Browse the evidence

Mineral deficiencies (specifically Magnesium, Zinc, Iron, Copper, and Selenium) impair immune competence by disrupting innate and adaptive immune cell function and inflammation regulation, whereas maintaining adequate levels through a balanced diet supports optimal immune defense.

Focus on eating a varied diet rich in vegetables, nuts, seeds, whole grains, and lean proteins to naturally cover your mineral needs. You likely do not need supplements unless you are in an at-risk group (like an athlete with a restricted diet, elderly, or pregnant) or have a diagnosed deficiency. If you do supplement, do so under medical guidance to avoid toxicity, as too much of certain minerals (like Iron or Zinc) can actually harm your immune system or feed pathogens.

Magnesium deficiency promotes a pro-inflammatory state by increasing cytokine production (IL-6, TNF-alpha) and oxidative stress, while adequate Magnesium levels help regulate inflammation and support T-cell function.

If you have chronic low-grade inflammation, check your Magnesium levels. Ensuring adequate intake through foods like spinach, nuts, and seeds may help lower inflammatory markers like CRP. Do not self-prescribe high-dose supplements without testing, as balance is key.

Zinc supplementation (>75 mg/day) significantly reduces the duration of common colds, and adequate Zinc status is critical for T-cell maturation and preventing thymic atrophy, though excessive doses (>40 mg/day long-term) can cause immune dysfunction.

If you catch a cold, starting Zinc lozenges or supplements (totaling >75mg/day) within 24 hours may shorten the illness. Do not take high-dose Zinc (over 40mg/day) as a daily long-term supplement, as it can harm your immune system and cause other health issues. Get your Zinc from food sources like beef, oysters, and nuts instead.

Dietary habits are the dominant factor explaining inter-individual variation in the plasma metabolome, accounting for more variance than genetics or the gut microbiome for the majority of metabolites.

Your diet has a significantly larger impact on your blood metabolite levels than your genetics or gut bacteria do for most metabolic markers. Focusing on food quality and specific food items (like coffee or fish) can directly alter your metabolic profile more effectively than trying to change your genetic makeup.

Plasma metabolite levels can accurately predict an individual's diet quality score, reflecting the relationship between diet and disease.

You can use blood metabolite profiles to objectively assess your diet quality, providing a more accurate picture than self-reported food surveys alone.

Females bear a disproportionately higher burden of malnutrition-related mortality and DALYs compared to males, while males experience higher obesity-related DALYs, indicating sex-specific vulnerabilities in the double burden of disease.

Nutrition and health policies must be sex-specific. Women face higher risks of malnutrition due to biological needs and social inequities in food access, while men face higher risks of obesity. Interventions should address these distinct vulnerabilities rather than using a one-size-fits-all approach.

GLP-1 receptor agonists (Liraglutide, Semaglutide, Dulaglutide) significantly reduce liver fat content and improve liver enzymes in patients with Type 2 Diabetes and NAFLD, with Semaglutide showing histological resolution of NASH in Phase II trials.

If you have Type 2 Diabetes and NAFLD, ask your doctor about GLP-1 receptor agonists like Semaglutide or Liraglutide. These injectable medications have been shown in clinical trials to reduce liver fat and improve liver inflammation, in addition to helping with weight and blood sugar control.

SGLT2 inhibitors (Empagliflozin, Dapagliflozin, Ipragliflozin) improve liver fat content and liver enzymes in patients with Type 2 Diabetes and NAFLD, with some evidence of improving liver fibrosis.

If you have Type 2 Diabetes and NAFLD, SGLT2 inhibitors like Empagliflozin or Dapagliflozin may help reduce liver fat and improve liver enzymes. Discuss these options with your doctor, especially if you are already managing your blood sugar with other medications.

Bariatric surgery is an effective treatment for severe obesity in adolescents and adults with NAFLD, significantly improving liver histology, fibrosis, and metabolic parameters, but carries risks of complications.

For severe obesity that hasn't responded to lifestyle changes, bariatric surgery is a recommended option that can significantly improve liver health and fibrosis. Discuss the risks and benefits with a specialist, especially if you have advanced liver disease.

Extending the dose-escalation period or temporarily suspending dose increases when gastrointestinal adverse events occur improves tolerability and treatment persistence without compromising long-term efficacy.

If you feel sick after a dose increase, don't rush to the next one. Stay at the current dose for a few extra weeks or pause until you feel better. This helps your body adjust and keeps you on the medication longer.

Pharmacological management of persistent nausea with domperidone (preferred over metoclopramide) or other anti-emetics/prokinetics is an effective strategy for managing GLP-1 RA-induced nausea when dietary and titration strategies fail.

If diet changes aren't enough, ask your doctor about domperidone. It is often preferred over other anti-nausea drugs because it has fewer serious side effects. Use it as needed for nausea.

Endurance and resistance exercise training lowers plasma BCAA levels and enhances BCAA oxidation, serving as a natural strategy to mitigate BCAA-related insulin resistance.

Engage in regular endurance and resistance training. This naturally lowers circulating BCAA levels and improves their oxidation, helping to counteract insulin resistance. You don't need extreme protocols; consistent training is effective.

Targeted modulation of mitochondrial function through drugs, exercise, diet, gene therapy, stem cell therapy, and physical therapy can prevent or treat skeletal muscle atrophy.

Consider a multi-faceted approach to managing muscle atrophy. Incorporate regular exercise and a balanced diet as foundational steps. For more severe cases, consult healthcare providers about other potential therapies like drug treatments or physical therapy.

Inflammation and oxidative stress are crucial triggering factors in skeletal muscle atrophy, leading to increased proteolysis and reduced protein synthesis.

Manage stress and inflammation through lifestyle choices. Regular exercise, a healthy diet, and adequate sleep can help reduce oxidative stress and inflammation, supporting muscle health.

Adhering to the American Heart Association's 'Life's Essential 8' cardiovascular health metrics is associated with a significantly reduced risk of all-cause and cardiovascular disease-specific mortality in a linear dose-response manner.

To lower your risk of dying from heart disease or other causes, aim for high scores in eight key areas: healthy diet, physical activity, no nicotine, good sleep, healthy weight, normal blood lipids, normal blood glucose, and normal blood pressure. You do not need to be perfect in all areas; even small improvements in any single metric reduce your risk. Prioritize physical activity and quitting nicotine, as these had the largest impact on mortality in this study.

Step intensity, specifically 'peak-30 cadence' (fastest 30 minutes of walking per day), provides additional risk reduction for mortality and morbidity beyond total step count.

Try to walk briskly for short bursts during your day. You don't need to exercise formally; just walk faster for 30 minutes total (consecutive or not). This 'peak-30' intensity adds extra protection against heart disease and cancer on top of just walking more steps.

Direct supplementation with Urolithin A (Uro-A) bypasses gut microbiota variability to achieve significantly higher plasma concentrations than consuming ellagitannin-rich foods like pomegranate juice.

If you consume pomegranates or walnuts, your body must convert them into Urolithin A using gut bacteria. Not everyone does this efficiently. If you want guaranteed high levels of Urolithin A (e.g., for anti-inflammatory or metabolic benefits), direct Uro-A supplementation is significantly more effective than relying on food sources alone.

Genetically predicted accelerometer-assessed physical activity causally decreases the risk of COVID-19 hospitalization.

Prioritize physical activity measured by devices (accelerometers) over self-reported estimates, as it is causally linked to reduced COVID-19 hospitalization risk. While the effect size is modest, combining this with reduced leisure sedentary time (like TV watching) may offer better protection.

Regular physical activity improves cortisol and dehydroepiandrosterone (sulphate) levels in older adults, contributing to healthy ageing.

Engage in regular physical activity, such as moderate-intensity exercise, to help regulate stress hormones like cortisol and DHEA(S), which supports healthy ageing and reduces frailty risk in older adults.

Sarcopenic obesity, defined as the coexistence of low muscle mass/strength and high adiposity, significantly increases the risk of all-cause mortality, cardiovascular disease, and frailty compared to having either condition alone.

If you are older or have obesity, do not rely on BMI alone. Muscle loss combined with fat gain is a specific, high-risk condition that increases mortality and heart disease risk. Focus on maintaining muscle mass through resistance exercise and adequate protein intake, rather than just weight loss, which can worsen muscle loss if not managed carefully.

Sarcopenic obesity drives cardiovascular disease and mortality through mechanisms of chronic low-grade inflammation, insulin resistance, and lipotoxicity, creating a vicious cycle with cardiovascular conditions.

Understanding that fat and muscle loss interact to cause inflammation and heart risk highlights why treating both is crucial. Managing inflammation and insulin sensitivity through lifestyle can break this cycle.

There is no minimal threshold for cognitive benefit from exercise; any amount of physical activity is better than none, though clinically meaningful changes require ~724 METs-min/week.

You do not need to exercise for hours to see brain benefits. Even small amounts of activity help. However, to see significant, clinically meaningful improvements, aim for approximately 724 METs-min per week (e.g., 150 minutes of moderate activity).

Obesity moderates the dose-response relationship for cognitive benefits, with overweight/obese older adults reaching maximal cognitive benefits at lower exercise doses (~600 METs-min/week) than those with healthy BMI.

If you are overweight or obese, you may achieve maximum cognitive benefits with around 600 METs-min of exercise per week. Pushing beyond this may not yield additional cognitive gains and could be unrealistic. Start with moderate doses.

Dietary fiber interventions consistently increase Bifidobacterium spp. abundance in healthy adults, regardless of whether SCFA levels change significantly.

You can generally expect your gut bacteria to respond to fiber by increasing Bifidobacterium levels. However, this taxonomic shift does not guarantee a measurable increase in beneficial metabolites (SCFAs) in your blood or stool, as metabolic output varies by fiber type and individual microbiome.