Browse the evidence

High circulating levels of the artificial sweetener erythritol are associated with a significantly increased risk of major adverse cardiovascular events (MACE), including heart attack and stroke, and directly enhance platelet reactivity and thrombosis potential.

If you consume erythritol (a common artificial sweetener in 'keto' products, sugar-free drinks, and baked goods), be aware that it can accumulate in your blood and make your platelets more likely to form clots. This risk is particularly relevant if you have existing heart disease, diabetes, or high blood pressure. While occasional use may not pose a significant risk for healthy individuals, those at higher cardiovascular risk should consider limiting erythritol intake and consulting their doctor, especially given that levels can remain elevated for days after consumption.

GLP-1 receptor agonists and DPP-4 inhibitors provide effective glucose lowering with weight loss (GLP-1) or weight neutrality (DPP-4) and minimal hypoglycemia risk, outweighing potential risks of pancreatitis or thyroid cancer which lack convincing human evidence.

For patients with Type 2 Diabetes, GLP-1 receptor agonists (like liraglutide or exenatide) and DPP-4 inhibitors (like sitagliptin) are effective, safe options for lowering blood sugar. GLP-1 agonists offer the added benefit of weight loss, while DPP-4 inhibitors are weight-neutral. Current evidence does not support fears of increased pancreatitis or thyroid cancer risk in humans, making these therapies favorable compared to older drugs that cause weight gain or hypoglycemia.

Smaller adipocytes resulting from weight loss exhibit higher insulin sensitivity and enhanced nutrient clearance capacity, which signals energy depletion to the brain and promotes the storage of ingested energy.

Your body's fat cells become more efficient at storing fat when they shrink. This biological efficiency makes it easier to regain weight when you eat, as your body prioritizes storing those calories over burning them.

Weight loss reduces circulating levels of leptin and insulin disproportionately to fat mass loss, signaling energy depletion to the hypothalamus and increasing appetite.

Your body uses hormones like leptin and insulin to signal energy status. After weight loss, these hormones drop more than expected, telling your brain you are starving, which increases hunger and drives you to eat more.

Higher consumption of ultra-processed foods (UPFs) increases the risk of developing multimorbidity, defined as the co-occurrence of at least two chronic diseases among cancer, cardiovascular disease, and type 2 diabetes.

To lower your risk of developing multiple chronic conditions (cancer, heart disease, diabetes) simultaneously, reduce your intake of ultra-processed foods. This includes items like soft drinks, packaged snacks, processed meats, and ready-to-eat meals. Aim to replace these with less processed options, as even a moderate reduction can significantly improve long-term health outcomes.

Among ultra-processed food subgroups, animal-based products and artificially/sugar-sweetened beverages are specifically associated with increased multimorbidity risk, while ultra-processed breads and cereals may be inversely associated.

Not all ultra-processed foods are equally risky. Prioritize reducing sugar-sweetened beverages and animal-based processed products (like processed meats), as these are most strongly linked to chronic disease multimorbidity. Ultra-processed breads and cereals may not carry the same risk, so focus your efforts on the highest-impact items.

Fortification of common foods (bread, milk, spreads) with long-chain n-3 polyunsaturated fatty acids (LCn-3PUFA) is an effective strategy to increase intake, but current commercial products often deliver insufficient doses per serving to meet therapeutic recommendations for cardiovascular disease prevention.

If you are trying to lower your cardiovascular risk, simply eating 'fortified' foods like bread or milk might not be enough. Check the label for the specific amount of EPA and DHA (in mg). Many products only offer a tiny fraction of the dose needed for heart health. To get therapeutic benefits, you may need to eat large quantities of these fortified foods, which is impractical. For high-risk individuals, high-dose supplements or significant increases in oily fish intake are likely more effective than standard fortified foods.

Microencapsulation of fish oil in food products can mask unpleasant flavors and improve oxidative stability, but the amount of LCn-3PUFA that can be delivered in these formats is often too low to meet recommended allowances.

Microencapsulated fish oil powders are useful for masking taste, but they are not a magic bullet for high-dose needs. Because these powders often contain only a small percentage of actual fish oil, you might need to eat a lot of them to get a therapeutic dose. For high-dose needs, standard high-quality capsules or direct fish intake may still be more efficient.

Activation of brown adipose tissue (BAT) via cold exposure, beta-3 agonists, or specific hormonal mediators (FGF21, IL-6, BMPs) improves glucose tolerance and insulin sensitivity in humans and rodents.

To leverage brown fat for metabolic health, expose yourself to mild cold (around 19°C or 66°F) for extended periods (e.g., 12 hours). This activates BAT, increasing energy expenditure and improving insulin sensitivity through the release of hormones like FGF21. While beta-3 agonists work in rodents, they are not yet viable for humans, making cold exposure the primary practical tool.

Chronic cold acclimation increases the volume and oxidative capacity of metabolically active brown adipose tissue in humans, leading to increased energy expenditure and improved insulin sensitivity.

Engage in chronic mild cold exposure (around 19°C or 66°F) for extended periods daily. Over time, this increases the volume and oxidative capacity of your brown fat, boosting your resting energy expenditure and improving how your body handles insulin after meals. This is a sustainable, non-pharmacological way to leverage your body's natural thermogenic machinery.

Tirzepatide, a dual GIP and GLP-1 receptor agonist, produces clinically significant reductions in HbA1c and body weight in patients with type 2 diabetes, with efficacy superior to the selective GLP-1RA dulaglutide.

For patients with type 2 diabetes, tirzepatide offers superior glucose and weight control compared to existing GLP-1 drugs. To minimize stomach upset, it is crucial to follow the prescribed slow dose-escalation schedule (starting at 2.5mg or 4mg and increasing gradually over 8 weeks). This approach balances high efficacy with better tolerability.

A daily intake of 600 mg caffeine combined with 270-1200 mg EGCG (from green tea and Guarana extracts) significantly increases 24-hour energy expenditure by approximately 750 kJ (8%) in healthy men compared to placebo, but does not significantly increase fat oxidation or heart rate.

Taking a supplement containing 600mg of caffeine and 270-1200mg of EGCG (from green tea/Guarana) three times a day before meals will increase your total daily energy expenditure by about 750 kJ (roughly 180 kcal). However, this does not translate to increased fat burning (lipid oxidation) and higher doses of EGCG do not provide extra metabolic benefits. Be aware of a slight increase in diastolic blood pressure, though heart rate remains stable.

Exogenous administration of Peptide YY (PYY) reduces appetite and food consumption by approximately 30% in both lean and obese humans, primarily through inhibition of gut motility and hypothalamic signaling.

Your gut produces a hormone called PYY to tell your brain you are full. In obesity, this signal is often weaker. While injecting PYY works in studies, it is not a standalone cure. Focus on foods that naturally stimulate PYY release (like those reaching the distal small bowel) and respect the satiety signals your body sends, as relying on a single 'magic bullet' hormone therapy is unlikely to succeed long-term.

Consumption of arachidonic acid (AA) and saturated fatty acids (SFAs) increases pro-inflammatory gene expression, specifically upregulating IL-8, IL-6, and TNF-alpha in adipocytes and peripheral blood mononuclear cells (PBMCs).

Be mindful of the types of fats you eat. Diets high in arachidonic acid (found in eggs, dairy, red meat) and saturated fats can trigger inflammatory gene expression. Prioritize anti-inflammatory fats like Omega-3s and monounsaturated fats to mitigate this response.

Dietary interventions rich in antioxidants, specifically extra virgin olive oil, fruits, and vegetables, lower levels of inflammatory markers (IL-6, TNF-alpha) and downregulate NF-kappaB pathway genes in PBMCs.

Incorporate antioxidant-rich foods like extra virgin olive oil, fruits, and vegetables into your diet. These foods actively lower inflammatory markers like IL-6 and reduce the activity of inflammatory pathways, helping to manage systemic inflammation.

Caloric restriction downregulates inflammatory gene expression in adipose tissue and PBMCs, including markers like IL-6, IL-8, and TNF-related proteins, often requiring sustained periods (e.g., 28 days) to observe significant changes.

Sustained caloric restriction is a powerful tool for reducing inflammation. Focus on maintaining a caloric deficit for at least several weeks to see significant downregulation of inflammatory genes in fat tissue and blood cells.

Energy compensation following a preload is significantly determined by the intermeal interval (IMI) and the physical form of the preload, with semisolid and solid forms yielding higher compensation than liquids, particularly when the IMI is between 30 and 120 minutes.

To maximize fullness from a snack or meal, choose semisolid or solid foods (like yogurt, jelly, or whole fruits) and wait 30 to 120 minutes before your next meal. Liquid calories (smoothies, juices) are less effective at suppressing subsequent hunger, especially if consumed too close to the next meal.

The ALDH2 genetic variant (rs671) associated with BMI has an antagonistic effect with alcohol consumption, showing a BMI-increasing effect primarily among non-drinkers.

For East Asians with the ALDH2 variant, the genetic link to BMI appears to be stronger in those who do not drink alcohol. This suggests that alcohol consumption might interact with this specific genetic risk factor, potentially masking or altering its effect on body weight.

Caloric restriction (CR) of 20-40% below ad libitum intake, while maintaining adequate nutrient intake, improves cardiovascular and glucoregulatory biomarkers and extends lifespan in animal models, with mixed but generally favorable effects on human health markers.

To potentially improve long-term health markers, consider reducing your daily caloric intake by 20-40% compared to your current maintenance level, while ensuring you still get all necessary vitamins and minerals. This is best done under guidance, and combining it with exercise (CE) may make it easier to stick to.

Chronic low-grade inflammation, driven by obesity and excess nutrient intake, is a primary mechanistic link that causes both insulin resistance and hypertension by impairing insulin signaling and promoting vasoconstriction.

Addressing the root cause of inflammation through weight management and reducing processed food intake can simultaneously improve insulin sensitivity and lower blood pressure, as inflammation drives both pathologies.

Sodium retention is an evolutionarily conserved mechanism linked to insulin resistance, where insulin promotes sodium reabsorption in the kidney, and high salt intake exacerbates hypertension in salt-sensitive individuals with insulin resistance.

For those with high blood pressure and insulin resistance, reducing sodium intake is particularly critical as their bodies are evolutionarily primed to retain salt, which insulin further exacerbates.

Physical exercise, cold exposure, and certain nutritional strategies (capsaicin, caffeine, EPA) can stimulate brown and beige fat activity, offering potential therapeutic targets for age-related metabolic disease.

You can potentially boost your body's fat-burning capacity (brown and beige fat) through lifestyle choices. Regular physical activity, exposure to cooler temperatures, and consuming certain foods like spicy peppers (capsaicin), green tea (catechins), or fatty fish (EPA) may help stimulate these tissues. While the effects might be less pronounced in older adults, these strategies offer non-pharmacological ways to support metabolic health.

Front-of-package nutrient warning labels on sugar-sweetened beverages and ultra-processed foods significantly increase consumer attention, comprehension, and negative affect, leading to reduced behavioral intentions to purchase these products compared to no-label controls.

Look for products with clear, binary warning labels (like octagons stating 'High in Sugar'). These labels are designed to grab your attention and signal health risks quickly. While they may not change your behavior instantly, they are more effective at helping you identify unhealthy options than complex rating systems. Use them as a quick filter to avoid products with high levels of added sugars, sodium, or saturated fats.

Postoperative oral dietary supplementation in patients undergoing elective gastrointestinal surgery significantly reduces postoperative complications and preserves nutritional status during the inpatient phase.

If you are having major stomach or bowel surgery, ask your medical team about providing you with oral nutritional supplements (like Fortisip) while you are in the hospital. Drinking these supplements between meals, as much as you can tolerate, can help you keep your strength, lose less weight, and significantly lower your risk of getting infections or other complications after the operation. However, continuing these supplements at home after you are discharged does not appear to provide additional benefits for your weight or well-being.