Browse the evidence

RYGB surgery increases faecal GABA and glutamate, which may stimulate GLP-1 release and contribute to metabolic enhancement and weight loss.

Surgery increases gut bacteria that produce GABA, which may help stimulate hormones that reduce appetite and improve blood sugar control.

Plant-based drinks are not nutritionally equivalent to cow's milk and should not be recommended as full substitutes without further evidence, as they often lack protein and may contain harmful additives or inorganic calcium.

Do not assume plant-based drinks are healthy substitutes for milk. They often have less protein and more added sugar or oil. If you use them, check the label. They are not nutritionally equivalent to cow's milk.

Human aging is characterized by a progressive increase in oxidative stress, evidenced by decreased plasma antioxidant capacity and increased lipid peroxidation (MDA) and protein oxidation (carbonyls) in erythrocytes.

Aging is biologically linked to accumulating oxidative damage. You can monitor this via biomarkers like MDA and antioxidant capacity, but this paper does not prescribe a specific intervention to reverse it, only to measure it.

Erythrocyte Plasma Membrane Redox System (PMRS) and Ascorbate Free Radical (AFR) reductase activity increase with age as a compensatory mechanism to maintain plasma ascorbic acid levels and minimize oxidative stress.

Your body naturally tries to protect itself from oxidative stress during aging by increasing certain enzyme activities in red blood cells to recycle Vitamin C. This is an internal biological process, not something you can directly control.

Galegine, isolated from Galega officinalis, has a chemical structure similar to metformin and is responsible for the blood glucose-lowering effects of the plant extract.

Galegine is the active compound in Goat's Rue that resembles Metformin, explaining why this plant has been used historically to treat diabetes.

The decline in physical activity is slightly more pronounced in males than in females during the transition to adulthood.

Males may experience a steeper drop in activity (approx 6.5 min/day less) compared to females (approx 5.5 min/day less) during this life transition. Pay extra attention to maintaining activity levels if you are male.

In female athletes engaged in sports emphasizing strength over leanness (e.g., swimming, rowing), reproductive dysfunction is characterized by hyperandrogenism (elevated DHEA-S) rather than hypoestrogenism, potentially due to adrenal axis activation or self-selection of high androgens for performance.

If you are a strength-focused athlete (swimmer, rower) experiencing menstrual irregularities, your hormonal profile may be different from endurance athletes. You may have elevated androgens (like DHEA-S) rather than low estrogen. This may be due to training effects on the adrenal glands or natural selection. Medical evaluation should distinguish between hypoestrogenism and hyperandrogenism to guide treatment.

Higher urinary concentrations of specific phthalate metabolites (MBzP, MEP, MEHHP, MEOHP) are positively associated with increased BMI and waist circumference in adult males (20-59 years), suggesting an obesogenic effect of endocrine-disrupting chemicals.

For adult men, minimizing exposure to plastics containing phthalates (e.g., avoiding heating food in plastic containers, reducing use of certain personal care products) may be a supportive strategy for weight management, given the observed association between higher phthalate levels and increased BMI/waist circumference.

Higher urinary concentrations of MEHP (a metabolite of DEHP) are inversely associated with BMI and waist circumference in adolescent and adult females, suggesting a complex, potentially anti-androgenic or metabolic effect distinct from males.

For women, the relationship between phthalate exposure (specifically DEHP metabolites) and weight is complex and potentially inverse, unlike in men. This highlights the importance of considering hormonal context when evaluating environmental health risks.

Higher genetically predicted fat-free mass index is inversely associated with the risk of atrial fibrillation, ischaemic stroke, and abdominal aortic aneurysm.

Maintaining or increasing fat-free mass (muscle) may offer protective benefits against atrial fibrillation, ischaemic stroke, and abdominal aortic aneurysm. Incorporate resistance training to build muscle, while also managing fat mass to optimize cardiovascular health.

Aggressive tobacco control reducing male smoking prevalence to 10% by 2030 prevents significant cardiovascular and noncardiovascular deaths in men, but fails to prevent cardiovascular deaths in women.

Aggressive national tobacco control policies targeting male smoking prevalence (down to 10% by 2030) can prevent millions of total deaths in men, though this specific intervention does not reduce cardiovascular mortality in women.

Circulating soluble DPP4 (sDPP4) acts as an adipokine that contributes to vascular dysfunction and cardiovascular disease risk in obese and diabetic individuals.

In people with obesity and type 2 diabetes, higher levels of a specific form of the DPP4 enzyme found in the blood are linked to an increased risk of heart and blood vessel problems. Managing blood sugar may help mitigate these risks.

DPP4 inhibitors exert effects beyond incretin regulation by interacting with non-incretin substrates such as SDF-1, NPY, PYY, and Substance P, potentially influencing inflammation, angiogenesis, and appetite.

DPP4 inhibitors may have additional benefits beyond lowering blood sugar, potentially affecting inflammation, appetite, and blood vessel health by preserving other important peptides in the body.

Elevated plasma levels of branched-chain amino acids (BCAAs) are associated with an increased risk of insulin resistance and type 2 diabetes, potentially through the persistent activation of mTORC1 and subsequent serine phosphorylation of IRS-1.

If you have insulin resistance or type 2 diabetes, your blood BCAAs might be high, which is linked to worsening insulin sensitivity. While BCAAs are good for muscle building in healthy individuals, chronically high levels in your blood might be a sign of metabolic dysfunction rather than just a supplement effect. Focus on overall metabolic health and protein quality rather than just high-dose BCAA supplementation if you are at risk for diabetes.

BCAA supplementation or high BCAA diets can improve metabolic parameters such as body composition, glucose tolerance, and insulin sensitivity in specific contexts, such as in high-fat diet-fed mice or by stimulating protein synthesis.

BCAAs can have metabolic benefits, such as improving glucose tolerance in high-fat diet scenarios, but this does not mean they are safe for everyone with insulin resistance. The effect depends heavily on the metabolic context. If you are trying to manage insulin resistance, do not assume BCAA supplements are beneficial without considering your overall metabolic health.

Impaired BCAA metabolism, specifically reduced activity of enzymes like BCATm and BCKDC, leads to the accumulation of BCAAs and their toxic intermediates, contributing to insulin resistance and mitochondrial dysfunction.

If you have insulin resistance, your body might not be breaking down BCAAs efficiently, leading to high levels in your blood. This is not necessarily because you are eating too much protein, but because your metabolic enzymes are less active. Focus on improving overall metabolic health rather than just restricting protein.

Routine screening of serum 25(OH)D levels is not recommended for any population (children, adults, pregnant, obese, dark complexion) in the absence of established clinical indications.

Do not get your vitamin D levels tested unless you have a specific medical condition like hypocalcemia. The guideline states that no specific blood level has been proven to prevent disease, so testing will not change your advice: just take the standard recommended dose.

Increased population-level sugar availability is independently associated with higher type 2 diabetes prevalence, regardless of obesity rates, physical activity, or total caloric intake.

At a population level, higher availability of added sugars correlates with higher diabetes rates, independent of how much people weigh or exercise. While this doesn't mean one soda causes diabetes in one person, reducing sugar availability in communities may help lower overall diabetes prevalence.

Berberine supplementation reduces atherosclerotic plaque area and inflammatory markers in animal models of cardiovascular disease.

Berberine shows promise in reducing atherosclerosis in animal studies by lowering inflammation and oxidative stress. While human trials are limited, it may be a supportive supplement for cardiovascular health, particularly for those with metabolic issues. Consult a doctor before use, especially if taking other medications.

Berberine may have bidirectional effects on tissue factor expression, potentially promoting thrombosis in some contexts.

Berberine's effect on blood clotting is complex. While it generally inhibits platelet aggregation, it may increase tissue factor expression in some cell types, potentially promoting thrombosis. This highlights the need for caution in individuals with clotting disorders or those taking anticoagulants.

Dysbiosis in gut microbiota, characterized by harmful microbial activities such as lipopolysaccharide (LPS) supply and toxin production, is directly linked to the development of obesity, metabolic syndrome, and inflammatory bowel disease (IBD).

Prioritize dietary patterns that support a balanced gut microbiome to prevent dysbiosis, which is linked to obesity, IBD, and metabolic disorders. This involves consuming diverse fibers and fermented foods to maintain the balance between beneficial and harmful microbial activities, thereby reducing systemic inflammation and metabolic risk.

Sirtuin activation (via overexpression or activators like resveratrol/STACs) delays cellular senescence and extends organismal lifespan in model organisms, primarily through DNA repair, telomere maintenance, and interaction with longevity pathways like IIS and AMPK.

Focus on lifestyle factors that naturally boost Sirtuin activity, such as calorie restriction and exercise, which increase NAD+ levels and activate AMPK. While supplements like resveratrol are popular, their direct efficacy in humans is unproven and potentially mediated by off-target effects. Prioritize sleep, stress management, and balanced nutrition to support genomic stability.

Calorie restriction (CR) extends lifespan in many organisms, and this effect is mediated by Sirtuins, although the requirement for Sirtuins varies by species, strain, and CR protocol.

Consider modest calorie restriction or time-restricted eating as a strategy to potentially activate Sirtuin pathways. Focus on nutrient-dense foods. Be aware that individual responses vary, and extreme restriction is unnecessary and potentially harmful.

Myostatin acts as a negative regulator of skeletal muscle mass by inhibiting protein synthesis and promoting degradation; blocking myostatin signaling increases muscle mass in animal models but has failed to show clinical efficacy in elevating muscle strength in human muscular dystrophy trials.

While myostatin is a key regulator of muscle size, simply targeting it (e.g., via drugs or genetic mutation) increases mass but has not reliably improved strength in human clinical trials. Current research suggests targeting myostatin alone is insufficient for treating muscle wasting in humans, and other factors like activin A may play larger roles in primates.