Browse the evidence

Obesity in Type 1 Diabetes is associated with increased cardiometabolic risk, higher insulin requirements, and an enhanced risk of chronic complications compared to normal-weight T1D patients.

Obesity in T1D is not just about weight; it significantly increases the risk of heart disease, kidney issues, and eye problems due to insulin resistance. Managing weight is critical for long-term complication prevention.

Combining a GLP-1 receptor agonist (GLP-1RA) with an SGLT2 inhibitor provides superior glucose control, greater weight loss, and greater reductions in systolic blood pressure compared to either drug alone.

If your blood sugar remains high despite taking metformin, ask your doctor about combining a GLP-1 receptor agonist (like exenatide) with an SGLT2 inhibitor (like dapagliflozin). This combination lowers blood sugar more effectively than either drug alone, helps you lose more weight, and reduces blood pressure.

Low-carbohydrate diets improve cardiovascular risk markers (triglycerides, HDL, blood sugar, inflammation) and reduce 10-year ASCVD risk scores, despite potential increases in LDL-C in lean individuals.

If you are on a low-carbohydrate diet, expect improvements in triglycerides, HDL, and blood sugar. If your LDL-C rises, discuss with your provider whether it correlates with other risk factors, as overall cardiovascular risk may still decrease.

Low-dose empagliflozin (2.5-5 mg) as adjunct therapy to hybrid closed-loop systems improves postprandial glycemic control and reduces insulin requirements in adults with type 1 diabetes, though it increases the risk of hypoglycemia and requires management of side effects like increased urination.

If you have Type 1 Diabetes and use a hybrid closed-loop system but still struggle with post-meal spikes or high insulin doses, low-dose empagliflozin (2.5-5mg) can significantly improve your time in range and reduce insulin needs. Be aware that it may cause more frequent urination and a higher risk of post-meal lows, which you can manage by adjusting your pump settings. The benefit of better control often outweighs the inconvenience of taking one extra pill.

A non-carbohydrate counting (non-CC) meal bolus strategy based on preprandial glucose levels, when used with open-source automated insulin delivery (AID), significantly improves time in range (TIR) and reduces glycemic variability compared to manual open-loop modes in adults with Type 1 Diabetes.

If you have Type 1 Diabetes and find carbohydrate counting stressful or error-prone, consider using an open-source automated insulin delivery system (like AndroidAPS) with a simplified bolus strategy. Instead of counting carbs, you calculate your insulin based on your pre-meal glucose level and your average mealtime insulin needs. This approach can significantly improve your time in range and reduce glycemic variability, especially at night, without increasing the risk of hypoglycemia. It is a viable alternative for those who find traditional carb counting burdensome.

Intensive lifestyle interventions (ILI) involving caloric restriction and physical activity cause a significant increase in 25-hydroxyvitamin D [25(OH)D] and suppress parathyroid hormone (PTH) elevation during the period of maximal weight loss in adults with type 2 diabetes.

If you have type 2 diabetes and are losing weight through diet and exercise, expect your Vitamin D levels to rise and your Parathyroid Hormone (PTH) to decrease, especially in the first year. This is a normal and likely beneficial response to weight loss, though it may normalize over time. Monitor your bone health as weight loss can also lead to bone loss.

Intensive glycemic control (target HbA1c < 6%) significantly reduces the development of diabetic peripheral neuropathy (DPN) in patients with Type 1 Diabetes Mellitus (T1DM), but this benefit is not observed in patients with Type 2 Diabetes Mellitus (T2DM).

If you have Type 1 Diabetes, aiming for an HbA1c below 6% is the most effective way to prevent nerve damage. However, if you have Type 2 Diabetes, this aggressive target is not recommended due to lack of neuropathy benefit and increased mortality risk; standard control (7.0-7.9%) is advised instead.

VLCKD improves glycemic profiles (fasting glucose, HbA1c, HOMA-IR) and lipid profiles (triglycerides, total cholesterol) significantly, with some improvements (glycemia, LDL) being similar to other weight loss interventions.

You can expect your blood sugar, insulin resistance, and cholesterol numbers to improve significantly on VLCKD. However, for these specific metabolic markers, the improvement is comparable to what you might get from any other effective weight loss diet, whereas fat loss is specifically better on VLCKD.

Semaglutide significantly improves glycemic control (HbA1c and fasting blood glucose) and systolic blood pressure in overweight or obese adults, with or without type 2 diabetes.

Semaglutide not only helps with weight loss but also significantly improves blood sugar control (HbA1c and fasting glucose) and lowers systolic blood pressure in overweight or obese individuals, offering potential cardiovascular benefits.

Once-weekly semaglutide (1.0 mg) reduces ad libitum energy intake by approximately 24% through mechanisms of reduced appetite, improved control of eating, and lower preference for high-fat foods, leading to significant body weight loss without compensatory increases in energy expenditure.

Take once-weekly semaglutide (titrated to 1.0 mg over 12 weeks) to reduce hunger, improve control over eating, and lower preference for high-fat foods. This leads to a ~24% reduction in daily calorie intake and significant fat loss, without needing to increase exercise or metabolic rate. Expect mild GI side effects initially.

The 5:2 diet improves liver stiffness (a marker of fibrosis/inflammation) and reduces LDL cholesterol, whereas LCHF does not improve liver stiffness and may increase LDL.

If you have high cholesterol or heart disease risk, the 5:2 diet might be a better choice than LCHF because it lowers LDL and improves liver stiffness. LCHF reduces liver fat just as well but may not help with stiffness or cholesterol as much.

Intermittent fasting significantly increases adiponectin and decreases leptin levels, which may contribute to improved insulin sensitivity independent of significant fat mass loss.

Fasting may improve your metabolic health markers (like adiponectin) even if the scale doesn't move much, suggesting benefits beyond just weight loss.

A ketogenic diet is more effective than low-fat diets for improving glycemic control (HbA1c and HOMA-IR) in patients with type 2 diabetes, but shows comparable effects in non-diabetic patients.

If you have type 2 diabetes and are overweight, switching to a ketogenic diet (very low carb, high fat) is likely to improve your blood sugar control more effectively than a standard low-fat diet. If you do not have diabetes, the blood sugar benefits are similar to low-fat diets, though weight loss may still be superior.

Intermittent energy restriction (IER) significantly reduces fasting insulin levels compared to continuous energy restriction (CER), although the clinical relevance is uncertain.

IER may offer a slight advantage in lowering fasting insulin compared to daily restriction, which could be beneficial for metabolic health. However, since weight loss is the same, do not expect dramatic changes in body composition solely from this hormonal shift.

Reducing the intake of specific amino acids, particularly leucine and histidine, which are abundant in animal proteins, is associated with decreased fat mass and improved insulin resistance independent of total caloric intake.

Focus on the source of your protein. Plant proteins are naturally lower in leucine and histidine compared to animal proteins. This specific amino acid profile may help improve insulin sensitivity and reduce fat mass, even if total protein intake is adequate.

Achieving and maintaining diabetes remission (HbA1c <48 mmol/mol off glucose-lowering medications) is associated with a significantly lower incidence of Major Adverse Diabetic Events (MADE) compared to those not in remission.

Achieving diabetes remission is not just about feeling better; it actively protects your kidneys, eyes, and nerves from long-term damage. By maintaining remission through weight loss and lifestyle changes, you significantly lower your risk of serious diabetic complications.

Newer GLP-1 receptor agonists (semaglutide) and dual agonists (tirzepatide) significantly outperform older medications and lifestyle interventions alone, achieving weight losses of 12-17%.

Newer injectable medications like semaglutide (2.4mg weekly) and tirzepatide are significantly more effective than older drugs, achieving 12-17% weight loss. They represent a major step forward in pharmacotherapy for obesity.

A ketogenic diet significantly reduces HbA1c levels in overweight T2DM patients, though it does not significantly affect fasting glucose, fasting insulin, or HOMA-IR compared to control diets.

While a ketogenic diet effectively lowers long-term average blood sugar (HbA1c) in T2DM patients, it may not immediately change fasting blood glucose or insulin resistance scores (HOMA-IR) compared to other diets. This suggests the benefit is in sustained glucose regulation rather than acute fasting metrics.

Genetic variants in GLP1R (rs6923761) and TCF7L2 (rs7903146) influence the response to liraglutide, with specific genotypes associated with greater reductions in body fat and weight.

If you are taking liraglutide, your genetic makeup might influence how much fat or weight you lose. Some genetic variants are linked to better outcomes with this drug. This is not a reason to start or stop treatment, but may help explain individual differences in response.

A ketogenic very-low-energy diet (VLED) induces a transient increase in subjective hunger and desire to eat during the first 3 weeks (up to 5% weight loss), despite the presence of ketosis, with appetite suppression only emerging after 10% weight loss.

If you start a ketogenic very-low-energy diet, expect your hunger to increase significantly during the first 3 weeks, even if you are in ketosis. This is a normal, transient phase. Do not mistake this hunger for the diet not working; appetite suppression typically emerges only after you have lost about 10% of your body weight. Preparing for this initial hunger spike can help you stick with the diet.

Upon refeeding (cessation of ketosis) after significant weight loss (10-17%) on a ketogenic diet, hunger feelings and active ghrelin (AG) concentrations increase significantly, potentially undermining long-term weight maintenance.

When you stop the ketogenic diet and return to normal eating, expect your hunger and ghrelin levels to rise significantly. This is a physiological response to losing ketosis and weight. To mitigate this, transition gradually to your maintenance diet rather than stopping abruptly, and be aware that your body will signal for more food.

Time-restricted feeding (TRF) improves insulin sensitivity and glycemic control (including reduced glucose variability and HbA1c) in individuals with overweight or obesity, independent of significant weight loss in some studies.

If you have insulin resistance or pre-diabetes, try shifting your eating window to end earlier in the evening (e.g., 8 PM) and start later in the morning (e.g., 4 PM). This timing aligns with your body's natural circadian rhythms, helping to lower blood sugar spikes and improve how your body uses insulin, even if the scale doesn't move dramatically.

Alternate-Day Fasting (ADF) improves insulin sensitivity (HOMA-IR) more than Continuous Energy Restriction (CER).

If you are using Alternate-Day Fasting, you may see improvements in insulin sensitivity that are not seen with standard calorie restriction. This is a potential metabolic benefit of ADF.

Semaglutide and Liraglutide reduce the risk of Major Adverse Cardiovascular Events (MACEs), whereas Naltrexone/Bupropion increases the risk of elevated blood pressure.

If you have obesity and cardiovascular risks, Semaglutide or Liraglutide are preferred because they reduce MACE risk. Avoid Naltrexone/Bupropion if you have hypertension, as it increases blood pressure risk.