Browse the evidence

Loss of proteostasis, characterized by the accumulation of abnormal proteins due to decreased cellular capacity to degrade them, is a hallmark of aging and contributes to age-related pathologies like neurodegenerative diseases.

As we age, our cells become less efficient at cleaning up damaged proteins, leading to accumulation that can cause diseases like Alzheimer's. Maintaining cellular 'housekeeping' through healthy lifestyle choices (like exercise and diet) may help support these natural degradation pathways.

Oral zinc supplementation may decrease the absorption of certain drugs, including ciprofloxacin, doxycycline, and risedronate.

If you take ciprofloxacin, doxycycline, or risedronate, separate your zinc supplementation from these medications by a few hours to ensure proper drug absorption.

The higher n-3 PUFA content in organic meat is primarily caused by the high grazing/forage-based diets required by organic farming standards.

The nutritional advantage of organic meat comes from the animals' diet. Organic standards require more forage and grazing, which naturally increases the healthy fats in the meat. This is a direct result of the farming method, not just a labeling difference.

Organic meat does not have significantly different concentrations of saturated fatty acids (SFA) or monounsaturated fatty acids (MUFA) compared to conventional meat.

You should not expect organic meat to have less saturated fat than conventional meat. The main nutritional difference is in the healthy unsaturated fats (n-3), not the saturated fats.

Immune-modulating nutrition (supplementation with glutamine, arginine, omega-3 fatty acids, and antioxidants) does not improve outcomes in general critically ill patients and may increase mortality, although it may benefit specific subgroups like severe burn patients.

Do not routinely use immune-modulating supplements (glutamine, arginine, omega-3s) for general critically ill patients. These supplements have been shown to increase mortality or provide no benefit in large trials. They may be considered for specific subgroups like severe burn patients, but this requires specialist judgment.

Supplementation with high-dose Vitamin E and/or Vitamin C blunts skeletal muscle adaptations to endurance and resistance training, including mitochondrial biogenesis and hypertrophy signaling pathways, without improving performance metrics like VO2max.

If you are training to improve fitness or build muscle, avoid high-dose Vitamin C and E supplements. They block the cellular signals your body needs to adapt to exercise. Instead, get your antioxidants from whole foods like fruits and vegetables, which support health without interfering with your training progress.

PPARα and FXR have opposing effects on autophagy: PPARα induces autophagy during fasting to recover nutrients, while FXR suppresses it during the fed state.

Your body uses autophagy (cellular recycling) to recover nutrients when you are fasting, driven by PPARα. When you eat, FXR suppresses this process. This natural cycle suggests that intermittent fasting may leverage this mechanism to clear cellular debris and recover nutrients, provided the fasting periods are sufficient to trigger PPARα activation.

High-dose phenolic compound supplementation can exhibit pro-oxidant effects and cause toxicity, including liver damage and accelerated tumorigenesis, in certain contexts.

Avoid high-dose polyphenol supplements. While dietary sources are safe, concentrated supplements can become pro-oxidant and cause liver stress or other toxic effects.

Iodine supplementation during preconception, pregnancy, and postpartum periods corrects maternal iodine insufficiency but shows no significant benefit for preventing preterm birth, low birthweight, or improving child neurodevelopment.

If you are pregnant or planning pregnancy, iodine supplementation is recommended to correct iodine deficiency, which is common. However, do not expect this supplementation to prevent preterm birth, low birth weight, or significantly boost your child's intelligence or motor development beyond what is achieved by correcting the deficiency. Stick to recommended prenatal doses.

Daily supplementation with 400 IU or less of vitamin D and 1000 mg or less of calcium provides no benefit for the primary prevention of fractures in community-dwelling, postmenopausal women.

If you are a postmenopausal woman living independently (not in a nursing home) and do not have diagnosed osteoporosis or vitamin D deficiency, you should not take daily supplements of 400 IU vitamin D and 1000 mg calcium specifically to prevent fractures. Current evidence shows this combination does not reduce fracture risk and may increase the risk of kidney stones. Focus on diet and exercise instead.

Supplementation with vitamin D and calcium increases the incidence of kidney stones in community-dwelling adults.

Be aware that taking combined vitamin D and calcium supplements increases your risk of developing kidney stones. While the absolute risk is small (about 1 extra case per 273 women over 7 years), it is a confirmed side effect. If you are not deficient, the risks may outweigh the unproven benefits.

Non-nutritive sweeteners are less acidogenic than sugar and may increase oral pH, potentially reducing the risk of dental caries.

If you are concerned about tooth decay, switching from sugar-sweetened drinks to those with non-nutritive sweeteners is a beneficial change. The research indicates that NNSs produce less acid in the mouth than sugar, leading to a higher oral pH which is protective against cavities.

Vitamin D3 supplementation (2500 IU/day) does not improve cardiovascular risk markers (endothelial function, arterial stiffness, or inflammation) in post-menopausal women, regardless of baseline vitamin D status.

If you are a post-menopausal woman taking Vitamin D for heart health, this study suggests it likely won't improve your artery stiffness or blood vessel function, even if it successfully raises your blood Vitamin D levels. Continue taking it if recommended for bone health, but do not rely on it as a strategy to prevent cardiovascular disease.

Oral administration of pure ergothioneine (5mg or 25mg daily for 7 days) to healthy humans results in avid absorption and retention, but produces no statistically significant reduction in biomarkers of oxidative damage or inflammation.

Taking ergothioneine (5-25mg daily) is safe and your body will store it efficiently, but if you are healthy and not under extreme stress, you should not expect it to lower your oxidative stress or inflammation markers. The body likely stores it for times of actual injury or high stress rather than using it as a daily antioxidant in healthy states.

Obese women exhibit altered caffeine metabolism, specifically excreting significantly higher amounts of the metabolite theobromine compared to lean women, despite similar caffeine excretion levels.

Obese individuals metabolize caffeine differently, producing more theobromine. This metabolic difference may contribute to the blunted thermogenic response observed in obesity, suggesting that standard caffeine dosing may not yield identical metabolic effects across different body compositions.

In obese youth, gut microbiota exhibit a higher capability to ferment carbohydrates into short-chain fatty acids (SCFAs) compared to lean youth, and these SCFAs serve as substrates for hepatic de novo lipogenesis (DNL), thereby increasing energy harvest and fat partitioning.

For obese youth, the gut microbiome may extract more energy from carbohydrates than in lean individuals by converting them into short-chain fatty acids (SCFAs) like acetate and butyrate. These SCFAs are then used by the liver to create new fat (DNL). Simply eating 'healthy' carbs might not be enough if the gut microbiome is highly efficient at fermentation; the resulting SCFAs fuel fat storage. This suggests that interventions might need to target gut microbiota composition or fermentation rates, not just caloric intake.

Supplementation with NAD+ intermediates (NMN or NR) restores declining NAD+ levels in aged animals, thereby reversing age-associated metabolic dysfunction, improving mitochondrial function, and extending healthspan.

Aging is associated with a measurable drop in cellular NAD+, which impairs energy metabolism and mitochondrial function. Supplementing with precursors like Nicotinamide Mononucleotide (NMN) or Nicotinamide Riboside (NR) can restore NAD+ levels. In animal studies, this restoration reverses metabolic dysfunction, improves energy expenditure, and enhances physical activity, suggesting a viable strategy to mitigate age-related decline.

Magnesium supplementation above the Tolerable Upper Intake Level (UL) of 250 mg/day from supplements can cause mild diarrhea.

Do not exceed 250 mg/day from magnesium supplements, as this can cause diarrhea. This limit applies to supplements and fortified foods, not naturally occurring magnesium in whole foods.

Melatonin acts as a potent antioxidant by scavenging reactive oxygen and nitrogen species, protecting against oxidative stress, and enhancing mitochondrial efficiency, independent of receptor binding.

Melatonin's role as an antioxidant helps protect cells from damage caused by stress and metabolism. This function supports overall cellular health and may be particularly relevant for brain health and aging, as melatonin protects against mitochondrial dysfunction associated with neurodegenerative diseases.

Reduced glutathione (GSH) levels in serum are increased by Lactobacilli supplementation and mediate the improvement of hepatic mitochondrial function and systemic glucose metabolism.

Lactobacilli supplementation increases serum glutathione, a key antioxidant. This increase helps protect liver mitochondria from damage caused by high sugar/fat diets, thereby improving blood sugar control. This highlights the importance of antioxidant pathways in metabolic health.

Choline metabolism by gut bacteria into Trimethylamine (TMA) and subsequently Trimethylamine-N-oxide (TMAO) contributes to NAFLD by decreasing VLDL export and promoting insulin resistance.

Be cautious with high-dose choline supplements if you have NAFLD. Your gut bacteria may convert it to TMAO, which is linked to liver steatosis and insulin resistance.

Treatment of iron deficiency after gastric bypass is often refractory to oral supplementation, frequently requiring parenteral (IV/IM) iron, blood transfusions, or surgical reversal/conversion for severe or persistent cases.

If oral iron doesn't fix your anemia after bypass surgery, don't give up. You likely need IV iron, which bypasses your gut. This is common and safe. If even IV iron fails, surgical options like converting to a banding procedure or reversing the bypass might be considered to restore absorption.

Monthly high-dose vitamin D3 supplementation (200,000 IU initial bolus followed by 100,000 IU monthly) without calcium does not reduce the incidence of invasive or in situ cancer in adults aged 50-84.

Taking 100,000 IU of vitamin D3 once a month (after an initial 200,000 IU dose) does not appear to lower your risk of developing cancer. If you are taking vitamin D for cancer prevention, this specific high-dose monthly regimen is not supported by this evidence. You might discuss daily or weekly lower-dose strategies with your doctor, as this study suggests those methods warrant further investigation.

Excessive consumption of certain seaweeds, particularly those high in iodine or accumulating toxic metals like arsenic, cadmium, or lead, poses potential health risks and requires adherence to safety regulations regarding toxic element limits.

Be mindful of the source and type of seaweed you consume. Some seaweeds, especially brown varieties like Kombu, are extremely high in iodine, which can be harmful in excess. Others may accumulate toxic metals like arsenic or lead. To minimize risk, choose seaweeds from regulated aquaculture sources and vary your intake to avoid excessive exposure to any single mineral or toxin.