Browse the evidence

Among men, higher consumption of vitamin E supplements is not associated with a reduced risk of coronary heart disease.

If you are a man, taking high-dose vitamin E supplements (400 IU or more daily) will not lower your risk of heart disease. The study of health professionals showed no significant benefit. Do not rely on supplements for heart protection; instead, focus on a balanced diet rich in natural sources of vitamin E, such as vegetable oils, nuts, and seeds.

Omega-3 PUFA supplementation does not reduce the risk of stroke (ischemic or hemorrhagic) in primary or secondary prevention settings.

Taking fish oil supplements will not prevent you from having a stroke, whether you have had one before or not. Do not take them for stroke prevention.

Engineered E. coli Nissle strains (SYNB1618 and SYNB1934) expressing phenylalanine-degrading enzymes successfully reduce fasting plasma phenylalanine levels in patients with Phenylketonuria (PKU) in Phase 1/2a and Phase 2 trials.

For PKU patients, engineered bacteria are showing promise in clinical trials to lower blood phenylalanine levels. This could eventually offer more dietary flexibility, but these treatments are not yet widely available.

Increasing fruit and vegetable consumption does not significantly reduce the risk of cancer mortality.

While eating fruits and vegetables is crucial for heart health and overall longevity, relying on them alone to prevent cancer death may not be effective based on current large-scale data. Focus on them for cardiovascular benefits and general health.

Increasing micronutrient (Fe, Zn) content in seeds enhances crop yield and seedling vigor, particularly when grown in micronutrient-poor soils, creating a 'win-win' for farmers and nutrition.

Farmers in nutrient-poor regions should consider using biofortified seeds (high Fe/Zn) not just for health, but because they often produce higher yields and better seedling vigor than standard seeds in those specific soils.

Selenium supplementation does not protect against cardiovascular disease or mortality in the general population, despite lower selenium levels being associated with higher risk in observational studies.

Do not take selenium supplements for heart disease prevention. While low levels are associated with higher risk, trials show supplements do not reduce that risk.

Breast milk oligosaccharides (HMOs) selectively promote the growth of specific beneficial bacteria (Bifidobacterium longum subsp. infantis) and shape the infant gut microbiota towards a state that supports immune development and digestion.

For parents, breast milk is the optimal source for establishing a healthy infant gut microbiota due to HMOs. If breastfeeding is not possible, look for formulas containing prebiotics (GOS/FOS) to help mimic some of these beneficial microbial shifts.

Higher frequency of fish and shellfish consumption is directly associated with significantly higher blood organic (methyl) mercury concentrations in adult women.

If you eat fish frequently (more than twice a week), your blood mercury levels will be significantly higher than non-consumers. To minimize risk, vary your seafood choices, limiting high-mercury species like shark, swordfish, and king mackerel, and stick to lower-mercury options like salmon and shrimp.

A significant portion of newborns in the US are exposed in utero to methyl mercury levels considered to carry an increased risk of adverse neurodevelopmental effects, primarily driven by high fish consumption in specific demographic groups.

If you are pregnant or planning to be, your fish choices directly impact your baby's brain development. Over 300,000 US babies are exposed to risky mercury levels annually. To protect your baby, avoid high-mercury fish (shark, swordfish, king mackerel, tilefish) and choose low-mercury options (salmon, shrimp, canned light tuna, pollock).

Genetic overexpression of autophagy-related proteins (e.g., ATG5, LC3/ATG8) is sufficient to extend life span in model organisms.

In animals, genetically boosting autophagy proteins extends life. This proves that enhancing the body's natural cleanup system is enough to live longer. However, this is not a practical human intervention yet, as it requires genetic modification.

CoQ10 supplementation (2400 mg/day) is safe and well-tolerated in patients with early-stage Huntington's disease, but does not slow functional decline.

If you or a family member has early-stage Huntington's disease, high-dose CoQ10 (2400mg/day) is safe but has not been shown to slow the disease's progression. Do not rely on it as a treatment for slowing decline.

Manipulation of specific branches of methionine metabolism, including the methionine cycle, transsulfuration pathway, and polyamine biosynthesis, can extend lifespan.

Targeting specific metabolic pathways involved in methionine metabolism, such as the transsulfuration pathway or polyamine biosynthesis, may offer longevity benefits. This can be achieved through genetic manipulation or dietary interventions that affect these pathways.

Supplementing infant formula with preformed DHA and AA, rather than just precursors, significantly improves mental development scores and visual acuity in infants compared to formulas containing only precursors.

If you are formula-feeding your infant, choose a formula that explicitly lists DHA and Arachidonic Acid (AA) as ingredients, not just alpha-linolenic acid (ALA). The paper indicates that preformed DHA and AA are necessary to support optimal mental and visual development, as infants cannot efficiently convert plant-based precursors into these critical fats.

Administration of ethanolamine increases intracellular phosphatidylethanolamine (PE) levels, which positively regulates autophagic flux and extends chronological lifespan in yeast, mammalian cells, and Drosophila.

To potentially support longevity and cellular cleanup (autophagy), consider increasing your intake of ethanolamine. This can be done through diet (foods rich in phosphatidylethanolamine precursors) or supplementation. Research in yeast, cells, and flies shows that 10 mM ethanolamine extends lifespan by about 5% in flies and boosts autophagy in mammalian cells. While human data is not yet available, ethanolamine is a naturally occurring compound with a favorable safety profile. It works by increasing levels of phosphatidylethanolamine (PE), which is essential for the autophagy process.

Methionine restriction extends chronological lifespan in yeast by inducing autophagy, which subsequently stimulates vacuolar acidification; this pathway is strictly dependent on functional autophagy genes (ATG5, ATG7, ATG8).

In yeast models, restricting the amino acid methionine significantly extends lifespan by triggering a cellular cleanup process called autophagy, which requires the vacuole to become more acidic. This effect is lost if the autophagy genes are disabled. While this is a yeast model, it suggests that amino acid composition, specifically methionine levels, may play a critical role in triggering cellular maintenance pathways relevant to aging.

Long-term supplementation with 300 µg/day of selenium (as selenium-enriched yeast) in populations with moderately low baseline selenium status significantly increases all-cause mortality approximately 10 years after treatment cessation.

If you live in a region with low soil selenium (like parts of Europe), standard supplementation (100-200 µg/day) may be safe, but you should avoid high-dose supplements (300 µg/day or more) taken long-term. The study suggests that exceeding 300 µg/day of total selenium intake (diet + supplements) for 5+ years may increase your risk of death, particularly if you are under 65. Consult a doctor to check your baseline selenium levels before supplementing.

A 12-week supplementation of 500 mg/day resveratrol does not significantly improve anthropometric measurements, insulin resistance markers, lipid profiles, or blood pressure in patients with NAFLD compared to placebo.

Do not expect 500 mg of resveratrol to fix your cholesterol, blood pressure, or insulin resistance. It may help your liver enzymes, but you still need to manage your weight, diet, and exercise to improve these broader metabolic health markers.

Dietary resveratrol intake, as measured by urinary metabolites in older adults, does not reduce all-cause mortality, inflammation, or risk of cardiovascular disease and cancer.

If you are eating a normal diet, your intake of resveratrol (from grapes, wine, etc.) is not enough to extend your life or prevent heart disease and cancer. Do not rely on dietary resveratrol for longevity benefits.