Browse the evidence

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.

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.

Adding Very Low Calorie Diets (VLCD, ≤800 kcal/day) to a standard low-intensity weight management program (WMP1) is not cost-effective compared to WMP1 alone.

For patients with severe obesity, adding very low-calorie diet meal replacements (≤800 kcal/day) to a standard 12-week behavioral weight management program is not a cost-effective strategy. The standard program alone provides better value for money. Patients should focus on sustainable behavioral changes rather than expensive, restrictive meal replacements.

Deletion of the p38α kinase in adipose tissue protects against high-fat diet-induced obesity by increasing energy expenditure and brown adipose tissue (BAT) thermogenesis.

Current research suggests that low levels of the p38α protein in fat tissue are associated with higher body mass index in humans. In mice, removing p38α from fat cells prevents obesity by boosting heat production. This implies that therapies aiming to reduce p38α activity in fat might help treat obesity, but this is currently only a mechanistic finding in animals, not a human treatment protocol.

The p38δ kinase isoform promotes brown adipose tissue thermogenesis, and its deletion leads to obesity and reduced energy expenditure.

In mice, the p38δ protein is required for fat-burning. Removing it causes obesity. This suggests that maintaining or activating p38δ in fat tissue could be a potential strategy to prevent obesity, though no human treatments exist yet.

A diagnosis of Type 2 Diabetes acts as a 'teachable moment' that significantly accelerates smoking cessation compared to the general population, but fails to trigger positive changes in physical activity, alcohol consumption, or fruit and vegetable intake.

Getting a Type 2 Diabetes diagnosis is a strong motivator to quit smoking, but it rarely changes your diet or exercise habits on its own. Do not rely on the diagnosis to fix your lifestyle. You must actively implement specific plans for nutrition and physical activity, as these habits are resistant to change without targeted intervention.

Older anti-obesity medications (Orlistat, Sibutramine, Phentermine, Naltrexone/Bupropion, Phentermine/Topiramate) achieve mean weight loss between 5-10%, which is often insufficient to meet patient expectations and leads to lower long-term adherence.

Older anti-obesity medications (like Orlistat, Sibutramine, and combination drugs) typically produce 5-10% weight loss, which is beneficial but often fails to meet patient expectations, leading to higher discontinuation rates compared to newer agents.

Self-reported dietary energy intake in population surveys is systematically biased by macronutrient composition, specifically under-reporting protein and over-reporting fat relative to actual expenditure.

When analyzing dietary data or tracking your own intake, do not assume that your macronutrient ratios are accurate if your total calorie count is off. People who under-report calories tend to under-report protein and over-report fat. This bias distorts the perceived relationship between diet and health outcomes, meaning 'healthy' diets may appear even healthier than they are in self-reported data.

Semaglutide is associated with an increased incidence of neoplasms (cancer) in clinical trials, specifically involving the thyroid, bladder, colorectal, and pancreas, although the absolute number of cases is often low and causality is not conclusive.

If you are taking semaglutide (Ozempic/Wegovy), be aware that clinical trials showed a small number of cancer cases, particularly in the thyroid, bladder, and pancreas. However, the paper notes this is not conclusive proof that the drug causes cancer, as obesity and diabetes themselves increase cancer risk. You should discuss your personal risk factors (especially family history of thyroid cancer) with your doctor.

Protein hydrolysates do not provide superior muscle protein synthesis (MPS) or anabolic properties compared to intact non-hydrolysed proteins or free amino acids.

If you are taking protein hydrolysates expecting better muscle growth than regular protein, you are likely wasting money. Current evidence shows that intact proteins (like whey isolate or casein) and free amino acids are just as effective for muscle recovery and adaptation. Stick to cost-effective, intact protein sources unless you have specific digestive issues.

Diet-induced weight loss in obese individuals with or without type 2 diabetes significantly increases plasma Lipoprotein(a) [Lp(a)] levels, potentially antagonizing the cardiovascular benefits of conventional risk factor improvement.

If you are obese and have type 2 diabetes, losing weight through diet will likely improve your blood sugar and cholesterol, but it may also raise your Lipoprotein(a) levels. This rise is a known biological response to calorie restriction in this population and might partially cancel out the heart benefits of weight loss. You should still lose weight, but discuss monitoring your Lp(a) levels with your doctor to see if additional interventions are needed.

High variability in bodyweight is associated with an increased risk of incident atrial fibrillation in patients with type 2 diabetes mellitus, independent of baseline BMI and overall weight change direction.

If you have type 2 diabetes, avoid extreme weight cycling. Whether you are trying to lose weight or maintain it, try to do so gradually. Large swings in body weight (e.g., losing 10% and regaining it quickly) are linked to a higher risk of atrial fibrillation. Focus on stable, sustainable weight management rather than rapid, drastic changes.

Current dietary assessment methods for UPF intake are limited and require improvement, including better classification algorithms and exposure assessment tools.

Be aware that current estimates of UPF intake may be inaccurate due to limitations in dietary assessment tools. Future research aims to improve these methods, which will lead to better public health guidance.

GLP-1 receptor agonists (GLP-1RAs) cause a significantly higher rate of intolerable gastrointestinal adverse reactions leading to drug withdrawal compared to other hypoglycemic agents (Insulin, SGLT2i, DPP4i, TZD) and placebo.

If you are considering a GLP-1RA, expect a higher likelihood of gastrointestinal side effects (nausea, vomiting, diarrhea) compared to other common diabetes drugs like Metformin or SGLT2 inhibitors. These side effects are the most common reason for stopping the medication. However, not all GLP-1RAs carry the same risk; Dulaglutide appears to have the lowest risk of intolerable GI reactions, while Semaglutide and Liraglutide have higher risks, especially at higher doses.

Leptin analogs (metreleptin) are effective for treating obesity only in patients with generalized lipodystrophy or congenital leptin deficiency, but are ineffective and contraindicated for general diet-based obesity due to leptin resistance.

Leptin analogs like metreleptin are not for general weight loss. They are reserved for rare genetic conditions like generalized lipodystrophy where the body cannot produce leptin. For most people with obesity, leptin levels are already high, and adding more does not help.