Browse the evidence

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.

In obese patients with type 2 diabetes (BMI ≥30), intentional weight loss is associated with a statistically significant increase in all-cause mortality.

If you are obese (BMI ≥30) and have type 2 diabetes, intentional weight loss might actually increase your risk of death compared to maintaining your weight. Discuss this specific risk with your doctor, as standard weight loss advice may not apply to your long-term survival.

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.

Higher dietary intake of alpha-linolenic acid (ALA) is associated with a lower risk of total and non-cardiovascular mortality in older adults, but is not associated with cardiovascular mortality, coronary heart disease, or stroke.

If you are over 65, increasing your intake of plant-based alpha-linolenic acid (found in flaxseed, chia, and walnuts) is associated with a lower risk of dying from non-heart-related causes. However, relying on these plant sources to prevent heart attacks or strokes is not supported by this data. Focus on a balanced diet for cardiovascular health rather than expecting ALA to replace marine omega-3s for heart protection.

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.

MC4R agonists (setmelanotide) are effective for treating obesity in individuals with specific genetic deficiencies (POMC, PCSK1, LEPR) or Bardet-Biedl syndrome, but are not approved for general obesity.

If you have a rare genetic condition like POMC deficiency or Bardet-Biedl syndrome, ask your doctor about setmelanotide. It is a daily injection approved for these specific conditions. It is not approved for general obesity.

The association between ultra-processed food consumption and colorectal cancer risk is significant in men but not in women, and there is no significant association with prostate, rectal, pancreatic, or central nervous system cancers.

If you are male, be particularly mindful of UPF intake as it is linked to a higher risk of colorectal cancer. For women, the link to colorectal cancer was not statistically significant in this study. There was no significant link found for prostate, rectal, pancreatic, or brain cancers.

In individuals with type 2 diabetes and obesity, treatment with glucagon-like peptide-1 receptor agonists (GLP-1RA) does not increase the risk of suicidal ideation or self-injury (SIS) compared to sodium-glucose cotransporter 2 inhibitors (SGLT-2i).

If you have type 2 diabetes and obesity, current evidence suggests that GLP-1RA medications do not increase your risk of suicidal thoughts or self-harm compared to other common diabetes drugs like SGLT-2 inhibitors. While regulators are reviewing safety data based on early reports, this large study found no such link. However, because these events are rare, the possibility of a small increased risk cannot be completely excluded, so monitoring your mental health remains important.

High-dose GLP-1 receptor agonists and treatment of patients with higher baseline BMI are associated with a significantly increased risk of ventricular arrhythmias (VAs).

If you are taking a high dose of a GLP-1 medication (like the maximum weight-loss doses of Ozempic or Saxenda), especially if you have a higher body weight, there is a slightly increased risk of ventricular arrhythmias. Doctors should monitor these patients more closely. However, this risk is specific to high doses and higher BMI, not the standard doses used for diabetes.

Oral semaglutide is associated with a significantly lower risk of incident atrial fibrillation (AF), while dulaglutide shows an increasing trend toward higher AF risk compared to controls.

Among GLP-1 medications, oral semaglutide (Rybelsus) may actually lower the risk of atrial fibrillation, while dulaglutide (Trulicity) might slightly increase it. This difference is drug-specific and not seen with all GLP-1s. If you have a history of AF, discuss the specific drug choice with your doctor.

GLP-1 receptor agonists (GLP-1 RAs) significantly increase the risk of gastrointestinal adverse events, specifically intestinal obstruction and perioperative aspiration, due to delayed gastric emptying.

If you are taking a GLP-1 medication (like Ozempic or Wegovy) and have surgery or an endoscopy, tell your medical team. You may need to adjust your fasting time or pause the medication to prevent stomach contents from entering your lungs, which is a known risk of these drugs.

GLP-1 receptor agonists are associated with an increased risk of gallbladder and biliary tract diseases, particularly with weight-loss focused dosing and specific agents like liraglutide.

Be aware that GLP-1 medications can increase the risk of gallstones, especially if you are losing weight rapidly. Report any abdominal pain to your doctor. This risk is higher with weight-loss doses compared to diabetes doses.

Current evidence does not support a significant increased risk of acute pancreatitis or pancreatic cancer associated with GLP-1 receptor agonists in human populations, despite early animal studies and spontaneous reports.

You do not need to worry about developing pancreatitis or pancreatic cancer from GLP-1 medications. Large studies have confirmed they are safe in this regard, although you should stop the medication if you experience severe abdominal pain.

An acute high-fat diet increases the activity of AMPK and SIRT1 in skeletal muscle (via phosphorylation and deacetylation, respectively) without changing the total protein or mRNA levels of these enzymes.

Your body can rapidly switch on fat-burning enzymes in your muscles just by changing what you eat, even if the total amount of those enzymes doesn't change. This happens through chemical tags (phosphorylation/deacetylation) that activate the enzymes. This is a fast-acting regulatory mechanism, not a slow structural change.