Browse the evidence

Visceral adipose tissue (VAT) is the primary driver of cardiometabolic complications (hypertension, T2DM, dyslipidemia) through endocrine dysfunction, RAAS activation, and inflammation, rather than total body weight alone.

Stop relying on BMI to assess your health risk. Focus on reducing visceral fat through lifestyle changes, as this specific fat type drives heart disease and diabetes. Use waist-to-height ratio as a better metric than weight alone.

Semaglutide 2.4 mg is cost-effective for patients with BMI ≥ 30 kg/m² (ICER 18,459 EUR) but may not be cost-effective for patients with BMI ≥ 35 kg/m² (ICER 22,657 EUR) compared to the willingness-to-pay threshold of 20,000 EUR.

For patients with BMI ≥ 35 kg/m², semaglutide 2.4 mg may exceed the willingness-to-pay threshold for cost-effectiveness in Portugal, whereas it remains cost-effective for those with BMI ≥ 30 kg/m².

Diabetes remission, rather than weight loss itself, is the primary driver for reducing the risk of new-onset microvascular complications.

While weight loss is important, achieving diabetes remission (normal blood sugar without medication) is what actually protects against microvascular complications like kidney and eye damage. Weight loss without remission may not provide this specific protection.

Dulaglutide 1.5 mg reduces systolic blood pressure (SBP) and pulse pressure in patients with type 2 diabetes, with the majority of this reduction (64% for SBP, 86% for pulse pressure) being independent of weight loss.

If you have Type 2 Diabetes, taking dulaglutide (1.5 mg weekly) can lower your systolic blood pressure by about 2.6 mmHg after 6 months. Crucially, most of this benefit comes from the drug's direct effect on your blood vessels and nervous system, not just from losing weight. This means you may see blood pressure improvements even if your weight remains stable.

Higher doses of dulaglutide (4.5 mg) provide additional blood pressure reduction compared to 1.5 mg, but this additional benefit is primarily driven by greater weight loss rather than enhanced weight-independent mechanisms.

Increasing your dulaglutide dose from 1.5 mg to 4.5 mg may lower your blood pressure a bit more, but this extra benefit comes mostly from losing more weight, not from a stronger direct effect on your blood vessels. If you are not losing enough weight on 1.5 mg, the higher dose might help your BP by helping you lose more weight.

Obesity significantly increases the risk of cardiovascular disease, heart failure, and cerebrovascular disease, even in individuals classified as 'metabolically healthy'.

If you have obesity, your risk for heart disease and heart failure is significantly higher than someone with a normal weight, even if your blood pressure and cholesterol are currently normal. You should prioritize cardiovascular health monitoring and weight management strategies to mitigate this elevated risk.

Tirzepatide improves hepatic steatosis and renal outcomes in patients with type 2 diabetes, independent of or additive to weight loss.

Tirzepatide not only helps with blood sugar and weight but also significantly reduces liver fat and protects kidney function in people with type 2 diabetes. This makes it a valuable option for those at risk of liver or kidney complications.

Women with obesity exhibit distinct physiological and psychological responses to weight management compared to men, including greater neural sensitivity to food rewards, higher baseline leptin levels, and a tendency toward peripheral (gluteo-femoral) fat distribution which offers metabolic protection until menopause.

If you are a woman with obesity, your body may respond differently to food and stress than a man's due to hormonal and neural factors. This is not a failure of willpower. Post-menopause, your fat distribution may shift to the abdomen, increasing health risks. Work with providers who assess your specific hormonal status and mental relationship with food, rather than just applying a generic 'calories in, calories out' model.

Post-menopausal women face a significantly increased risk of cardiovascular disease and metabolic complications due to the shift from protective gluteo-femoral fat to visceral, perivascular, and epicardial fat accumulation following estrogen decline.

After menopause, your body stores fat differently, often around organs (visceral/epicardial fat), which increases heart disease risk even if your BMI stays the same. Focus on maintaining muscle mass and reducing visceral fat through exercise and diet, as standard BMI checks may not capture this new risk.

Tirzepatide (5, 10, and 15 mg once weekly) achieves glycaemic targets (HbA1c < 7.0% and ≤ 6.5%) significantly faster than semaglutide 1 mg and insulin degludec in patients with type 2 diabetes.

If you have type 2 diabetes, starting tirzepatide will likely lower your blood sugar (HbA1c) to target levels faster than starting semaglutide 1 mg or insulin degludec, even though you start on a low dose. You will need to wait 4-20 weeks to reach your full maintenance dose depending on the strength chosen, but clinical targets are met sooner with tirzepatide than with the comparators.

Semaglutide demonstrates superior efficacy compared to Liraglutide in reducing hemoglobin A1c (HbA1c) levels, though it shows no significant difference in weight loss or fasting blood sugar (FBS) reduction compared to Liraglutide.

If you are managing Type 2 Diabetes without metformin, switching from Liraglutide to Semaglutide is likely to improve your blood sugar control (HbA1c) more effectively. However, do not expect significantly more weight loss from this switch alone, as both drugs appear to offer similar weight reduction benefits.

Semaglutide demonstrates superior efficacy compared to Dulaglutide in reducing both HbA1c and Fasting Blood Sugar (FBS), but shows no significant difference in weight loss or BMI reduction.

If you are using Dulaglutide and your blood sugar (HbA1c and FBS) is not well-controlled, switching to Semaglutide may offer better glycemic results. However, if your primary goal is weight loss, switching is unlikely to yield additional weight reduction compared to staying on Dulaglutide.

Higher BMI and central obesity are strongly associated with poor glycemic control (HbA1c ≥ 7%) in Japanese adults with Type 2 Diabetes, with over 50% of obese patients failing to meet glycemic targets.

If you have Type 2 Diabetes and are in an obesity class (BMI ≥ 25 kg/m² in Japan), your risk of having high blood sugar (HbA1c ≥ 7%) is over 50%. Managing your body weight is a critical step to improving your glycemic control, especially if you are under 45 years old.

Younger adults (18-44 years) with Type 2 Diabetes and obesity exhibit significantly higher rates of poor glycemic control compared to older adults, despite having higher mean BMI and waist circumference.

If you are under 45 and have Type 2 Diabetes, your blood sugar control is likely worse than older patients with the disease, especially if you carry extra weight around your waist. You need to prioritize weight management and dietary habits more aggressively than older patients to achieve similar glycemic targets.

Liraglutide 3.0 mg administered subcutaneously once daily produces significant but numerically lower weight loss compared to semaglutide and is less cost-effective, though it remains a safe and efficacious option for obesity management.

Liraglutide 3.0mg once daily is an effective treatment for obesity, producing an average 5.6kg weight loss. It is less effective than semaglutide and tirzepatide. It remains a safe option, particularly for those who may not respond as well to other agents or have specific contraindications.

High body mass index (BMI) and obesity are strong, independent risk factors for the development and progression of chronic kidney disease (CKD), end-stage renal disease (ESRD), and obesity-related glomerulopathy (ORG).

Maintaining a healthy body weight is one of the most effective ways to prevent chronic kidney disease. High BMI increases pressure inside the kidney's filtering units (glomeruli) and triggers inflammatory hormones from fat tissue that directly damage kidney structure over time. Even if you do not have diabetes or high blood pressure, excess weight—especially around the waist—increases your risk of kidney failure. Weight management through diet and exercise is a primary preventive strategy for kidney health.

Obesity increases the risk of nephrolithiasis (kidney stones) through mechanisms including lower urine pH, increased urinary oxalate, uric acid, and sodium excretion, and insulin resistance-induced acidic urine.

If you are overweight, you are at higher risk for kidney stones because your body's metabolism changes how your urine is made. Insulin resistance makes your urine more acidic and increases the amount of stone-forming minerals like oxalate and uric acid you excrete. Managing your weight and insulin sensitivity is key to preventing stones, not just avoiding specific stone-causing foods.

Low-carbohydrate diets (20% of energy) increase Total Energy Expenditure (TEE) by approximately 250 kcal/day compared to high-carbohydrate diets (60% of energy) during weight-loss maintenance, supporting the carbohydrate-insulin model.

Adopting a low-carbohydrate diet (around 20% of calories from carbs) may increase your daily energy expenditure by about 250 calories compared to a high-carb diet, even when maintaining the same weight. This metabolic advantage may facilitate long-term weight management.

Higher estimated glucose disposal rate (eGDR), indicating lower insulin resistance, is independently associated with a reduced risk of incident cardiovascular disease in individuals with Cardiovascular-Kidney-Metabolic (CKM) syndrome stages 0-3.

For individuals with metabolic risk factors (obesity, high blood pressure, or pre-diabetes), improving insulin sensitivity is a primary strategy for preventing heart disease. While eGDR is a clinical metric, the underlying principle is that reducing insulin resistance—through weight management, physical activity, and dietary quality—lowers cardiovascular risk. This benefit is most pronounced in early stages of metabolic dysfunction (CKM 0-1).

Tirzepatide treatment significantly reduces the prevalence of metabolic syndrome in patients with type 2 diabetes compared to placebo, semaglutide, and insulin therapies.

If you have type 2 diabetes, tirzepatide (a once-weekly injection) is highly effective at reducing the cluster of risk factors that make up metabolic syndrome (like high blood sugar, high blood pressure, and high triglycerides). It works better than standard insulin or other common diabetes medications in clinical trials. While lifestyle changes are important, they are often not enough on their own to resolve metabolic syndrome, making this medication a powerful tool for improving your cardiovascular risk profile.

GLP-1 receptor agonists (specifically semaglutide and liraglutide) significantly reduce hepatic fat content and resolve NASH in patients with NAFLD, primarily through delayed gastric emptying and direct metabolic effects on the liver.

If you have NAFLD or NASH, especially if you are overweight or have type 2 diabetes, GLP-1 receptor agonists like semaglutide (once weekly) and liraglutide are currently the most promising pharmacological treatments for resolving liver fat and NASH. While they can cause temporary gastrointestinal issues like nausea, clinical trials show they significantly improve liver outcomes compared to placebo. Discuss these options with your doctor, as they may offer resolution of steatosis and metabolic improvement.

Incretin receptor agonists (IRAs), including GLP-1RAs and dual GIP/GLP-1RAs, reduce the risk of major adverse cardiovascular events (MACE) and improve lipid profiles and blood pressure in patients with type 2 diabetes.

If you have Type 2 Diabetes and are at risk for heart disease, ask your doctor about GLP-1 receptor agonists (like liraglutide, semaglutide, or dulaglutide). These medications not only help control blood sugar but have been proven in large studies to significantly reduce the risk of heart attacks, strokes, and cardiovascular death. They also help lower blood pressure and improve cholesterol levels. While they are often injectable (with some oral options available), the cardiovascular protection they offer is a major benefit for patients with existing heart conditions.

Statin therapy is safe and effective for cardiovascular risk reduction in patients with MASLD and MASH, and elevated transaminases should not prevent prescription.

If you have fatty liver disease (MASLD/MASH), do not avoid statins due to fear of liver damage. Statins are safe, effective for heart health, and may even improve liver markers. Consult your doctor for appropriate intensity based on your overall cardiovascular risk.

Once-weekly semaglutide (2.4 mg) significantly improves health-related quality of life and reduces body weight in obese patients with HFpEF.

If you are obese and have HFpEF, ask your doctor about semaglutide (Ozempic/Wegovy). The STEP-HFpEF trial showed that taking 2.4 mg once weekly significantly improved quality of life and reduced body weight by over 13% compared to placebo.