Browse the evidence

DPP-4 inhibitors (sitagliptin, saxagliptin, vildagliptin, linagliptin, alogliptin) are cardiovascularly safe (neutral effect on MACE) but do not significantly reduce cardiovascular events or mortality compared to placebo.

DPP-4 inhibitors (like sitagliptin) are safe for your heart and do not increase the risk of heart attacks or strokes, but they also do not reduce these risks. They are a good option for blood sugar control if you cannot tolerate other drugs, but if you have existing heart disease, doctors usually prefer SGLT-2 inhibitors or GLP-1 agonists because those have proven heart benefits.

Moderate alcohol consumption (1-3 drinks/day) is associated with a significantly lower risk of coronary heart disease in women compared to abstainers, while heavy consumption increases risk.

For women aged 40-65 who do not smoke and have no history of heart disease, consuming 1-3 drinks per day is associated with a lower risk of coronary heart disease compared to not drinking at all. However, this does not apply to stroke risk, and heavy drinking increases risk. Individuals should consider their personal health history and local guidelines before making changes.

In nonobese humans, there is a weak inverse correlation between serum resistin and insulin sensitivity, but this association disappears when adjusting for body fat percentage.

In lean individuals, higher resistin levels are weakly associated with lower insulin sensitivity, but this is likely driven by body fat levels rather than resistin itself. Adjusting for body fat eliminates this link.

Using weight-dependent prediction equations (Goldberg or pTEE methods) to exclude implausible energy reporters in epidemiologic studies of diet and BMI introduces selection bias and reverses observed associations compared to using simple absolute caloric cutoffs.

When analyzing diet and weight data, avoid using complex formulas that exclude people based on their weight if your outcome is also weight-based (like BMI). This creates a statistical illusion. Simple cutoffs for extreme calorie reporting (e.g., <500 or >3500 kcal/day) are often sufficient and less prone to bias. For prospective changes in weight, the method of exclusion matters less.

Mutations in the preproghrelin/ghrelin gene are associated with obesity in humans, suggesting a genetic basis for energy balance regulation via the ghrelin pathway.

If you have a family history of obesity, it may be partly due to genetics affecting your hunger hormones (ghrelin). This doesn't mean you are doomed, but it does mean you might need to be more mindful of hunger cues and food environments than someone without this genetic risk. Consult a healthcare provider for personalized advice.

In postmenopausal women who have never used hormone replacement therapy, greater waist circumference is significantly associated with an increased risk of invasive breast cancer, independent of overall body mass index.

If you are postmenopausal, your body shape matters for breast cancer risk, not just your weight. Specifically, carrying more weight around your waist increases your risk, even if your overall weight (BMI) is healthy. This risk is most pronounced if you do not take hormone replacement therapy. To mitigate this, focus on reducing central adiposity through lifestyle changes, as waist circumference is a stronger predictor of risk than BMI alone in this group.

In postmenopausal women, the association between central adiposity (waist circumference) and breast cancer risk is significantly modified by hormone replacement therapy use, with the association being strongest in never-users and non-significant in current users.

If you are postmenopausal and take hormone replacement therapy, your breast cancer risk is elevated regardless of your waist size. However, if you do not take hormones, keeping your waist circumference low is a critical way to reduce your risk. The protective effect of a smaller waist is most visible in those not taking hormones.

The coexistence of depression and type 2 diabetes is associated with a significantly higher risk of all-cause and cardiovascular disease (CVD) mortality compared to either condition alone, with the risk being particularly elevated in women with long-duration diabetes or those on insulin therapy.

If you have both diabetes and depression, your risk of dying from heart disease or other causes is significantly higher than if you had only one of these conditions. This risk is even higher if your diabetes has been present for 10+ years or if you require insulin. To mitigate this, it is crucial to actively treat both conditions. Treating depression is not just about mood; it is a critical component of reducing mortality risk in diabetic patients, likely by improving adherence to diabetes management and reducing biological stress responses.

In institutionalized elderly residents with dementia, higher physical and cognitive dependency and decreased appetite are significant predictors of body weight loss, whereas higher baseline BMI and fat intake predict weight gain.

For elderly nursing home residents with dementia, do not automatically assume weight loss is due to illness or medication. The study shows that physical/cognitive dependency and decreased appetite are the key drivers of weight loss. Conversely, higher fat intake and higher baseline BMI are associated with weight gain. Care plans should focus on managing dependency levels and addressing appetite issues (possibly linked to dementia/depression) rather than restricting fat or focusing solely on chronic disease management, as these were not associated with weight changes in this specific population.

Computed Tomography (CT) mean muscle attenuation (MA) is significantly correlated with intramyocellular lipid (IMCL) measured by Magnetic Resonance Spectroscopy (MRS) in the soleus muscle, validating CT as a reliable proxy for assessing intramuscular triglyceride stores.

For clinical or research purposes, CT scans can be used to estimate intramuscular fat levels by measuring muscle attenuation, providing a reliable alternative to more complex MRS techniques. This is particularly useful for assessing insulin resistance risk in sedentary, overweight, or obese populations.

Adherence to a Mediterranean diet supplemented with extra-virgin olive oil or nuts does not significantly reduce the incidence of heart failure compared to a low-fat control diet in high cardiovascular risk individuals, although point estimates suggest a potential benefit that requires larger trials to confirm.

For individuals at high cardiovascular risk, following a Mediterranean diet supplemented with olive oil or nuts did not statistically significantly reduce the risk of developing heart failure compared to a low-fat diet in this specific trial. However, the trend favored the Mediterranean diet, and the study may have been underpowered. It remains a heart-healthy dietary pattern for other cardiovascular benefits, but should not be relied upon as a guaranteed prevention method for heart failure based on this data alone.

The RECODe risk equations provide more accurate predictions for microvascular and cardiovascular complications in diverse U.S. populations with type 2 diabetes compared to older models like UKPDS OM2 and ACC/AHA PCEs, which tend to substantially overestimate risk.

For clinicians managing diverse type 2 diabetes patients, using the RECODe risk equations instead of older models (like UKPDS or ACC/AHA PCEs) leads to more accurate risk assessment. This accuracy helps avoid unnecessary aggressive treatments for patients at lower actual risk and ensures high-risk patients receive appropriate intensive care, thereby reducing drug-related morbidity and improving overall population health management.

The Nutri-Score front-of-pack labeling system fails to identify unhealthy ultra-processed foods because it evaluates only nutrient composition and ignores the degree of food processing.

Do not rely solely on the Nutri-Score letter (A-E) to judge if a food is healthy. A product can receive an 'A' rating for nutrients but still be an ultra-processed food (NOVA 4) with additives and low nutritional value in terms of food matrix. Look for the degree of processing (NOVA classification) alongside or instead of Nutri-Score to make better choices.

Gluten-free diets do not appear to impact IBD disease activity, hospitalization, or surgery rates, despite many patients self-reporting symptom improvement.

For most IBD patients, a gluten-free diet does not reduce disease activity, hospitalizations, or surgery rates. While some patients report subjective symptom improvement, this does not translate to better clinical outcomes. It is not recommended as a primary treatment for IBD unless Celiac Disease is diagnosed.

In patients with type 2 diabetes, total adipocyte number is significantly lower than in BMI-matched obese subjects, indicating a failure of adipose tissue hyperplasia (cell number increase) to buffer excess fat.

For individuals with Type 2 Diabetes, the body's ability to expand fat storage capacity by creating new fat cells (hyperplasia) is impaired compared to non-diabetic obese individuals. This leads to larger existing fat cells (hypertrophy) and forces excess fat into visceral organs and muscles, worsening insulin resistance. Management should focus on preventing further fat accumulation to avoid ectopic fat deposition, as the structural capacity to store fat safely in subcutaneous tissue is limited.

Carbohydrate loading does not improve performance in 100-km stochastic cycling time trials when carbohydrate is ingested during exercise, likely because concurrent intake prevents hypoglycemia regardless of pre-exercise glycogen stores.

If you are eating carbohydrates during your long ride, you likely do not need to perform a strict carbohydrate loading protocol in the days leading up to it. Your performance will be similar whether you load or eat normally, provided you fuel during the event. Save the loading protocol for events where you cannot eat during the activity.

Calorie restriction reduces the production of Prostaglandin E2 (PGE2), a suppressive factor for T-cells, which contributes to enhanced immune function.

Reducing calories, especially by 30%, lowers PGE2, a compound that suppresses T-cells. This reduction helps your immune system work better.

Obesity is associated with a blunted increase in muscle sympathetic nerve activity (MSNA) in response to oral glucose ingestion, despite higher plasma insulin levels, which may contribute to reduced thermic effect of food.

In obesity, the body's ability to increase energy expenditure (via sympathetic nervous system activation) in response to eating is impaired. This blunted response, despite high insulin levels, likely contributes to a lower thermic effect of food, making weight management more difficult. This is a physiological feature of insulin resistance, not just a behavioral issue.

The timing of daily metabolic responses to nutritional challenges differs significantly between serum and skeletal muscle, with serum metabolites showing robust time-of-day oscillations that are reprogrammed by diet type, whereas skeletal muscle metabolome shows less time-of-day variation.

For metabolic health, the timing of your meals matters as much as what you eat. Serum metabolites show strong daily oscillations that are reprogrammed by diet type (high fat vs high carb). While muscle metabolome is less responsive to time-of-day, serum shows significant differences between morning and evening states. This suggests that aligning meal timing with circadian rhythms may be a lever for metabolic optimization, particularly for lipid metabolism in the blood.

In low-income countries (LIC), the excess cardiovascular and all-cause mortality associated with diabetes remains high and is not significantly attenuated by standard pharmacological treatments (antidiabetes, antihypertensive, lipid-lowering drugs, and aspirin), unlike in high-income countries where treatment substantially reduces this risk.

For patients in low-income settings, having a diabetes diagnosis carries a significantly higher mortality risk than in wealthy nations, and simply taking prescribed medications (for blood sugar, blood pressure, or cholesterol) does not fully mitigate this risk. This is due to systemic issues like low medication adherence, suboptimal dosing, lack of access to acute cardiac care (like angioplasty), and socioeconomic disparities. To reduce mortality, access to care must be improved beyond just medication availability, including affordable acute interventions and better disease management.

Higher white blood cell (WBC) counts in obese individuals are largely mediated by elevated fasting plasma leptin concentrations, which stimulate haemopoietic stem cell proliferation.

If you are obese, your body produces more leptin, which signals your bone marrow to produce more white blood cells. This is a normal physiological response to higher body fat levels, not necessarily a sign of infection or disease. Understanding this link helps contextualize lab results in the context of body composition.

Prolonged strenuous running (e.g., marathons, ultra-marathons) causes acute, transient elevations in biomarkers typically associated with pathology (such as creatine kinase, cardiac troponins, and liver enzymes), but these changes represent physiological stress and tissue microtrauma rather than chronic disease or injury.

If you have recently completed a long run or race, expect your blood work to show elevated markers for muscle, liver, or heart stress. These results are transient and reflect the physical effort, not disease. Inform your clinician about recent strenuous exercise to avoid misdiagnosis.

The age-related decline in resting metabolic rate (REE) is driven by the loss of body cell mass (BCM) rather than an intrinsic slowing of cellular metabolism, and this loss is only accurately captured by Total Body Potassium (TBK) measurement.

Your metabolism doesn't inherently slow down as you age; rather, you lose the metabolically active tissue (muscle and cells) that drives it. To maintain your energy expenditure, you must prioritize preserving muscle mass through resistance training and adequate protein intake, rather than accepting metabolic decline as inevitable.

Adhering to a low-carbohydrate diet (defined as the lowest quartile of carbohydrate intake, <42.7% of energy) is associated with a significantly higher risk of developing incident atrial fibrillation compared to higher carbohydrate intake, regardless of whether the replaced carbohydrates are substituted with animal or plant-based fats and proteins.

If you follow a low-carbohydrate diet, be aware that long-term adherence may be associated with a higher risk of developing atrial fibrillation (an irregular heart rhythm). This risk appears to exist regardless of whether you replace carbohydrates with animal or plant-based foods. If you have risk factors for heart disease or AF, consider discussing your carbohydrate intake with a healthcare provider to balance weight management goals with cardiac rhythm health.