Browse the evidence

The EAT-Lancet diet score without minimum intake values for nutrient-dense food groups negatively predicts micronutrient adequacy in rural women of reproductive age in low- and middle-income countries, whereas adding minimum intake values (>0 g/d) reverses this association to a positive one.

When evaluating diet quality in low-resource settings, do not use scoring systems that allow zero consumption of nutrient-dense foods (like meat, dairy, or legumes) to earn points. These scores will falsely label malnourished diets as 'healthy.' Always apply minimum intake thresholds to ensure the score reflects actual nutrient adequacy.

Short-term resistance exercise (3 bouts over 9 days) combined with a high-fat diet does not prevent the high-fat diet-induced upregulation of immune and inflammatory genes in skeletal muscle, although it does remodel genes associated with muscle growth and structure.

If you are eating a high-fat, low-carb diet, doing resistance exercise for just a few days will not stop your muscles from turning on inflammatory genes. While exercise does build muscle structure genes, it doesn't stop the inflammation caused by the diet. You likely need longer-term training to see protective effects, but don't assume a few workouts cancel out the dietary stress.

Short-term high-fat diet induces DNA hypermethylation and alters gene expression of PYGM (glycogen phosphorylase, muscle), an adaptive epigenetic response to glycogen depletion, which is preserved by resistance exercise.

When you switch to a low-carb/high-fat diet, your body epigenetically silences the gene responsible for breaking down glycogen (PYGM) because you aren't eating carbs. This is a smart adaptation. Exercise helps maintain this state but doesn't change this specific epigenetic switch.

Elevating plasma free fatty acid availability during intense exercise (approx. 80% VO2max) increases fat oxidation and spares carbohydrate, but does not enhance performance in exercise lasting approximately 1 hour.

For intense workouts lasting around an hour (like interval training or hard races), eating a high-fat meal beforehand will not help you perform better, even if it changes what fuel your body burns. Your body will still rely heavily on carbohydrates because the intensity is too high to use fat efficiently. Stick to your standard pre-workout nutrition strategy rather than experimenting with high-fat loads for these specific efforts.

No country globally achieves the combined WHO target of potassium intake >3.5 g/day and sodium intake <2 g/day.

It is currently impossible to meet both sodium and potassium guidelines simultaneously in most countries. Focus on reducing discretionary salt intake and increasing potassium-rich foods like fruits and vegetables, as this is the most feasible path to improving cardiovascular health.

Tirzepatide treatment is not significantly associated with an increased risk of pancreatitis compared to control groups (placebo, basal insulin, or GLP-1 RAs) in patients with type 2 diabetes and obesity.

If you have Type 2 Diabetes or Obesity and are considering Tirzepatide, current data from multiple clinical trials suggests it does not significantly increase your risk of pancreatitis compared to other common diabetes or weight-loss medications. This is reassuring news if you were avoiding the drug due to fears of pancreatic inflammation.

Tirzepatide is associated with a significantly increased risk of composite gallbladder or biliary diseases (including cholelithiasis, cholecystitis, and other gallbladder disorders) compared to placebo or basal insulin, but not compared to GLP-1 RAs.

Tirzepatide increases the risk of gallbladder or biliary issues (like gallstones or inflammation) compared to placebos or insulin. However, this risk appears similar to other GLP-1 medications. Be aware of symptoms like abdominal pain and report them to your doctor promptly, as early detection is key.

In patients with new-onset type 2 diabetes, a weight loss of 10% or more within the first two years is associated with the highest risk of all-cause mortality.

If you have recently been diagnosed with type 2 diabetes, avoid losing more than 10% of your body weight in the first two years. Significant weight loss in this context is linked to higher mortality, possibly due to muscle loss or other health issues. Focus on maintaining a stable weight rather than aggressive weight loss.

Food industry sponsorship of academic research systematically biases the research agenda toward physical activity and nutrient-specific interventions, thereby diverting attention from the health impacts of highly processed foods and ultra-processed diets.

When evaluating health advice or research, always check the funding source. If a study on obesity or nutrition is funded by a food or beverage company, be skeptical of conclusions that emphasize exercise or specific nutrients while ignoring the role of highly processed foods. Prioritize research that is independent of industry funding or focuses on whole dietary patterns rather than isolated components.

Use of GLP-1 receptor agonists (GLP1-RAs) is not associated with an increased risk of thyroid cancer compared to DPP-4 inhibitors in patients with type 2 diabetes.

If you have type 2 diabetes and are considering a GLP-1 medication like Ozempic or Wegovy, current large-scale evidence suggests it does not increase your risk of thyroid cancer compared to other common diabetes drugs. While rodent studies showed thyroid effects, this has not been observed in human population studies.

AMPK activation inhibits ribosome biogenesis by blocking mTORC1 signaling, while mTORC1 signaling may negatively affect mitochondrial biogenesis, creating a molecular competition.

This is a molecular detail. For training, it means high-energy demand (endurance) signals the body to build mitochondria, potentially suppressing the signal to build protein (muscle) if not managed.

Administration of the ketone metabolite BHB-Phe (N-beta-hydroxybutyryl phenylalanine) suppresses food intake and reduces body weight in obese mice.

This research identifies a specific metabolite, BHB-Phe, which is naturally produced during ketosis and actively suppresses hunger. While the study used high-dose injections in obese mice, it suggests that maintaining ketosis may naturally elevate this compound, contributing to reduced food intake. For now, this is a mechanistic insight rather than a direct supplement recommendation, as oral bioavailability and dosing in humans are not established.

GLP-1 receptor agonists delay gastric emptying, increasing the risk of aspiration during anesthesia, necessitating specific preoperative discontinuation guidelines.

If you take Ozempic and have surgery, tell your surgeon. You likely need to stop the drug 1-7 days before surgery to prevent vomiting during anesthesia. Follow your doctor's specific instructions.

Research funded by the sugar-sweetened beverage (SSB) industry is significantly more likely to reach weak or null conclusions regarding the adverse health effects of SSB consumption compared to independently funded research.

When evaluating health claims about sugary drinks, prioritize studies funded by government, universities, or independent foundations over those funded by the beverage industry. Industry-funded studies are statistically much more likely to downplay health risks, potentially delaying necessary public health interventions like taxes or labeling laws.

Bariatric surgery confers a protective effect against cancer mortality, potentially driven by weight loss and intrinsic surgical changes.

Bariatric surgery significantly reduces the risk of dying from cancer (by 60%). This benefit is a major driver of the overall mortality reduction seen in surgical patients.

Resistance training induces an acute and chronic expansion of the satellite cell (SC) pool in skeletal muscle, but this expansion does not result in a detectable increase in myonuclear content during the first 10 weeks of training in young, previously trained men.

If you are a young, previously trained man, expect your satellite cells to increase in number during the first few months of resistance training, but do not expect this to immediately translate into more muscle nuclei. Your muscle is likely adapting through increased protein synthesis and repair mechanisms rather than structural nuclear addition at this stage. Focus on consistent training; the nuclei may add up if you train long enough or intensely enough to exceed current transcriptional capacity.

Sustained caloric restriction in non-obese adults leads to a statistically significant but clinically small loss of bone mineral density (BMD) at the hip and spine, increasing fracture risk by an estimated 0.2% over 10 years.

If you restrict calories, expect some bone density loss. Take calcium and vitamin D as recommended, and monitor your bone health, although the increased fracture risk is very small.

Caloric restriction in non-obese adults increases the incidence of adverse events related to the nervous, musculoskeletal, and reproductive systems, particularly in normal-weight individuals compared to overweight individuals.

If you are already lean, be aware that CR may cause more side effects like fatigue, muscle pain, or menstrual issues than if you were overweight. Monitor these symptoms closely.

Dapagliflozin (SGLT2 inhibitor) lowers systolic blood pressure through an initial plasma volume contraction followed by a sustained reduction in sympathetic nervous system activity.

If you have type 2 diabetes and high blood pressure, dapagliflozin 10mg daily can help lower your blood pressure. It works by initially reducing blood volume and, over time, by calming the nervous system's stress response on your blood vessels. This happens even after the initial fluid loss stops.

Combining Dapagliflozin and Exenatide results in a synergistic blood pressure reduction that exceeds the sum of their individual effects, driven by plasma volume contraction and potentially other mechanisms beyond SNS reduction.

For patients with type 2 diabetes and obesity, combining dapagliflozin and exenatide offers a stronger blood pressure reduction than using either drug alone. This synergy helps achieve better cardiovascular protection, though the exact mechanism beyond fluid loss is still being studied.

Exenatide (GLP-1 RA) reduces parasympathetic nervous system activity, which may contribute to an increase in heart rate, but does not significantly lower systolic blood pressure on its own in this population.

Exenatide alone may not significantly lower blood pressure in people with type 2 diabetes and obesity, but it does reduce parasympathetic nervous system activity, which can increase heart rate. It is often used in combination with other drugs for better cardiovascular outcomes.

Tirzepatide does not increase the risk of major adverse cardiovascular events (MACEs) in patients with type 2 diabetes.

Tirzepatide does not increase the risk of major adverse cardiovascular events (MACEs) in patients with type 2 diabetes. This makes it a safe option for cardiovascular risk management.

Ethnic disparities in Type 2 Diabetes are influenced by genetic variations regulating lipid and amino acid metabolism, leading to distinct metabolic signatures and drug responses across populations.

Your ethnic background influences how your body metabolizes nutrients and responds to medications for Type 2 Diabetes. This is due to genetic variations affecting lipid and amino acid metabolism. Discuss your specific metabolic profile with your healthcare provider to tailor dietary and therapeutic strategies, as personalized approaches are more likely to succeed than generic ones.

SGLT2 inhibitors and GLP-1 receptor agonists reduce arrhythmia risk in diabetic patients by ameliorating intracellular sodium and calcium dysregulation and reducing fibrosis.

If you have type 2 diabetes, ask your doctor about SGLT2 inhibitors or GLP-1 agonists. These drugs do more than lower blood sugar; they help stabilize the electrical activity of your heart and reduce scarring, lowering your risk of sudden cardiac death.