Browse the evidence

A single acute bout of resistance exercise training (RET) does not induce mitochondrial remodelling (biogenesis, content, or quality control) in either untrained older adults or master athletes within the acute (1h) or delayed (48h) recovery periods.

If you are an older adult or a master athlete, do not expect a single resistance training session to improve your mitochondrial health or biogenesis. While long-term resistance training is crucial for muscle mass and strength, acute mitochondrial remodeling (like building more mitochondria) is not triggered by a single bout of resistance exercise in these populations. Focus on consistency for muscle health, but rely on endurance training for acute mitochondrial signaling responses.

None of the tested dietary supplements (protein, creatine, HMB) significantly increased lean body mass in athletes when combined with strength and conditioning training.

Do not expect supplements like protein, creatine, or HMB to significantly increase your muscle mass on their own. Focus on your training and overall diet. This analysis found no significant benefit for muscle mass from these supplements in trained athletes.

Diet-induced changes in endogenous gut-derived appetite hormones (GLP-1, GIP, PYY, ghrelin) do not reliably predict or control ad libitum energy intake in humans.

Do not rely on macronutrient manipulation (like Keto or Low-Fat) to regulate your appetite through hormones. This study proves that even when hormones change significantly, they do not predict how much you will eat. Instead, focus on food properties: lower energy density and fewer hyper-palatable combinations (fat/sugar/sodium) are more effective for controlling intake than hormone-targeting diets.

Endogenous gut hormone concentrations achieved through dietary changes are orders of magnitude lower than pharmacological doses, explaining why diet fails to suppress appetite while drugs succeed.

You cannot replicate the effects of GLP-1 drugs (like Ozempic) through diet alone because the hormonal concentrations achieved by eating are too low. Diet changes affect hormones, but not enough to significantly reduce appetite or energy intake.

Genetic loss-of-function variants of the GIP receptor are associated with lower body mass index (BMI) and reduced obesity prevalence in humans.

People with certain genetic variations that reduce GIP receptor function tend to have lower body weight. This genetic insight supports the development of drugs that block GIP receptors to achieve similar weight loss benefits.

Positive Airway Pressure (PAP) therapy, while effective for reducing AHI and improving symptoms, has not demonstrated a benefit on composite cardiovascular endpoints in randomized controlled trials.

PAP is the standard treatment for OSA and effectively reduces breathing interruptions and daytime sleepiness. However, it does not appear to reduce long-term cardiovascular risks like heart attacks or strokes in large studies, and many patients struggle with adherence due to discomfort. It remains a good option for symptomatic relief and blood pressure control, but may not be a 'one-size-fits-all' solution.

Semaglutide increases the risk of non-serious gastrointestinal adverse events, specifically nausea, vomiting, and diarrhea, in patients at increased risk of cardiovascular events.

Expect stomach issues like nausea, vomiting, or diarrhea when starting semaglutide. These are common, usually get better over time, and are not considered 'serious' adverse events. Managing diet and starting with a low dose can help mitigate these effects.

High-dose tirzepatide (15mg/week) is associated with a significantly increased risk of overall gynecologic tumors compared to controls, with an odds ratio of 2.37.

If you are taking high-dose tirzepatide (15mg/week), be aware that this network meta-analysis found a statistically significant increase in gynecologic tumor risk compared to controls. The absolute risk increase is small (0.57%), but it exists. Discuss this with your doctor to weigh the metabolic benefits against this potential risk, especially if you have other predisposing factors for gynecologic cancers.

Both high-dose (15mg/week) and low-dose (5mg/week) tirzepatide are associated with a significantly elevated risk of intra-uterus tumors.

If you are taking tirzepatide (whether 5mg or 15mg weekly), be aware that this network meta-analysis found a statistically significant increase in the risk of intra-uterus tumors. The risk appears to be present at both low and high doses. Discuss this with your doctor to weigh the metabolic benefits against this potential risk, especially if you have other predisposing factors for gynecologic cancers.

Sleeve gastrectomy is associated with a higher risk of new-onset or worsening gastroesophageal reflux disease (GERD) compared to Roux-en-Y gastric bypass (RYGB).

If you have existing or severe acid reflux, Roux-en-Y gastric bypass is likely a safer choice than sleeve gastrectomy, as the sleeve procedure carries a higher risk of causing or worsening reflux.

Tirzepatide reduces the incidence of heart failure hospitalizations, need for treatment intensification, and mortality due to cardiovascular causes in patients with heart failure and reduced ejection fraction.

If you have heart failure and reduced ejection fraction, Tirzepatide can reduce your risk of hospitalization and cardiovascular mortality.

Obeticholic acid reduces liver fibrosis but does not resolve NASH, and is associated with significant side effects like pruritus and increased LDL.

Obeticholic acid can reduce liver scarring (fibrosis) but does not cure the underlying inflammation (NASH). It causes itching in over 50% of patients at higher doses and raises LDL cholesterol, which may need to be managed with statins. It is not a first-line cure.

Metabolic/bariatric surgery (MBS) is the most cost-effective intervention for class II and III obesity, often demonstrating dominance (cost-saving) over non-surgical management.

For individuals with Class II or III obesity, metabolic/bariatric surgery is the most economically and clinically effective long-term solution, often paying for itself through reduced healthcare costs from comorbidity remission. It should be prioritized over pharmacotherapy for this group.

Discontinuation of GLP-1 receptor agonists (GLP-1 RA) is significantly higher and reinitiation is significantly lower in patients without type 2 diabetes (T2D) compared to those with T2D, driven largely by insurance coverage and cost barriers rather than efficacy.

If you are taking a GLP-1 RA for weight loss without diabetes, be aware that insurance coverage is a major hurdle. Discontinuation rates are significantly higher for non-diabetics, often due to cost. If you face financial barriers, discuss coverage options or assistance programs with your provider immediately, as these factors heavily influence long-term adherence.

Increases in lean mass (hypertrophy) are not significantly associated with improvements in muscle strength, endurance, or power in resistance-trained young males, indicating that functional adaptations occur independently of muscle size gains.

If you are a trained individual, do not assume that your strength gains are limited by your muscle size. You can improve your strength, power, and endurance significantly without necessarily gaining large amounts of lean mass. Focus on technical proficiency and neural adaptation (e.g., heavy loads, specific power drills) rather than just volume for hypertrophy, as these functional improvements can occur independently of muscle growth.

Improvements in cardiorespiratory fitness (VO2peak) do not consistently correlate with improvements in Metabolic Syndrome risk factors (blood pressure, lipids, glucose) following exercise training.

Do not assume that an increase in your maximum oxygen uptake (VO2peak) means your blood pressure or cholesterol has automatically improved. This study shows these two improvements are not consistently linked. You must monitor your specific risk factors (blood pressure, lipids, glucose) separately to assess the metabolic benefit of your exercise routine.

Prescribed physical activity interventions alone, without dietary restriction, do not significantly influence weight loss outcomes in overweight adults.

If your goal is weight loss, exercise alone is not enough. You must also manage your calorie intake. While exercise improves health and fitness, it does not significantly drive weight loss without dietary changes.

A 20-minute documentary appealing to health, environmental, and animal welfare concerns does not reduce actual meat and animal product (MAP) consumption over a 12-day period when social desirability bias is minimized.

Watching a documentary about the benefits of reducing meat consumption is unlikely to change your actual eating habits, even if it makes you feel good about the idea. The study shows that while intentions to eat less meat may increase, actual consumption remains unchanged. To make real changes, focus on practical, small-scale adjustments to your environment and habits rather than relying on informational interventions.

Obesity lacks standardized diagnostic criteria and treatment targets compared to T2DM, leading to inconsistent care, underdiagnosis, and undertreatment.

If your doctor only uses BMI to diagnose obesity, ask for a more comprehensive assessment. This should include metabolic markers (blood pressure, lipids, glucose) and possibly the Edmonton Obesity Staging System to determine the severity of your condition and the appropriate treatment.

Initiation of GLP-1 receptor agonists (GLP-1RA) in older adults with type 2 diabetes on stable levothyroxine therapy significantly increases the risk of new-onset atrial fibrillation or flutter (AF/Aflutter) compared to SGLT2 inhibitors.

If you take levothyroxine and start a GLP-1RA (like Ozempic or Wegovy), your thyroid hormone levels may become too high because you lose weight or absorb the medication differently. This increases your risk of irregular heartbeats (AF). You need closer monitoring of your TSH levels and likely a reduction in your levothyroxine dose shortly after starting the GLP-1RA to prevent this.

GLP-1 receptor agonists (exenatide, liraglutide, dulaglutide, semaglutide, tirzepatide) reduce hepatic lipid accumulation in MASLD patients, primarily through indirect mechanisms involving weight loss and reduced fatty acid deposition, and directly by improving insulin sensitivity and suppressing de novo lipogenesis.

GLP-1 agonists like semaglutide and tirzepatide are effective treatments for reducing liver fat in people with MASLD, especially if they also have type 2 diabetes or obesity. They work by improving insulin sensitivity and directly reducing fat production in the liver, in addition to helping with weight loss. While they significantly reduce liver fat, they may not reverse advanced scarring (fibrosis). Consistency is key, as side effects and cost can lead to stopping treatment.

GLP-1 receptor agonists have limited efficacy in reversing advanced hepatic fibrosis compared to their ability to reduce hepatic steatosis.

If you have advanced liver scarring (fibrosis), GLP-1 medications may not reverse it, even though they will likely reduce liver fat. Newer multi-agonists (like resmetirom or dual agonists) might be needed for fibrosis.

Retatrutide increases the incidence of adverse events, particularly nausea, vomiting, and decreased appetite, in a dose-dependent manner compared to placebo.

While effective, retatrutide causes more side effects than placebo, including nausea, vomiting, and constipation. These side effects increase with higher doses (8mg and 12mg). Patients should be prepared for these potential issues, which may affect adherence.

Obesity pharmacotherapy is recommended against for compounded medications or unapproved medications due to safety and efficacy concerns.

Avoid compounded weight loss medications. They are not approved, may be unsafe, and are not proven to work. Stick to FDA/Health Canada-approved medications prescribed by your doctor.