instead of trying to maximize hormonal spikes.

Macroscopic increases in muscle size (hypertrophy) do not necessarily reflect proportional increases in contractile (myofibrillar) protein; instead, they often result from sarcoplasmic expansion (fluid, glycogen, non-contractile proteins), leading to a dilution of myofibrillar protein concentration.

When you see muscle size increase, do not automatically assume it is all 'quality' contractile tissue. A significant portion of early or even chronic hypertrophy can be 'sarcoplasmic'—driven by fluid, glycogen, and non-contractile proteins. This means your strength-to-size ratio might not improve as much as your tape measure suggests. Focus on strength metrics and protein synthesis markers, not just visual size, to gauge true contractile adaptation.

Ketogenic diets increase LDL cholesterol and total cholesterol, which may accelerate atherosclerosis and increase cardiovascular disease risk, despite improving triglycerides and HDL.

Monitor your LDL cholesterol closely when starting a ketogenic diet. While your triglycerides may drop and HDL rise, your LDL may increase significantly. If you have a history of cardiovascular disease or high baseline LDL, consult your provider, as this increase may pose a risk. Consider shifting fat sources to plant-based options (nuts, vegetables) to potentially mitigate LDL elevation.

Adding carbohydrates to a sufficient protein dose post-exercise does not further increase muscle protein synthesis in young men.

You don't need to eat carbs after your workout to build muscle, as long as you've eaten enough protein (20-25g). Carbs won't hurt, but they won't build extra muscle either. Eat them if you want to replenish energy for your next session.

In obese and noninsulin-dependent diabetic subjects, the thermic effect of infused glucose and insulin is significantly decreased or abolished due to a greater suppression of hepatic gluconeogenesis and lower glucose storage rates compared to normal-weight subjects.

If you are obese or have type 2 diabetes, your body may not generate as much heat (energy expenditure) in response to eating carbohydrates as a lean person's would. This is largely due to how your liver handles glucose production (gluconeogenesis) and storage under the influence of insulin. Improving insulin sensitivity through weight loss and metabolic health management can help restore this normal thermogenic response.