Browse the evidence

Using pedometers is associated with decreased levels of physical activity in adults with Type 2 diabetes, particularly older adults.

Do not assume giving a patient with Type 2 diabetes (especially if over 60) a pedometer will increase their activity. This study found pedometer use was associated with decreased activity. Consider if the patient finds the device burdensome or confusing, and prioritize other behavior change techniques like barrier identification instead.

Obesity is a neurobehavioral disorder resulting from the interaction of a 'vulnerable brain' (biological dysregulation of homeostatic and hedonic pathways) and an obesogenic food environment, rather than solely a failure of willpower.

If you struggle with obesity, understand that it is not just a lack of willpower. Your brain's biological signaling for hunger and satiety, combined with the modern food environment, creates a 'vulnerable brain' state. Effective management requires addressing both the biological signals (e.g., through medical or behavioral interventions) and the environment (e.g., reducing access to hyper-palatable foods).

Gut peptides such as GLP-1 and PYY, along with vagal afferent signaling, play a critical role in homeostatic appetite suppression and satiety signaling.

Your gut produces hormones like GLP-1 and PYY when you eat, which signal your brain to stop eating. This is a natural biological process. Understanding this can help explain why certain foods or eating patterns might affect your satiety levels.

Adipocyte ATP-citrate lyase (ACLY) is essential for handling dietary carbohydrates and maintaining metabolic homeostasis in females, as its deficiency leads to lipodystrophy-like phenotypes, hepatic steatosis, and insulin resistance when consuming high-carbohydrate diets.

For women, high-carbohydrate diets may pose a higher metabolic risk if adipose tissue function is compromised, potentially leading to fat storage in the liver and insulin resistance. Men may tolerate similar carbohydrate loads better. This suggests that women might benefit from monitoring carbohydrate quality and quantity more closely, especially if they have underlying metabolic vulnerabilities.

The presence of cardiometabolic risk factor clusters (CMRFCs)—defined as BMI ≥ 25 plus two of diabetes, hypertension, or hyperlipidemia—results in significant direct medical expenditures independent of cardiovascular disease, totaling approximately $80 billion annually in the U.S.

If you have obesity plus two other metabolic risks (high blood pressure, high cholesterol, or diabetes), your healthcare costs are significantly higher than those with just one risk factor, even if you haven't had a heart attack. This cluster costs the U.S. economy roughly $80 billion a year, largely driven by prescription drugs. Early management of these clusters is critical to preventing the even higher costs of overt cardiovascular disease.

Brainstem cholecystokinin-expressing (CCKAP/NTS) neurons are required for the appetite-suppressing and body-weight-lowering effects of GLP-1 receptor agonists.

GLP-1 medications like semaglutide or liraglutide work by activating specific neurons in the brainstem (CCK neurons). If these neurons are blocked or non-functional, the medication will not suppress appetite or reduce body weight. This highlights that the drug's efficacy depends on this specific neural pathway.

GIP receptor activation reduces the recruitment of CCKAP/NTS neurons and selectively reduces conditioned taste avoidance without abolishing weight loss.

Adding GIP receptor activation to GLP-1 therapy reduces the activation of brainstem neurons responsible for nausea, thereby reducing side effects like nausea without significantly compromising the weight-loss benefits. This suggests dual-agonists may offer a better tolerability profile.

BMI is an imperfect individual predictor of obesity-related risk because metabolically healthy individuals with high BMI may still have elevated cardiovascular risk and mortality compared to normal-weight individuals.

Even if your blood sugar and cholesterol are normal, carrying excess weight (BMI ≥ 30) still increases your risk of heart problems and early death compared to being a normal weight. You should still aim for weight loss to reduce this residual risk.

Higher intake of unprocessed red meat and total meat is associated with a significantly higher incidence of atherosclerotic cardiovascular disease (ASCVD) in older adults, partly mediated by gut microbiota-derived metabolites TMAO, gamma-butyrobetaine, and crotonobetaine.

If you are over 65, be mindful of your red meat consumption. This study links higher intake of unprocessed red meat and total meat to a higher risk of heart disease and stroke. The risk is partly explained by how gut bacteria process compounds in red meat into substances like TMAO. You don't need to eliminate red meat entirely, but balancing it with fish, poultry, and plant-based proteins may help lower your cardiovascular risk.

Intake of fish, poultry, and eggs is not significantly associated with incident atherosclerotic cardiovascular disease (ASCVD) in older adults.

You can likely continue to eat fish, poultry, and eggs without increasing your risk of heart disease or stroke, according to this study of older adults. These foods do not show the same negative association with cardiovascular health that red meat does. Focus on reducing red meat intake while maintaining these other protein sources.

There is no conclusive evidence that varying the relative quantities of dietary carbohydrates and fats (macronutrient partitioning) significantly affects the degree of weight loss or the duration of weight maintenance beyond the effects of total caloric intake.

Do not expect a specific macronutrient ratio (low-carb vs. low-fat) to give you a metabolic advantage for long-term weight loss if you are eating the same number of calories. The science shows that both diets work equally well for weight maintenance when calories are matched. Focus on finding a diet you can adhere to long-term, as compliance is the primary driver of success, not the specific ratio of carbs to fats.

Intensive lifestyle interventions (diet and exercise) alone do not significantly reduce cardiovascular event risk in overweight/obese adults with type 2 diabetes compared to usual care, whereas weight loss achieved through metabolic surgery significantly reduces complications and mortality.

While healthy eating and exercise are important, they might not be enough to protect your heart if you have type 2 diabetes and are overweight. The Look AHEAD study showed that intensive lifestyle changes didn't lower heart attack or stroke risk compared to standard care. However, losing a significant amount of weight (10% or more) did help. For some, metabolic surgery offers the best chance to reduce complications and live longer. Talk to your doctor about combining lifestyle changes with medications or other treatments.

Longitudinal changes in body composition (fat mass, lean mass, or waist circumference) are not significantly associated with the risk of myocardial infarction (MI) in patients with type 2 diabetes.

In type 2 diabetes, losing weight and fat does not significantly reduce your risk of having a heart attack (myocardial infarction). However, it does significantly reduce your risk of heart failure. Therefore, weight loss remains crucial for heart health, but for different reasons than preventing heart attacks.

Acute muscle protein synthesis (MPS) response to resistance exercise is not quantitatively correlated with long-term muscle hypertrophy in individuals, meaning acute MPS measurements cannot predict individual hypertrophic outcomes.

Do not use acute muscle protein synthesis tests to predict your muscle growth potential. While MPS is necessary for growth, its acute magnitude does not predict how much muscle you will gain from training. Focus on consistent training volume and nutrition rather than trying to maximize acute MPS spikes.

Resistance training induces 'anabolic resistance' in older adults, characterized by lower muscle protein synthesis rates in response to protein feeding and exercise compared to younger individuals.

Older adults experience 'anabolic resistance,' meaning their muscles respond less strongly to protein and exercise than younger people's. To overcome this, older adults may need higher protein intakes and more consistent resistance training to stimulate muscle growth.

Acute muscle protein synthesis measurements are useful for understanding mechanistic differences between exercise and nutritional interventions but are not sufficient to predict individual hypertrophic responses.

Use acute MPS data to compare the *potential* of different training or nutritional strategies (e.g., milk vs. soy), but do not use it to predict how much muscle a specific person will gain.

A Mediterranean eating plan supplemented with either extra-virgin olive oil or mixed nuts does NOT significantly reduce the need for initiating insulin therapy in patients with type 2 diabetes compared to a low-fat control diet.

While a Mediterranean diet with olive oil or nuts can help delay starting oral diabetes medications, it may not prevent the need for insulin therapy in all patients. Do not rely on diet alone to avoid insulin if your doctor recommends it based on your blood sugar levels.

When inequalities in behavioral weight management interventions do exist, they tend to favor 'more advantaged' groups (e.g., older, higher SES, employed) in terms of trial uptake, intervention adherence, and trial attrition.

If you are from a 'less advantaged' background (e.g., lower income, rural, younger), you may face higher barriers to starting or sticking with a weight loss program. This is not a reflection of your ability but of the program's design requiring high personal agency. Seek programs that reduce these barriers.

Approximately half of patients with type 2 diabetes discontinue SGLT-2 inhibitors or GLP-1 receptor agonists within five years, but a significant portion (approx. 25%) reinitiates therapy within one year of discontinuation, suggesting many discontinuations are temporary pauses rather than permanent abandonment.

If you stop your SGLT-2 inhibitor or GLP-1 RA, it doesn't mean you are done with it. About 1 in 4 people restart within a year. This often happens after a hospital stay. If you pause your medication due to illness or surgery, ask your doctor to help you restart it as soon as it is safe, so you don't lose the long-term heart and kidney benefits.

Metabolic adaptation (a reduction in resting metabolic rate beyond what is predicted by body composition changes) is minimal, transient, and does not predict long-term weight regain in overweight women following weight loss.

Do not blame persistent weight regain on a 'slowed metabolism' or 'adaptive thermogenesis.' While your metabolism does drop slightly when you lose weight, this effect is small, temporary, and does not predict who will regain weight. Focus on sustainable lifestyle changes and long-term support rather than trying to 'trick' your metabolism.

The doubly labeled water technique provides accurate measurements of total energy expenditure in healthy adults when performed in experienced laboratories, but significant between-laboratory variability exists that can lead to physiologically impossible results in less experienced settings.

If you are using Doubly Labeled Water to measure energy expenditure, ensure your laboratory is experienced with the technique. The method is accurate, but results vary significantly between labs. Use standardized isotope standards and calculation methods (like the 2-point or modified methods) to minimize error, especially if your subject has a low ratio of water intake to energy expenditure.

Co-ingesting 10g of citrulline with 15g of whey protein does not enhance myofibrillar protein synthesis (MPS) or blood flow in elderly men compared to 15g of whey protein alone, despite increasing arginine levels.

For elderly men, adding 10g of citrulline to a small dose of protein (15g) after exercise does not boost muscle building or blood flow any more than the protein alone. To maximize muscle protein synthesis, consume a larger dose of high-quality protein (like 45g of whey) instead of relying on citrulline to make a small dose work better.

One-repetition maximum (1RM) tests and isokinetic peak torque (PT) tests produce conflicting results for assessing alterations in muscle strength, meaning they are not equivalent measures of individual responsiveness to resistance training.

Do not use different testing methods to evaluate the same training program. If you train with free weights or machines (isoinertial), test using 1RM on similar movements. If you use an isokinetic dynamometer, stick to that for tracking. Using 1RM to judge an isokinetic program (or vice versa) will likely lead you to believe the program failed or succeeded when it actually produced standard adaptations, just measured differently.

Chronic high-fat diet consumption increases the formation and activation of mTOR complexes 1 and 2 in skeletal muscle, leading to insulin resistance via S6K1-mediated inhibition of IRS1, whereas exercise training reverses this process by enhancing AMPK activation.

Chronic overconsumption of fats can trigger molecular switches (mTOR) in your muscles that block insulin, leading to resistance. Regular exercise acts as a counter-switch by activating AMPK, which turns off mTOR and restores insulin sensitivity. To maintain metabolic health, balance fat intake with consistent physical activity.