Browse the evidence

Approximately half of patients with type 2 diabetes discontinue SGLT-2 inhibitors or GLP-1 receptor agonists within five years, but a significant portion (approx. 25%) reinitiates therapy within one year of discontinuation, suggesting many discontinuations are temporary pauses rather than permanent abandonment.

If you stop your SGLT-2 inhibitor or GLP-1 RA, it doesn't mean you are done with it. About 1 in 4 people restart within a year. This often happens after a hospital stay. If you pause your medication due to illness or surgery, ask your doctor to help you restart it as soon as it is safe, so you don't lose the long-term heart and kidney benefits.

Metabolic adaptation (a reduction in resting metabolic rate beyond what is predicted by body composition changes) is minimal, transient, and does not predict long-term weight regain in overweight women following weight loss.

Do not blame persistent weight regain on a 'slowed metabolism' or 'adaptive thermogenesis.' While your metabolism does drop slightly when you lose weight, this effect is small, temporary, and does not predict who will regain weight. Focus on sustainable lifestyle changes and long-term support rather than trying to 'trick' your metabolism.

One-repetition maximum (1RM) tests and isokinetic peak torque (PT) tests produce conflicting results for assessing alterations in muscle strength, meaning they are not equivalent measures of individual responsiveness to resistance training.

Do not use different testing methods to evaluate the same training program. If you train with free weights or machines (isoinertial), test using 1RM on similar movements. If you use an isokinetic dynamometer, stick to that for tracking. Using 1RM to judge an isokinetic program (or vice versa) will likely lead you to believe the program failed or succeeded when it actually produced standard adaptations, just measured differently.

Protein intake proportion (20-30%) is not significantly associated with all-cause mortality in Korean adults, although it yields the longest warranty period for mortality exceeding 1%.

For Korean adults, the specific proportion of protein (20-30%) does not significantly impact all-cause mortality risk. However, since traditional Korean diets are high in plant-based proteins, focusing on plant protein sources may be beneficial, as animal protein has been linked to higher mortality in other studies.

Intensive glucose-lowering strategies significantly increase the risk of severe hypoglycemia compared to standard therapy.

If you are on intensive diabetes treatment to lower your blood sugar significantly, be aware that your risk of severe low blood sugar (hypoglycemia) nearly doubles compared to standard treatment. This risk must be weighed against the benefits for your eyes and kidneys. Regular monitoring and awareness of hypoglycemia symptoms are crucial.

Systematically manipulating resistance training variables (load, volume, contraction type, rest intervals) does not produce greater muscle hypertrophy than a standard progressive resistance training protocol in trained young men, despite generating higher total training volume and slightly greater acute myofibrillar protein synthesis.

If you are a trained individual, you do not need to constantly vary your resistance training variables (like load, volume, or rest periods) to maximize muscle growth. A standard progressive resistance training program, performed with high effort (to failure), is just as effective for hypertrophy as a complex, variable program. Focus on consistency and progressive overload rather than frequent changes in exercise selection or parameters.

Mitochondrial dynamics, specifically regulated by Drp1-mediated fission, are essential for maintaining muscle stem cell (satellite cell) regenerative competence and metabolic health throughout adult life.

As you age, your muscle stem cells rely on healthy mitochondrial function to repair tissue. While you cannot directly 'dose' Drp1, you can support mitochondrial health through regular physical activity and adequate nutrition, which are known to promote mitochondrial biogenesis and dynamics. This biological maintenance is key to preserving muscle mass and regenerative ability in adulthood.

Adding phenotypic and genotypic data to personalized nutrition advice does not provide added benefit over advice based solely on current diet analysis.

Do not pay for expensive genetic or phenotypic testing for personalized nutrition advice. The Food4Me study showed that advice based only on your current diet is just as effective as advice that includes your genes or body metrics.

Providing individualized genetic risk information alone does not motivate behavior change in diet or physical activity.

Do not rely on genetic testing to motivate you to eat better or exercise. Knowing your genetic risk does not change your behavior. Focus on actionable dietary advice instead.

Pioglitazone improves NASH histology without worsening fibrosis in patients with T2DM and MAFLD, but its use is limited by side effects including weight gain, fluid retention, and potential bladder cancer risk.

Pioglitazone (45mg daily) can improve liver inflammation (NASH) in people with type 2 diabetes and fatty liver without worsening scarring. However, it can cause weight gain, fluid retention, and may increase the risk of bladder cancer in some people. It is not recommended for everyone and should be used with caution, especially if you have a history of heart failure or bladder cancer.

In advanced CKD and dialysis patients, higher BMI (including morbid obesity) is associated with better survival outcomes, a phenomenon known as the 'obesity paradox'.

If you are on dialysis, do not try to lose weight. Your higher body weight is actually protecting your life. Focus on eating enough protein and calories to maintain your muscle mass, as losing weight is dangerous for dialysis patients.

Obesity accelerates biological cardiovascular ageing by inducing structural and functional cardiac and vascular changes that mimic those of chronological ageing, independent of traditional risk factors.

Your heart ages based on how you treat it, not just your birth year. Obesity forces your heart to work harder and remodels it to look and function like an older, non-obese heart. Losing weight can reverse these changes, effectively turning back the biological clock of your cardiovascular system.

Central nervous system (CNS) activation of the Glucose-dependent Insulinotropic Polypeptide Receptor (GIPR) is required for the synergistic weight loss observed with dual GIPR/GLP-1R agonists.

If you are using a GLP-1 medication for weight loss or diabetes and struggle with side effects or plateauing results, newer dual-acting medications (targeting both GIP and GLP-1 receptors) may offer better weight loss with potentially fewer gastrointestinal side effects. This is because these drugs work on brain pathways that suppress appetite and may reduce the nausea often caused by older GLP-1-only drugs. Consult your doctor about whether a dual-agonist is appropriate for your metabolic health.

Liraglutide-induced weight loss is significantly attenuated in individuals consuming high-carbohydrate diets when hepatic FGF21 signaling is absent, indicating that FGF21 mediates the appetite-suppressing effects of GLP-1 receptor agonists specifically in the context of high carbohydrate intake.

If you are using a GLP-1 receptor agonist like liraglutide, your weight loss results may be suboptimal if you consume a high-carbohydrate diet. This is because the drug relies on a hormone called FGF21 to help suppress appetite, and this hormone is most effective at reducing food intake when carbohydrates are present. To maximize weight loss, consider reducing your carbohydrate intake, as this may enhance the drug's ability to engage the FGF21 pathway and promote greater weight reduction.

A three-week ketogenic diet shifts tryptophan metabolism to increase kynurenic acid and decrease quinolinic acid, potentially promoting mitochondrial protection and reducing neuroinflammation.

Following a ketogenic diet may shift your body's processing of tryptophan away from potentially neurotoxic byproducts (quinolinic acid) toward protective ones (kynurenic acid). This suggests a potential neuroprotective benefit of long-term ketosis.

Transforming urban provisioning systems through integrated spatial planning and supply-side innovations (e.g., active mobility, green infrastructure, clean energy) reduces cardiometabolic risk factors and improves cardiovascular health outcomes.

Advocate for and utilize urban designs that prioritize walking, cycling, and access to green spaces. If you live in a city, look for 'walkable' neighborhoods with mixed land use. If infrastructure is lacking, support policy changes for better transit and pedestrian safety, as these systemic changes directly lower your risk of cardiovascular disease and help maintain a healthy weight.

In Mexican adults, general adiposity (BMI or height-adjusted weight) is a stronger independent predictor of blood pressure than central adiposity (waist circumference, waist-hip ratio, or waist-height ratio), with no evidence of threshold effects.

For Mexican adults, maintaining a healthy overall body weight is more critical for controlling blood pressure than focusing solely on waist size. Since there is no 'safe' threshold for adiposity, lower general body weight is consistently associated with lower blood pressure, regardless of where the fat is stored.

GLP-1R signaling primarily occurs through the Gαs/cAMP pathway, leading to insulin secretion, but also involves Gαq and β-arrestin pathways which contribute to receptor internalization and other metabolic effects.

GLP-1 drugs work by activating specific pathways in the body. The main pathway increases insulin when blood sugar is high. Other pathways help with receptor recycling and may contribute to other effects like cell survival.

Non-POMC neurons, specifically GABAergic neurons, mediate leptin's direct effects on energy balance and food intake, influencing POMC neurons indirectly.

This suggests that treatments targeting only POMC neurons may fail to reduce appetite. Future therapies might need to target GABAergic neurons or other non-POMC pathways to effectively manage obesity via leptin signaling.

POMC neurons expressing the glucagon-like peptide 1 receptor (Glp1r) are a distinct subpopulation from those expressing the leptin receptor (Lepr), and Glp1r-expressing POMC neurons may regulate energy balance.

This heterogeneity explains why broad activation of POMC neurons might have mixed results. Targeted therapies might need to distinguish between Lepr-expressing (glucose) and Glp1r-expressing (energy balance) subsets.

Metabolic surgery, which yields approximately 25% weight loss at 10 years, is associated with a 44% lower risk of invasive cancer compared to non-surgical patients.

For individuals with severe obesity, metabolic surgery can lead to significant weight loss and a substantially lower risk of invasive cancer. Discuss with your doctor if you are a candidate.

Overfeeding-induced insulin resistance is driven by the depletion of small, peripherally located intramyocellular lipid droplets and the subsequent accumulation of large lipid droplets and ceramides, rather than by an increase in total intramyocellular lipid content.

If you are concerned about insulin resistance, focus on maintaining physical activity levels that preserve small, peripheral muscle lipid droplets. High physical activity and efficient lipid oxidation are associated with resistance to weight gain and better insulin sensitivity, even during periods of overfeeding. The total amount of fat in your muscles matters less than how your body organizes that fat.

Increasing protein intake to 1.6 g/kg/day during resistance training does not enhance strength or lean body mass gains compared to moderate intake (1.0 g/kg/day) in previously untrained middle-aged adults.

If you are middle-aged and new to resistance training, you do not need to obsess over high protein intakes (1.6g/kg+). Getting your protein to around 1.0-1.2 g/kg of body weight is sufficient to maximize your strength and muscle gains. Focus on consistent training and hitting that moderate target rather than over-consuming protein, which offers no additional muscle-building benefit in this group.

Supplementation with commercially available leucine metabolites (α-HICA, HMB-FA, or HMB-Ca) does not enhance resistance training-induced gains in muscle thickness, strength, or power in young, moderately trained men consuming a high-protein diet.

If you are a young, moderately trained man eating enough protein and training consistently, taking HMB or α-HICA will not give you better muscles or strength than if you just took a placebo. Focus on your training and diet instead of spending money on these supplements.