Browse the evidence

Anthropometric measures (BMI, waist circumference, waist-to-hip ratio) are recommended as feasible, cost-effective core measures for obesity clinical trials, despite being less accurate than imaging methods like DXA or MRI.

For obesity research, simple measurements like height, weight, and waist circumference are the standard starting point because they are feasible and cost-effective. While they are less precise than advanced imaging, they are sufficient for tracking general trends in body composition across large groups.

Leptin, amylin, and adiponectin are recommended as core biomarkers for obesity trials to assess energy homeostasis and predict treatment response.

Obesity trials should measure leptin, amylin, and adiponectin to understand energy homeostasis. Leptin reflects fat stores, amylin promotes satiation, and adiponectin is linked to insulin sensitivity and inflammation.

Intensive glycaemic control reduces microvascular complications (retinopathy, nephropathy, neuropathy) but has limited or potentially harmful effects on macrovascular outcomes and all-cause mortality.

Intensive blood sugar control helps prevent eye, kidney, and nerve damage, but it doesn't significantly prevent heart attacks and may increase the risk of low blood sugar events. Work with your doctor to find a safe blood sugar target that minimizes risks.

Long-term remission of Type 2 Diabetes following metabolic surgery is not sustained for the majority of patients, with remission rates dropping significantly after 5 years.

While surgery often puts Type 2 Diabetes into remission initially, this effect often wears off after several years. Most patients will eventually need to restart diabetes medications to maintain blood sugar control, meaning surgery is a tool for disease management rather than a permanent cure.

There is no evidence supporting the practice of periodizing resistance exercise training for females according to specific phases of the menstrual cycle to promote greater hypertrophic adaptations.

Do not waste time or energy trying to periodize your training based on your menstrual cycle. There is no evidence that training differently in the follicular vs. luteal phase leads to better muscle growth. Stick to a consistent, progressive resistance training program regardless of where you are in your cycle.

Current energy intake recommendations for pregnant women with obesity overestimate total daily energy expenditure (TDEE), potentially promoting excess gestational weight gain.

Standard calorie recommendations for pregnant women with obesity are likely too high. This study suggests that following these standard guidelines may lead to excessive weight gain because they overestimate how many calories these women actually burn. Healthcare providers should consider lower energy targets or more personalized metabolic assessments for obese pregnant women to prevent excess gestational weight gain.

Low sleeping energy expenditure (SleepEE) in early pregnancy is associated with insulin resistance and low triiodothyronine (T3) concentrations.

For obese pregnant women, a lower-than-expected metabolic rate is linked to higher insulin resistance and lower thyroid hormone (T3) levels. This suggests that metabolic health issues may drive lower energy expenditure, contributing to weight gain risk.

Specific lipid metabolites, Diacylglycerols (DAGs) and Ceramides, are inversely associated with insulin sensitivity and mitochondrial capacity, suggesting they are the primary drivers of insulin resistance rather than total intramyocellular lipid (IMCL) content.

Your body's ability to handle sugar depends less on how much total fat is stored in your muscles and more on specific toxic fat byproducts called ceramides and DAGs. These toxic lipids build up when you are sedentary or diabetic, blocking insulin signals. Keeping your muscles active helps clear these toxic lipids, improving insulin sensitivity even if total muscle fat remains high.

Vagus nerve stimulation (VNS) and GLP-1 analogs are emerging therapeutic tools that harness brain-body communication to treat obesity and diabetes, though more invasive and long-lasting approaches are needed.

If lifestyle changes are insufficient, medical interventions like GLP-1 analogs (e.g., semaglutide) and vagus nerve stimulation are proven to help reverse metabolic disease by targeting brain-body signals. These are powerful tools, but they may be invasive or expensive. Work with your healthcare provider to determine if these options are appropriate for your specific situation, keeping in mind that more accessible long-term solutions are still being developed.

Current clinical evidence from randomized controlled trials and meta-analyses does not support a causal link between GLP-1 receptor agonist use and an increased risk of thyroid cancer in humans.

If you are considering or taking a GLP-1 medication (like Ozempic or Wegovy) and are worried about thyroid cancer, know that large human studies have not found a proven link. The warning on the label comes from animal studies, not human outcomes. While you should be aware of symptoms, the proven benefits for weight loss and heart health generally outweigh this unproven risk. Do not stop your medication without talking to your doctor, especially if you have a family history of specific thyroid cancers (MTC), which is a separate contraindication.

Setmelanotide treatment is associated with a high incidence of skin hyperpigmentation and injection site reactions, though these are generally mild and manageable.

Patients should expect skin darkening (hyperpigmentation) and injection site reactions as common side effects of Setmelanotide. These are generally mild, do not indicate serious harm, and do not necessarily require discontinuation of therapy, but patients should be counseled on these expected outcomes.

Chronic consumption of high-calorie/obesogenic diets causes maladaptive perturbations in gut-brain signaling, leading to desensitization of vagal afferents and reduced efficacy of appetite-suppressing gut hormones (GLP-1, CCK, PYY), which contributes to the exacerbation of metabolic dysregulation and obesity.

If you have a history of obesity or high-calorie eating, your body's natural 'stop eating' signals (hormones and nerve feedback) may be desensitized. This isn't a failure of willpower; it's a physiological state. To counter this, focus on strategies that naturally stimulate these pathways, such as consuming protein and fiber before carbohydrates (meal sequencing), which has been shown to enhance GLP-1 secretion and improve metabolic control.

High-fat diets, specifically saturated lipids like palmitic acid, disturb gastrointestinal feedback and promote overconsumption independently of food palatability.

Be mindful of high-saturated-fat foods (like those high in palmitic acid). They can disrupt your body's natural 'fullness' signals, leading you to eat more than you need, regardless of how tasty they are. Balancing fats with fiber and protein can help mitigate this effect.

Sleep duration is primarily determined by environmental factors with low heritability, whereas body composition measures (adiposity and lean mass) are strongly influenced by genetic factors with high heritability.

You cannot change your genetic predisposition to body fat or lean mass, which accounts for a large portion of your body composition. However, sleep duration is largely environmentally determined, meaning you have significant control over how much you sleep. This suggests that improving sleep habits is a viable lever for health, even if it doesn't directly dictate your genetic body type.

Higher body mass index (BMI) is independently associated with elevated plasma levels of acylcarnitines (ACs) and large neutral amino acids (LNAAs), serving as biomarkers of metabolic dysregulation and increased cardiometabolic risk.

Your weight (BMI) is a rough proxy for metabolic health, but it's not the whole story. This research shows that as BMI increases, your body's metabolic byproducts (specifically acylcarnitines and large neutral amino acids) also increase, signaling higher metabolic stress and disease risk. Focus on metabolic health markers and lifestyle factors rather than just the number on the scale.

Sympathomimetic drugs (e.g., phentermine) reduce hunger and increase energy expenditure but are limited by adverse cardiovascular and central nervous system effects, leading to withdrawal of many agents from the market.

Older stimulant-based weight loss drugs can work by suppressing appetite and increasing energy expenditure, but they carry higher risks of heart and nervous system side effects. Many have been removed from the market. If prescribed, they are typically for short-term use (12 weeks) and require careful monitoring.

The early improvement in hepatic insulin sensitivity after RYGB is primarily driven by postoperative caloric restriction and reduced liver fat, rather than surgery-specific anatomical effects.

Early improvements in liver function after gastric bypass are largely due to the immediate reduction in calorie intake and liver fat, not just the surgery itself. Maintaining a caloric deficit is essential to sustain these early metabolic benefits.

Intensive glucose control using sulphonylurea-insulin therapy in type 2 diabetes reduces long-term cardiovascular events and mortality, with a legacy effect persisting after the active intervention ends.

For patients with type 2 diabetes, achieving tight blood sugar control early in the disease course using intensive therapy (like insulin or sulphonylureas) significantly lowers the risk of heart attacks and death. This benefit persists for at least 10 years after treatment stops, highlighting the importance of not delaying effective therapy.

Adding glutamine to a post-exercise beverage containing essential amino acids and carbohydrate does not enhance muscle protein synthesis or glycogen resynthesis in healthy young males.

If you are drinking a post-workout shake with essential amino acids and carbs, adding glutamine will not help your muscles grow or recover faster. Your muscles are already getting the signal they need from the essential amino acids. You can save your money on glutamine supplements without losing any muscle-building benefits.

Long-term weight loss maintenance is not significantly predicted by dietary adherence or caloric restriction, but is associated with baseline proteomic and gut microbiome signatures.

If you struggle to maintain weight loss despite good adherence, your baseline biology (proteins and gut bacteria) may be a factor. This suggests that personalized dietary strategies based on biological markers might be more effective than generic advice for long-term maintenance.

A 12-month multi-component exercise program combined with daily multi-nutrient supplementation (whey protein, calcium, vitamin D) has limited effect on ameliorating adverse musculoskeletal consequences (bone density, muscle mass, physical function) in men with prostate cancer undergoing androgen deprivation therapy, primarily due to modest intervention adherence.

For men on prostate cancer hormone therapy, combining exercise and supplements is challenging to maintain long-term. While leg strength can improve, bone density loss often continues. Prioritize sustainable adherence over complex protocols; if you can't do 3 gym sessions and take daily supplements, focus on what you can consistently do, as the study showed low adherence led to negligible bone benefits.

WB-EMS does not provide additional benefits for dynamic arm strength, balance, or flexibility in postmenopausal women compared to standard resistance and aerobic training.

Do not rely on WB-EMS to improve your balance, flexibility, or arm strength. Stick to traditional stretching and upper-body specific exercises for those goals. WB-EMS is best used as a tool to boost leg power and heart health when combined with standard exercise.

ChREBP acts as a central regulator linking carbohydrate intake to metabolic disease; its overexpression causes fatty liver and insulin resistance, while its deletion prevents obesity and fatty liver but may cause other metabolic issues like insulin resistance in adipose tissue.

While high sugar intake drives disease via ChREBP, completely eliminating carbohydrates or targeting this pathway aggressively may have unintended metabolic consequences. A balanced approach focusing on reducing HFCS while maintaining adequate complex carbohydrate intake is likely optimal.

Ingesting 3 g/kg body mass of carbohydrate during the 3-hour recovery period following eccentric exercise-induced muscle injury increases local skeletal muscle mRNA expression of pro-inflammatory myokines (IL-6, IL-8, MCP-1) rather than attenuating inflammation.

If you perform heavy eccentric exercise (like heavy leg presses or downhill running), eating carbohydrates immediately after (3g/kg) will increase the genetic signals for inflammation inside your muscles. However, this did not change blood inflammation levels or muscle damage markers in this study. The practical impact on soreness or recovery time is unknown, but you should not avoid carbs for fear of 'increasing inflammation' as the systemic response was unchanged.