Browse the evidence

Multimodal nonsurgical aesthetic treatments are recommended for addressing aesthetic issues in GLP-1 weight loss patients.

Practitioners should consider a combination of treatments for optimal aesthetic outcomes.

MitoQ supplementation reduced mitochondrial H2O2 emission capacity in skeletal muscle.

MitoQ may reduce oxidative stress in skeletal muscle for older adults.

Individuals with type 2 diabetes have significantly higher levels of inflammatory markers compared to an unaffected population.

Practitioners should consider monitoring inflammatory markers in patients with type 2 diabetes.

There is a significant positive association between C-reactive protein (CRP) levels and body mass index (BMI) in individuals with type 2 diabetes.

Monitoring BMI may provide insights into inflammation levels in diabetic patients.

The paper developed the first consensual definition of functional training using an international e-Delphi method.

Practitioners can refer to this consensual definition for clarity in functional training.

A proposal was made to avoid the distinction between functional training and the general concept of training.

Practitioners should consider this proposal when defining and applying functional training.

The incidence of peripheral neuropathy (PN) differs by type 2 diabetes (T2D) subgroup.

Healthcare providers should consider T2D subgroups when assessing PN risk.

Long-term metformin (850 mg twice daily) and intensive lifestyle interventions do not reduce major cardiovascular events in individuals with prediabetes, despite significantly delaying or preventing the onset of type 2 diabetes.

Taking metformin or following a strict lifestyle program to prevent diabetes does not guarantee protection against heart attacks or strokes, even if you successfully avoid developing diabetes. In this long-term study, these interventions prevented diabetes but did not lower cardiovascular event rates compared to placebo, likely because other risk factors (blood pressure, cholesterol) were managed by standard care. Focus on comprehensive risk management, not just glucose control.

Statin therapy causes a moderate, dose-dependent increase in the diagnosis of new-onset diabetes and worsening glycaemia, with high-intensity regimens producing a 36% relative increase compared to a 10% increase for low/moderate-intensity regimens.

If you are taking statins, be aware that they can slightly raise your blood sugar, especially at higher doses. This increases your risk of being diagnosed with diabetes, particularly if your blood sugar was already near the threshold. However, the heart protection benefits of statins far outweigh this small risk. Regular monitoring of your blood sugar is recommended.

The absolute excess risk of new-onset diabetes from statins is highest in individuals whose baseline glycaemic markers are already close to the diagnostic threshold for diabetes.

If you have pre-diabetes or high-normal blood sugar, your risk of developing diabetes while on statins is higher than someone with normal blood sugar. This does not mean you should stop the statin, but it does mean you should monitor your blood sugar more closely and focus on lifestyle changes to keep your blood sugar in check.

Visceral feedback from the gut activates GCG neurons in the cNTS to promote long-lasting satiety (tens of minutes) that tracks cumulative food intake.

The physical presence of food in your stomach and intestines activates GCG neurons, which promote a feeling of fullness that lasts for tens of minutes. This visceral feedback tracks how much you have eaten, contributing to long-lasting satiety after a meal.

Rare deleterious variants in six specific effector genes (MC4R, PCSK1, POMC, CALCR, BSN, and CORO1A) are significantly associated with BMI at the population level, with CORO1A being a newly identified genetic risk factor for obesity.

Genetic testing can identify individuals with rare variants in genes like CORO1A, MC4R, or PCSK1 who are at higher risk for severe obesity. Knowing this early can guide personalized prevention strategies, such as early lifestyle interventions or targeted pharmacological therapies, before significant weight gain occurs.

Genetic variants (SNPs) associated with obesity, diabetes, and cardiovascular disease generally have small effect sizes and explain a small fraction of the overall variance in these conditions.

Understanding your genetics does not give you a free pass or a guaranteed outcome. Most genetic risks are small and can be managed. Focus on modifiable risk factors like BMI, blood pressure, and diet quality.

Implementation of Enhanced Recovery After Surgery (ERAS) protocols in bariatric surgery significantly reduces postoperative nausea and vomiting, intraoperative time, time to mobilization, intensive care unit stay, and total/functional hospital stay compared to standard care, without increasing complication rates.

For bariatric surgery units, adopting ERAS protocols is a high-value intervention. It significantly reduces patient suffering (nausea/vomiting), shortens hospital stays, and speeds up mobilization without increasing surgical risks like leaks or bleeding. Implementation should be prioritized where feasible.

Race and geographic region significantly modify the risk of new-onset diabetes in people with HIV, with higher rates observed in South Asia and among Black or African American individuals in high-income regions.

If you are from South Asia or are Black/African American, you may have a higher baseline risk for diabetes. Work with your healthcare provider to monitor your blood sugar and weight closely, as these risks can be managed with lifestyle changes.

SGLT-2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) reduce cardiovascular death and heart failure hospitalizations in patients with type 2 diabetes, heart failure, or chronic kidney disease, regardless of baseline glycemic control.

If you have heart failure, kidney disease, or high-risk diabetes, ask your doctor about SGLT-2 inhibitors (like Jardiance, Farxiga, or Invokana). These drugs protect your heart and kidneys, not just your blood sugar. The benefits are proven to reduce hospital stays and death, even if your blood sugar is already well-controlled.

Existing FDA-approved smoking cessation medications (varenicline, nicotine replacement therapy, and bupropion alone) provide only modest attenuation of post-cessation weight gain and do not eliminate it.

Standard smoking cessation drugs like patches, gum, or varenicline will help you quit, but they are not designed to stop you from gaining weight afterward. Expect modest weight changes, but do not rely on them to maintain your weight.

Aggressive blood glucose lowering (targeting HbA1c < 6.5%) in type 2 diabetes does not necessarily reduce cardiovascular risk and may increase overall mortality due to side effects like hypoglycemia and weight gain.

Do not aim for an HbA1c below 6.5% if it requires strong medications that cause low blood sugar or weight gain. The goal is stable, safe blood sugar levels, not the lowest possible number.

SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin, ertugliflozin, sotagliflozin) significantly reduce major adverse cardiovascular events (MACE-3), cardiovascular death, and heart failure hospitalizations in patients with type 2 diabetes and established cardiovascular disease, independent of glycemic control.

If you have Type 2 Diabetes and heart disease or heart failure, SGLT2 inhibitors are a first-line treatment option that protects your heart and reduces hospitalization risk, regardless of your blood sugar levels. Consult your doctor about these specific medications.

Bariatric surgery significantly reduces the incidence of mortality and cardiovascular diseases compared to best non-surgical care in patients with obesity.

Bariatric surgery offers a dramatic reduction in mortality and cardiovascular disease risk compared to non-surgical weight loss methods. For patients with obesity, surgery is the most effective intervention for long-term survival and cardiovascular health.

Cardiovascular-Kidney-Metabolic (CKM) syndrome is a systemic disorder characterized by pathophysiological interactions among metabolic risk factors, chronic kidney disease (CKD), and the cardiovascular system, leading to multiorgan dysfunction and high adverse outcome rates.

If you have high blood pressure, diabetes, or kidney issues, recognize that these conditions are linked and worsen each other. Managing one without addressing the others is less effective. Seek integrated care that looks at your heart, kidneys, and metabolic health together to prevent serious complications like heart failure or kidney failure.

Dysfunctional adipose tissue, particularly visceral fat, drives CKM syndrome by secreting proinflammatory and prooxidative products that damage arterial, cardiac, and kidney tissues, leading to insulin resistance and systemic inflammation.

Excess visceral fat is not just stored energy; it actively releases harmful substances that damage your heart, kidneys, and blood vessels. Managing your weight, specifically reducing visceral fat, is a key medical strategy to reduce inflammation and protect your organs.

Chronic Kidney Disease (CKD) significantly amplifies cardiovascular risk, with albuminuria and low GFR being strong predictors of major atherosclerotic and heart failure events, often making CVD the leading cause of death in CKD patients.

If you have kidney disease, your risk of heart problems is significantly higher. Regular monitoring of your heart health, along with managing blood pressure and blood sugar, is essential to prevent heart failure and heart attacks.

Obesity is a disorder of the energy homeostasis system involving the biological defense of an elevated body-fat mass set point, rather than simply the passive accumulation of excess calories.

Understand that your body has a biological 'set point' for body fat that it actively defends. This is why weight loss programs often fail long-term; your body fights back by increasing hunger and decreasing energy expenditure. Effective treatment requires addressing this biological defense, not just relying on willpower or specific diet compositions.