Browse the evidence

Fermentation of non-starch polysaccharides by colonic microflora produces short-chain fatty acids (SCFAs), particularly butyrate, which promotes large bowel health, inhibits pathogenic organisms, and may offer a prebiotic effect.

Include a variety of fibrous plant foods in your diet to feed your gut bacteria. These bacteria ferment the fiber into beneficial compounds like butyrate, which support colon health and may help protect against colorectal issues.

Chronic exposure to an obesogenic diet induces low-grade systemic inflammation that causes loss of muscle integrity (intramuscular lipid accumulation, fibrosis, and reduced satellite cell function), which acts as a central driver for musculoskeletal diseases including osteoarthritis, tendinopathy, and osteoporosis.

If you have obesity and joint/muscle pain, weight loss alone may not restore function because the underlying muscle tissue may be damaged by inflammation (fat infiltration, fibrosis). Focus on preserving or rebuilding muscle quality through resistance training and anti-inflammatory dietary patterns, not just weight reduction, as muscle integrity appears to be the key to preventing musculoskeletal disease.

Childhood stunting and low birth weight are associated with an increased risk of obesity and metabolic complications later in life, particularly in Asian populations.

Ensure adequate nutrition during pregnancy and early childhood to prevent stunting, which is a risk factor for obesity and metabolic disease later in life.

Milk products have a low glycaemic index (GI) but a high insulinaemic index (II), meaning they elicit an insulin response similar to white bread despite low blood glucose impact.

Be aware that while milk has a low glycaemic index, it can still stimulate a significant insulin response. This is due to milk proteins, not lactose. For most people, this is not a concern, but those monitoring insulin levels should be aware of this discrepancy.

In elderly men (aged 70-79), a rapid rate of leukocyte telomere shortening over a 2.5-year period predicts a threefold increase in subsequent 12-year cardiovascular disease mortality, whereas baseline telomere length does not.

For elderly men, monitoring the rate of biological aging (specifically telomere attrition) may be a more useful prognostic indicator for heart disease risk than a single snapshot of telomere length. While this is a biomarker and not an intervention, it suggests that maintaining cellular health and minimizing oxidative stress/inflammation over time is critical for longevity.

Transitioning to telehealth for eating disorder treatment during lockdown was associated with perceived lower quality of care compared to face-to-face interactions, though continuity of care was maintained for many.

If you are receiving telehealth for an eating disorder, recognize that it may feel less effective than in-person care. Communicate this to your provider. They can adapt strategies to make remote sessions more effective, but you must be proactive in discussing what is and isn't working.

The PER3 VNTR polymorphism in humans affects sleep homeostasis, specifically accelerating the buildup of sleep pressure and altering slow-wave sleep, independent of circadian phase shifts.

If you have the PER3 long variant (often associated with morningness), your brain builds sleep pressure faster. This means you may feel sleepier earlier in the day and have more slow-wave sleep. Align your schedule with this faster buildup to avoid excessive sleepiness during the day or difficulty staying awake.

Light-to-moderate alcohol consumption is associated with a reduced risk of incident dementia and Alzheimer's disease, but evidence for vascular dementia is only suggestive.

If you already drink alcohol, light-to-moderate consumption (e.g., wine with meals) may be associated with a lower risk of Alzheimer's disease. Do not start drinking if you do not already. The evidence for vascular dementia is less clear.

Activation of the Nrf2/Keap1/ARE pathway improves insulin sensitivity, reduces hyperglycemia, and protects pancreatic beta-cells in type II diabetes models, whereas classic direct antioxidants have failed to show benefit.

Focus on lifestyle and dietary choices that naturally support your body's antioxidant defenses (like the Nrf2 pathway) rather than relying on high-dose direct antioxidant supplements. The paper highlights that compounds like sulforaphane (found in cruciferous vegetables) and resveratrol (found in grapes/berries) may help activate this pathway, potentially improving insulin sensitivity and protecting cells, whereas direct antioxidant supplements have not shown clinical benefit for diabetic complications.

Intermittent fasting lowers blood pressure through increased parasympathetic activity mediated by Brain-Derived Neurotrophic Factor (BDNF), leading to reduced heart rate and blood pressure.

If you have high blood pressure, intermittent fasting might help lower it by calming your nervous system (increasing parasympathetic tone). However, this effect is not guaranteed for everyone, and you should monitor your BP. Do not stop prescribed blood pressure medication without consulting your doctor.

Restricting food marketing to children, particularly on television and in schools, reduces children's exposure to unhealthy food advertisements.

For policymakers: Implement comprehensive marketing restrictions targeting children, focusing on TV, schools, and digital media. Define 'unhealthy' foods based on nutrient profiling and ban their marketing to minors. This reduces exposure to persuasive messaging that drives unhealthy consumption.

Elevated gut microbiome abundance of Christensenellaceae, Porphyromonadaceae, and Rikenellaceae is associated with reduced visceral adipose tissue (VAT) and a healthier metabolic profile in elderly individuals.

For elderly individuals, maintaining a gut microbiome enriched in Christensenellaceae, Porphyromonadaceae, and Rikenellaceae may be associated with lower visceral fat and better metabolic health. This suggests that dietary strategies supporting these specific bacteria could be beneficial for healthy aging.

Saturated fatty acids activate Toll-like receptors (TLR2 and TLR4) on immune and adipose cells, triggering proinflammatory cytokine production (TNF-α, IL-6) and contributing to insulin resistance, whereas unsaturated fatty acids inhibit this signaling.

Dietary fat quality matters for inflammation. Saturated fats can trigger immune receptors (TLRs) that promote inflammation and insulin resistance, while unsaturated fats (like those in fish oil) can block this pathway. Prioritize unsaturated fats to mitigate inflammatory signaling.

TLR4 deficiency protects mice from diet-induced obesity and improves insulin sensitivity, although effects on body weight are contradictory across studies.

Immune system activation via Toll-like receptors (specifically TLR4) by dietary saturated fats may drive insulin resistance and inflammation associated with obesity. While genetic modification of TLR4 shows benefits in mice, this highlights the importance of managing saturated fat intake to reduce inflammatory signaling.

Pharmacological activation of AMPK using metformin or berberine prevents oxidative stress-induced cellular senescence by restoring autophagic flux and elevating intracellular NAD+ levels.

This research suggests that maintaining cellular energy balance via AMPK activation (through lifestyle or pharmacological means like metformin/berberine) may help cells resist aging-related damage. However, this is based on cell cultures, not humans. Do not self-prescribe metformin or berberine for anti-aging without medical supervision, as the optimal dosing and long-term safety in healthy humans are not established by this study.

Lactic acid bacteria in fermented foods produce bioactive metabolites (postbiotics) such as biopeptides, vitamins, and GABA, which confer health benefits even if the bacteria themselves are not alive at consumption.

You don't always need live bacteria to get health benefits from fermentation. Look for fermented foods that produce bioactive compounds like biopeptides (which may help blood pressure), vitamins (B and K), and GABA (for stress/mood). These benefits exist even in heat-treated fermented products like some cheeses or baked sourdough, though live-culture foods offer an additional microbial boost.

Leg fat (appendicular fat) is inversely related to insulin resistance, suggesting that fat storage in the legs may be metabolically protective compared to trunk or liver fat.

Fat stored in the legs may be less harmful to metabolic health than fat stored in the liver or abdomen. While overall weight management is important, the location of fat storage is a key determinant of metabolic risk.

Short-term cold acclimation (10 days of intermittent exposure to 14-15°C) recruits brown adipose tissue (BAT) and enhances skeletal muscle glucose uptake in metabolically healthy obese men.

If you are obese, exposing yourself to mild cold (around 14-15°C or 57-59°F) for 10 days can help your body recruit brown fat and improve how your muscles handle glucose. Start with short exposures (2 hours) and gradually increase to 6 hours per day. You don't need to be freezing; just cool enough to trigger a response without shivering excessively. This adaptation may help counteract some metabolic risks associated with obesity.

Cold acclimation enhances basal GLUT4 translocation to the sarcolemma in skeletal muscle of obese men, facilitating increased glucose uptake.

Cold exposure not only activates brown fat but also improves your muscles' ability to take up glucose by moving glucose transporters (GLUT4) to the cell surface. This happens even in obese individuals and may help maintain better blood sugar control.

Short-term cold acclimation does not significantly increase non-shivering thermogenesis (NST) or energy expenditure in obese men, despite recruiting BAT.

While cold exposure recruits brown fat in obese individuals, it may not significantly increase your calorie burning (energy expenditure) compared to lean individuals. This means cold acclimation might not be a powerful weight-loss tool on its own for obese people, even if it improves metabolic health.

Obesity-associated gut dysbiosis contributes to cognitive and mood deficits through the activation of the HPA-axis, leading to glucocorticoid overproduction, and the promotion of a pro-inflammatory milieu (endotoxemia/leaky gut) that causes neuro-inflammation.

If you are obese and experiencing brain fog or mood issues, your gut health may be a contributing factor, not just your weight. The paper suggests that improving diet (fiber, prebiotics) or using specific probiotics might help restore gut balance, reduce inflammation, and lower stress hormones, potentially improving cognitive and emotional health. This is not a cure-all, but a modifiable lever.

Hyperinsulinemia is the primary etiological driver of insulin resistance, obesity, type 2 diabetes, and cardiovascular disease, rather than a compensatory response to insulin resistance.

Focus on lowering baseline insulin levels through dietary changes (e.g., reducing refined carbohydrates and sugars) and increasing hepatic insulin clearance. This may prevent or reverse the progression to insulin resistance, obesity, and type 2 diabetes, as high insulin is the primary driver of these conditions.

Hyperinsulinemia shifts the insulin-to-GH ratio towards insulin, suppressing Growth Hormone and IGF-I, which promotes fat accumulation and reduces energy expenditure.

Reducing insulin levels may restore the natural balance with Growth Hormone, potentially improving lipid breakdown and energy expenditure, aiding in obesity management.

Normal physiological levels of ceramide are necessary for glucose homeostasis; inhibiting ceramide synthesis in lean mice causes glucose intolerance and insulin resistance.

While blocking ceramide helps obese mice, it can harm lean mice by causing insulin resistance, suggesting a 'Goldilocks' zone for ceramide levels.