Browse the evidence

Testosterone replacement therapy increases fat-free mass, muscle size, and strength in hypogonadal men, even without resistance exercise training.

If you are a hypogonadal man, testosterone replacement therapy can significantly increase your muscle mass and strength, even if you do not engage in resistance exercise. The study used a standard replacement dose of 100 mg of testosterone enanthate weekly for 10 weeks. This resulted in an average increase of nearly 5 kg of fat-free mass and significant increases in muscle cross-sectional area. Ensure your testosterone levels are monitored by a healthcare provider.

Selenium-dependent selenoproteins (specifically deiodinases and glutathione peroxidases) are essential for thyroid hormone activation/inactivation and protecting thyroid cells from oxidative damage during hormone synthesis.

Support thyroid health with both iodine and selenium. Selenium is required for the enzymes that activate thyroid hormones and protect the thyroid gland from damage during hormone production.

Critical Power (CP) defines a physiological threshold separating exercise domains where metabolic responses stabilize (<CP) from those where they progressively drift toward intolerance (>CP).

Use Critical Power (CP) to define your training zones. If you exercise above CP, your body cannot stabilize its metabolic state (O2 and lactate will keep rising), and you will fatigue predictably based on your W' (work capacity above CP). If you stay below CP, your body can stabilize, allowing for longer durations. This is more accurate than using percentages of your max heart rate or lactate threshold for predicting how long you can sustain a specific power output.

Restoring Insulin-like Growth Factor 1 (IGF-I) levels or blocking Myostatin (Mstn) production can prevent or reverse glucocorticoid-induced muscle atrophy.

Current research suggests that therapies targeting IGF-I or Myostatin could protect muscle during steroid treatment. However, these are not yet standard clinical practices for all patients. Focus on maintaining protein intake and resistance training as foundational strategies while consulting your doctor about the specific risks and benefits of your steroid regimen.

Abdominal (visceral) obesity is an independent risk factor for coronary artery disease, hypertension, stroke, and type 2 diabetes, driven by a specific dyslipidemia phenotype characterized by hypertriglyceridemia, reduced HDL, and increased small, dense LDL particles.

If you have excess belly fat, your cardiovascular risk is significantly elevated regardless of your total cholesterol number. This is because your body produces more small, dense LDL particles and has lower HDL. To assess your true risk, ask your doctor for an Apo B test or an LDL particle size test, rather than relying solely on standard LDL cholesterol.

Obesity rates are significantly higher among African American and Hispanic children compared to white children, with specific demographic variations such as higher rates in African American girls and Hispanic boys.

Public health efforts must recognize that obesity is not distributed equally. African American and Hispanic children face higher risks, with specific vulnerabilities in African American girls and Hispanic boys. Interventions should be tailored to these high-risk groups, addressing their specific environmental and cultural contexts.

Insulin resistance in skeletal muscle and adipose tissue, characterized by impaired GLUT4 translocation, is a primary driver of whole-body hyperglycemia and type 2 diabetes.

Maintaining insulin sensitivity through regular physical activity (which stimulates GLUT4 translocation independently of insulin) and managing body fat levels are critical for preventing the transition from insulin resistance to type 2 diabetes.

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.

Caloric restriction extends lifespan and delays age-related pathologies by activating autophagy and reducing inflammasome activation.

Caloric restriction is a proven way to extend lifespan and delay disease by activating your body's cleanup processes. While strict restriction is hard, finding a sustainable way to eat slightly less or practice intermittent fasting can mimic these benefits.

Adjusting self-reported dietary intake data for total daily energy intake significantly reduces measurement error and improves the validity of relative risk estimates in nutritional epidemiology.

When analyzing diet-health relationships, always adjust intake data for total energy. This corrects for common reporting errors and makes your findings more reliable.

Skeletal muscle is responsible for over 80% of postprandial glucose uptake, making it the primary driver of whole-body insulin resistance and glucose homeostasis.

Your skeletal muscle is the main engine for processing sugar from your food. When muscle function declines (due to aging or inactivity), your body struggles to manage blood sugar, leading to insulin resistance. Prioritizing muscle maintenance through activity is a fundamental strategy for metabolic health.

Exercise and insulin stimulate glucose uptake via distinct, independent signaling pathways that both converge on GLUT4 translocation.

Exercise improves blood sugar control through mechanisms that are separate from insulin. This means exercise can be beneficial even for those with severe insulin resistance, as it bypasses some of the defective insulin signaling pathways.

Excess weight (overweight or obesity) and lack of sufficient physical activity are associated with increased incidence of several cancers, including adenocarcinoma of the esophagus, colon and rectum, kidney, pancreas, postmenopausal female breast, and endometrial cancer.

Maintain a healthy weight and engage in at least 150 minutes of moderate-intensity aerobic activity per week. This is not just about appearance; it is a primary defense against several types of cancer, including breast, colon, kidney, and pancreatic cancers. The risk increases significantly with higher BMI and lower activity levels.

Large-scale prospective cohort studies with repeated dietary assessments and biospecimen collection provide high-validity evidence for associations between lifestyle factors (diet, physical activity, obesity) and cancer incidence/mortality, superior to early cohorts limited by single-time exposure assessment.

To accurately study how diet and lifestyle affect long-term health outcomes like cancer, researchers need large groups of people tracked over many years with updated information, rather than just a one-time survey.

Digital cognitive behavioral therapy (dCBT) for insomnia significantly improves functional health, psychological well-being, and sleep-related quality of life compared to sleep hygiene education, with these improvements mediated by the reduction in insomnia symptoms.

If you suffer from insomnia, digital CBT (like the Sleepio program) is a highly effective, evidence-based treatment. It not only improves your sleep but also significantly boosts your daytime health, mood, and overall quality of life. This treatment is delivered online, making it accessible, and has been shown to be superior to standard sleep hygiene advice in large-scale trials.

Sleep restriction increases the percentage of calories derived from fat during late-night hours (22:00-03:59) compared to daytime and evening hours.

When you are sleep-deprived, you tend to eat more fat during late-night hours. To manage your fat intake, try to avoid eating late at night, especially if you are sleep-restricted.

Biological adaptations to energy-restricted weight loss—including reduced leptin/insulin, increased hypothalamic NPY/AgRP, and suppressed energy expenditure—create a persistent drive for weight regain that actively counteracts behavioral efforts to maintain weight loss.

If you have lost weight, expect your body to fight back. Your hormones (leptin, insulin) and brain signals (hunger peptides) will change to promote weight regain. This is not a failure of willpower but a biological defense mechanism. Long-term success requires strategies that are 'comprehensive, persistent, and redundant' to counter these specific biological adaptations, rather than relying on willpower alone.

Energy expenditure declines after weight loss due to both reduced body mass (less tissue to maintain and move) and enhanced metabolic efficiency (regulated by homeostatic feedback loops), creating a persistent energy gap.

Your body burns fewer calories after weight loss than expected for your new size. This is due to having less tissue to maintain and a more efficient metabolism driven by your brain. You must account for this drop in expenditure to avoid regaining weight.

Caloric restriction extends lifespan and delays aging in mammals, partly through mechanisms involving autophagy and Sirt1 activation.

Caloric restriction is a proven strategy to extend lifespan and improve heart health in animal models, likely by activating autophagy and Sirt1. While specific dosing varies, reducing caloric intake is a key lever for longevity.

Higher intake of polyunsaturated fatty acids (PUFA), particularly linoleic acid (omega-6), and monounsaturated fatty acids (MUFA) is associated with lower total mortality and cause-specific mortality.

Increase your intake of polyunsaturated (PUFA) and monounsaturated (MUFA) fats. Sources include nuts, seeds, vegetable oils (like soybean, corn, and olive oil), and fish. Higher intake of these fats is linked to lower total mortality. Specifically, linoleic acid (omega-6) and MUFA show strong inverse associations with mortality. Replace saturated fats with these unsaturated fats for the best health outcomes.

Chronic mechanical loading on healthy human tendons significantly increases tendon stiffness and Young's modulus, with adaptations driven primarily by material property changes rather than morphological (cross-sectional area) increases.

To strengthen your tendons, you must use high-intensity loading (greater than 70% of your maximum capacity). The type of contraction (isometric, concentric, or eccentric) matters less than the intensity. Aim for at least 12 weeks of consistent training, performed 2-4 times per week, to see significant improvements in tendon stiffness and material properties.

Class III obesity (BMI 40.0–59.9 kg/m2) is associated with substantially elevated total mortality and major reductions in life expectancy (6.5 to 13.7 years lost) compared to normal weight, primarily driven by increased risks of heart disease, cancer, and diabetes.

If you have a BMI between 40 and 60, your risk of dying earlier is significantly higher than someone with a normal BMI, costing you an average of 6.5 to 13.7 years of life. This risk is driven largely by heart disease, cancer, and diabetes. The risk increases as your BMI gets higher within this range. While individual outcomes vary, the population data is clear: reducing BMI towards the normal range is associated with regaining these years of life.

Metformin is marginally cost-saving compared to placebo over 10 years in high-risk adults, with slightly lower costs and nearly the same QALYs as placebo.

For high-risk individuals, metformin is a cost-saving option compared to no intervention, with slightly lower total medical costs and similar quality-adjusted life years over 10 years.

PPARγ agonists (glitazones) improve insulin sensitivity and lower glucose in type 2 diabetes by promoting fatty acid flux into adipose tissue, thereby reducing lipid interference with glucose utilization in muscle and liver.

Glitazones (like rosiglitazone and pioglitazone) treat type 2 diabetes by activating the PPARγ receptor. This shifts fatty acids into fat cells, allowing muscles and the liver to use glucose more effectively. They are insulin sensitizers, not insulin secretagogues.