Browse the evidence

Sprint interval training does not increase the muscle content of fatty acid transport proteins (FAT/CD36 or FABPpm) in humans, suggesting that lipid oxidation capacity may adapt differently or slower than carbohydrate metabolism.

Don't worry if you don't see immediate changes in your body's fat-burning machinery after starting sprint training. Your body adapts to handle glucose and energy production more efficiently first. Focus on the performance benefits and overall metabolic health improvements, as these are the primary drivers of long-term fitness gains from SIT.

Training with reduced carbohydrate availability does not necessarily improve exercise performance (e.g., time trial performance) despite enhancing molecular markers of adaptation.

Do not expect that training with low carbs will automatically make you faster. While it improves your body's metabolic efficiency, it may blunt your ability to train at high intensities. Use 'train low' strategically for specific sessions, but ensure you also train 'high' (with adequate carbs) to maintain your speed and power capacity for races.

Consuming carbohydrates before and during exercise blunts the molecular signaling pathways (AMPK, p38MAPK) that are normally enhanced by low carbohydrate availability.

If your goal is to improve your body's metabolic efficiency (mitochondria and fat burning), avoid eating carbohydrates before and during your training session. Eating carbs will blunt the specific cellular signals (AMPK, p38MAPK) that drive these adaptations. If you need to maintain intensity, try caffeine or mouth-rinsing instead of ingesting carbs.

Adults residing in low-income countries (LICs) exhibit significantly higher diabetes prevalence (12.3-14.0%) compared to those in high-income countries (6.6-5.6%), a disparity that persists even after adjusting for conventional risk factors such as BMI, physical activity, and diet.

This research highlights that diabetes risk is not uniform globally. Living in a low-income country is associated with a significantly higher risk of diabetes, independent of standard risk factors like weight or exercise. This suggests that environmental, genetic, or early-life factors in these regions play a critical role, and standard risk assessments based on high-income country norms may underestimate risk in low-income settings.

Increasing red meat consumption by at least half a serving per day over an eight-year period is associated with a 10% higher risk of all-cause mortality in the subsequent eight years, with processed meat showing a stronger association (13% higher risk) than unprocessed meat (9% higher risk).

If you are currently eating red meat, try to avoid increasing your intake by more than half a serving per day over time. If you do increase it, be aware that your risk of death increases, especially if it is processed meat. Simply reducing red meat without replacing it with healthier options may not lower your mortality risk; instead, focus on replacing red meat with healthier protein sources like nuts, fish, or legumes, or whole grains and vegetables.

Long-term metformin treatment (up to 2,000 mg/day) significantly alters gut microbiota composition by increasing Escherichia coli and Ruminococcus torques while decreasing Intestinibacter bartlettii and Roseburia species, effects that persist for at least 12 months.

If you take metformin, expect your gut bacteria to change in a specific way: more E. coli and Ruminococcus torques, less Intestinibacter bartlettii and Roseburia. These changes don't just happen briefly; they stick around for at least a year. Importantly, these changes happen regardless of how much weight you lose, meaning the drug itself is driving this shift. While this might sound concerning because E. coli can be harmful, in this context, it is linked to increased production of short-chain fatty acids like acetate, which may help improve insulin sensitivity. If you experience stomach upset, talk to your doctor about slow dose titration.

Metabolic surgery reduces long-term cardiovascular mortality and microvascular complications in patients with Type 2 Diabetes compared to medical management.

For patients with Type 2 Diabetes and obesity, metabolic surgery not only improves blood sugar but also significantly reduces the risk of heart disease death and kidney/eye complications over the long term compared to standard medical care.

Coffee consumption is inversely associated with mortality from cardiovascular disease, neurological diseases, and suicide, but not with cancer mortality.

Drinking coffee is associated with a lower risk of death from heart disease, neurological conditions, and suicide. It does not appear to increase the risk of dying from cancer. This supports the view that moderate coffee consumption is a safe and potentially beneficial habit for long-term health.

Whole grain intake is not significantly associated with cancer mortality, and substituting whole grains for refined grains or red meat does not significantly reduce cancer mortality.

Do not rely on whole grains alone to prevent cancer. While they are excellent for heart health and overall longevity, this study found no significant link to reduced cancer mortality. Maintain a balanced diet with various vegetables and fruits for cancer prevention, while using whole grains for cardiovascular benefits.

Higher plasma levels of trans-18:2 fatty acids (derived from linoleic acid) are associated with a significantly increased risk of fatal ischemic heart disease and sudden cardiac death in older adults.

Focus on minimizing the heat treatment of polyunsaturated oils (like soybean, corn, sunflower) as this process generates trans-18:2 fatty acids, which are linked to higher heart disease risk. While industrial trans fats are largely removed, the specific trans-18:2 isomer formed during refining and frying remains a concern. Prioritize oils with low trans-18:2 content or unrefined options where possible.

Oral administration of deuterated creatine (D3-creatine) allows for the accurate estimation of total body skeletal muscle mass via urine D3-creatinine enrichment, providing a method with less bias than DXA or 24-hour urine creatinine excretion.

To accurately measure total skeletal muscle mass, the D3-creatine dilution method is superior to DXA and standard urine creatinine tests. It involves taking a single oral dose of deuterated creatine and collecting urine for 5 days to measure isotopic enrichment. This method correlates strongly with MRI (r=0.868) and avoids the overestimation errors of DXA caused by body water fluctuations. It is currently a research tool, not a standard clinical test.

Disuse-induced muscle atrophy in humans is primarily driven by a sustained reduction in muscle protein synthesis (MPS) rather than an increase in muscle protein breakdown (MPB).

To prevent muscle loss during periods of inactivity (like injury recovery or bed rest), simply moving minimally is often insufficient to maintain normal synthesis rates. The primary driver of atrophy is the shutdown of muscle building processes. While you cannot always force training, understanding that synthesis drops significantly (40-50%) highlights why even minimal, involuntary movement or specific nutritional strategies (like amino acid provision, though noted as blunted) are critical to counteract this specific metabolic shutdown.

In preclinical rodent models, disuse atrophy involves both decreased protein synthesis and increased protein degradation, with the extent of degradation being muscle-specific and dependent on fiber type.

While rodent studies show that muscle breakdown increases during disuse, human studies suggest this is not the primary driver. This highlights the importance of not blindly applying animal research to human health advice. For humans, maintaining synthesis (via minimal movement/nutrition) is likely more critical than worrying about breakdown rates.

FAO food balance sheet estimates of national per capita food supply substantially overestimate actual individual-level dietary intakes for most food groups (e.g., by 74.5% for vegetables and 270% for whole grains) and underestimate others (e.g., by 250% for beans/legumes), rendering raw FAO data invalid for assessing individual dietary quality or diet-disease relations without calibration.

Do not use UN FAO food balance sheets to judge how much people actually eat. These numbers are systematically wrong, often overstating consumption by 50-270% for foods like vegetables and grains. If you must use FAO data for global comparisons, you must apply specific calibration equations that account for country, age, sex, and region to correct for this bias.

Dietary diversity measures (count, evenness, dissimilarity) are not standardized and do not consistently correlate with diet quality scores like HEI or DASH.

Do not rely on 'dietary diversity scores' to judge your diet's health. These scores are not standardized and often do not reflect actual diet quality. Focus on specific food groups (vegetables, fruits, whole grains) rather than the number of different foods you eat.

Higher circulating levels of total long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs) and specifically docosahexaenoic acid (DHA) are associated with a significantly lower risk of incident atrial fibrillation in older adults.

For older adults, maintaining higher blood levels of long-chain omega-3s (specifically DHA and total n-3 PUFAs) is linked to a lower risk of developing atrial fibrillation. This association was observed in people not taking fish oil supplements, suggesting that dietary intake of fatty fish (which raises these biomarkers) may be protective. While this study does not prove causation, it supports guidelines recommending regular consumption of fatty fish for cardiovascular health.

Ultraprocessed food (UPF) consumption does not have a unique mechanistic link to increased body mass index or obesity risk, as epidemiological associations are weak and mechanistic evidence is lacking or contradictory.

Do not avoid all processed foods based on the NOVA classification. Focus on nutrient density, portion control, and overall dietary patterns. Many processed foods are safe, nutritious, and affordable. Avoiding them entirely may lead to nutrient deficiencies and higher costs without proven health benefits.

Short-term fat adaptation (5-6 days of high-fat diet followed by carbohydrate restoration) increases fat oxidation and spares muscle glycogen during submaximal exercise but does not improve performance in prolonged endurance events.

Do not use a high-fat diet followed by carb loading to try to improve your race time. While this strategy successfully teaches your body to burn more fat and save glycogen, it does not make you faster or help you finish endurance events sooner. Stick to standard carbohydrate strategies for performance.

Longer duration of exposure to overweight or obesity in adulthood is associated with a graded, cumulative increase in carotid intima media thickness (cIMT) and adverse cardiovascular risk factors, independent of childhood adiposity.

The longer you carry excess weight in adulthood, the more your arteries thicken and your risk factors worsen. However, this damage is cumulative, meaning that reducing your exposure to excess weight at any point in adulthood can slow or reverse this progression.

Sustained weight loss (defined as >1 kg/year over 2 years) is an independent risk factor for higher all-cause and cardiovascular mortality in patients with diabetes/prediabetes and CV risk, compared to maintaining stable weight.

If you have diabetes and heart disease risks, do not try to lose weight. If you have lost weight, do not try to lose more. Your goal should be to stabilize your weight. Aggressive weight loss strategies may increase your risk of death.

In moderately trained individuals, preexercise muscle glycogen availability (low vs. high) does not influence the rate of plasma glucose disposal during low- or moderate-intensity exercise.

If you are moderately trained, your blood sugar management during moderate exercise does not depend on whether you ate carbs beforehand. Your body maintains stable glucose disposal rates whether your muscles are full of glycogen or depleted. Focus on exercise intensity and duration for metabolic benefits rather than manipulating glycogen to alter blood glucose handling.

Higher circulating levels of long-chain monounsaturated fatty acids (specifically 22:1 and 24:1) are associated with a significantly higher incidence of congestive heart failure in humans.

Focus on the specific type of fat rather than just the category. While common monounsaturated fats (like olive oil) are generally good, high levels of long-chain monounsaturated fats (specifically erucic acid 22:1 and nervonic acid 24:1) found in certain fish, mustard, and meats are linked to a higher risk of heart failure. If you have risk factors for heart failure, consider moderating intake of foods high in these specific long-chain fatty acids.

Household-level food expenditure and availability data (e.g., FAO Food Balance Sheets) are not reflective of individual dietary intakes and fail to capture intra-nation heterogeneity.

Do not rely on national food availability statistics to assess individual or subgroup dietary risks. These aggregate measures fail to capture individual consumption patterns and demographic disparities, leading to inaccurate health assessments.

Obesity is a neurobehavioral disorder resulting from the interaction of a 'vulnerable brain' (biological dysregulation of homeostatic and hedonic pathways) and an obesogenic food environment, rather than solely a failure of willpower.

If you struggle with obesity, understand that it is not just a lack of willpower. Your brain's biological signaling for hunger and satiety, combined with the modern food environment, creates a 'vulnerable brain' state. Effective management requires addressing both the biological signals (e.g., through medical or behavioral interventions) and the environment (e.g., reducing access to hyper-palatable foods).