Browse the evidence

Chronic chicken meat intake and resistance training do not drastically alter gut microbiota composition in elderly women, contradicting hypotheses that such interventions significantly shift microbial diversity.

You do not need to worry about chicken meat or resistance training negatively impacting or drastically altering your gut microbiota in a harmful way. The study found no significant changes in gut bacteria diversity, suggesting these interventions are safe for gut health in this demographic.

Under volume-matched conditions, increasing resistance training frequency from two to four sessions per week does not result in greater maximal strength gains in trained men.

If you are a trained lifter, you do not need to train every muscle group 4 times a week to maximize strength. Training 2 times per week is equally effective for strength gains as training 4 times per week, provided you perform the same total number of sets and intensity. You can choose the frequency that best fits your schedule and recovery capacity without sacrificing strength gains.

Intensive lifestyle intervention for weight loss in type 2 diabetes does not significantly reduce the primary composite cardiovascular endpoint (death from CV causes, nonfatal MI, nonfatal stroke, or hospitalization for angina) compared to diabetes support and education.

For people with type 2 diabetes, intensive lifestyle changes (diet and exercise) aiming for modest weight loss (7%) and activity (175 mins/week) did not statistically reduce the combined risk of heart attack, stroke, or CV death compared to standard support. However, achieving larger weight loss (10%+) and improved fitness was associated with reduced risk of CV death and major cardiac events. Continue lifestyle efforts for overall health and specific risk reduction, even if the broad 'heart attack prevention' claim is statistically unproven in this specific trial design.

Individuals with greater personal success in weight loss without medication exhibit higher obesity stigma and less favorable attitudes toward anti-obesity medications.

Healthcare providers should recognize that patients who have successfully lost weight through diet and exercise may be skeptical of or stigmatizing toward GLP-1 medications. Counseling should validate their success while explaining that biological factors can persist despite lifestyle efforts, making medication a valid and effective tool for others.

Male sex, older age (≥65 years), lower socioeconomic status (lower income, less education, higher area deprivation), and lack of insurance are associated with significantly lower odds of receiving anti-obesity medication (AOM) prescriptions and metabolic and bariatric surgery (MBS).

If you are male, older, or have limited income/insurance, you face significant systemic barriers to accessing obesity treatments like GLP-1s or surgery. This is not a reflection of your medical need but of socio-economic disparities. Seek providers who are aware of these disparities and advocate for coverage options or financial assistance programs.

Activation of Glucagon-Like Peptide-1 Receptors (GLP-1R) in the Gustatory Cortex (GC) reduces homeostatic food intake in mice.

This research identifies a specific brain region (Gustatory Cortex) where GLP-1 receptors are active and influence how much we eat. While this doesn't change current dietary advice, it explains part of the mechanism behind GLP-1 based weight loss drugs, suggesting they work by altering how the brain processes taste and hunger signals, not just by signaling fullness from the gut.

The effect of GC GLP-1R activation on food intake is conditional on the palatability and fat content of the food, particularly in mice chronically maintained on a high-fat diet.

If you are trying to lose weight, switching from a high-fat diet to a lower-fat diet might make appetite-suppressing medications (like GLP-1 agonists) more effective. The brain's response to these drugs seems to depend on the palatability of the food, and changing your diet may help reset these signals.

GIPR agonism in humans may not provide weight loss benefits and can negate the appetite-suppressing effects of GLP-1.

While GIPR agonists work in animals, human studies show that adding GIP to GLP-1 can actually stop GLP-1 from working as well for appetite control. This suggests the human body responds differently than mice.

DPP-4 inhibitors (specifically Saxagliptin and Alogliptin) may increase the risk of hospitalization for heart failure, whereas Sitagliptin and Linagliptin appear neutral.

If you have Type 2 Diabetes and Heart Failure, be cautious with DPP-4 inhibitors. Saxagliptin and Alogliptin have been linked to an increased risk of heart failure hospitalization. However, Sitagliptin and Linagliptin have shown neutral effects. Discuss the specific risks and benefits with your doctor to choose the safest option for your heart.

GLP1R-expressing neurons in the human hypothalamus, specifically those co-expressing POMC in the arcuate nucleus and AVP in the paraventricular/supraoptic nuclei, are the primary neural targets mediating the appetite-suppressing effects of GLP-1 receptor agonists like semaglutide.

If you are using a GLP-1 medication like semaglutide, its ability to reduce your appetite is biologically grounded in its action on specific neurons in your hypothalamus (brain). This confirms that the reduction in food intake is a direct neurological effect, not just a side effect of slower digestion.

GIPR (Gastric Inhibitory Polypeptide Receptor) is expressed in human hypothalamic ependymal cells surrounding the third ventricle, suggesting a potential mechanism for how GIPR-targeting drugs like tirzepatide access the brain.

This research suggests that drugs targeting the GIP receptor (like tirzepatide) may interact with cells lining the fluid spaces in your brain. This provides a biological basis for how these medications might influence brain function related to appetite, beyond just their effects on the stomach.

Rare deleterious variants in the gene CORO1A are significantly associated with changes in BMI at the population level, identifying it as a novel genetic factor in obesity risk.

Genetic testing may reveal variants in the CORO1A gene that predispose individuals to higher BMI. This is a newly identified genetic risk factor.

Joining US Free Trade Agreements (FTAs) causes a statistically significant increase in the per capita sales of ultra-processed foods, processed culinary ingredients, and infant formula.

If you are involved in policy or public health advocacy, recognize that Free Trade Agreements with the US are a key driver of increased ultra-processed food and infant formula sales in partner countries. To protect public health, advocate for health exemptions in trade agreements, similar to tobacco carve-outs, to allow governments to regulate or tax these products without fear of legal challenges from corporations.

Second-generation oral contraceptive pill phase (active vs. inactive) does not influence muscle protein synthesis or myofibrillar proteolysis at rest or in response to resistance exercise.

If you take second-generation birth control pills, you can train for muscle growth without worrying about your pill cycle. Your muscles build and break down protein at the same rate whether you are on the active pills or the placebo week. Focus on your training and nutrition; the pill phase does not matter for your results.

Adding the long-acting PYY3-36 analogue PYY1875 (1.0 mg/week) to semaglutide (2.4 mg/week) yields only modest, non-clinically meaningful additional weight loss in people with obesity and is poorly tolerated due to gastrointestinal adverse events.

For individuals already on semaglutide, adding PYY1875 at 1.0 mg weekly provides only a small, likely unnoticeable additional weight loss benefit while significantly increasing the risk of gastrointestinal side effects like nausea. The 2.0 mg dose was not tolerated. Current evidence suggests this combination is not a viable strategy for improving weight loss outcomes due to poor tolerability and lack of clinical significance.

Concerns about side effects, long-term health risks, and potential for weight regain are significant barriers to patient interest in incretin-based anti-obesity medications, with higher endorsement of these barriers associated with lower interest in using the therapies.

If you are considering incretin-based weight loss medications, know that your concerns about side effects, long-term risks, and weight regain are common and valid. These concerns directly impact your interest in the treatment. To overcome these barriers, engage in open discussions with your healthcare provider about the relative risks of the medication versus the risks of untreated obesity, and inquire about support for lifestyle programs designed for medication users.

Endogenous peripheral GLP-1 enhances glucose-induced insulin release primarily through a vago-vagal reflex mediated by GLP-1 receptors on vagal sensory fibers, rather than through direct endocrine action on pancreatic beta-cells.

Your body's natural response to eating involves a complex gut-brain-heart axis. GLP-1 released from your gut doesn't just float to your pancreas; it signals your vagus nerve to help manage insulin. This highlights the importance of the neural connection between digestion and metabolic control, suggesting that factors affecting nerve health or gut signaling might influence metabolic efficiency.

Central GLP-1 produced by hindbrain PPG neurons and peripheral GLP-1 from intestinal L-cells regulate food intake through independent pathways, rather than acting synergistically or additively.

Your body uses two separate GLP-1 systems—one in your gut and one in your brainstem—to control hunger. They don't necessarily rely on each other. This means issues with gut hormone production might not directly impair your brain's satiety signals, and vice versa.

Using percent body weight loss as the sole target for obesity management is not ideal because it is often not feasible or sustainable for most participants and fails to capture holistic health outcomes.

Stop fixating on a specific percentage of weight loss as the only measure of success. For many people, achieving even a modest weight loss is not sustainable. Instead, focus on patient-centered outcomes like improved blood pressure, better glycemic control, and increased quality of life, which can be achieved through various lifestyle changes regardless of the final number on the scale.

Hepatic protein kinase Cbeta (PKCβ) deficiency mitigates late-onset obesity in mice by increasing energy expenditure through β3-adrenergic receptor signaling, independent of FGF21.

This research suggests that as we age, our liver may produce more PKCβ, which can suppress our body's ability to burn fat and heat (thermogenesis). While you cannot change your genetics, maintaining liver health through regular physical activity—which is shown to repress PKCβ expression—may help preserve your metabolic rate and resistance to age-related weight gain.

Physiological levels of GIP promote fat accumulation and insulin resistance in the context of high-fat diets and aging, acting as a 'thrifty hormone' that stores nutrients.

In the context of a high-fat diet, your body's natural GIP hormone helps store fat and may contribute to insulin resistance. This is why blocking GIP (antagonism) can help reduce obesity, while stimulating it pharmacologically (agonism) works through different mechanisms like appetite suppression in the brain.

Utilization of newer non-insulin glucose-lowering drugs (SGLT2 inhibitors and GLP-1RAs) has increased significantly in Australia, driven by cardiovascular and renal benefits, while older agents (sulphonylureas, glitazones) have declined.

If you have Type 2 Diabetes, talk to your doctor about newer medications like SGLT2 inhibitors or GLP-1RAs. These drugs not only lower blood sugar but also protect your heart and kidneys. While they are more expensive than older medications, they are increasingly recommended as first-line treatments due to these additional benefits.

Tirzepatide (5-15 mg weekly) does not increase the risk of adjudication-confirmed pancreatitis compared to placebo, insulin, or GLP-1 receptor agonists, despite causing greater elevations in serum pancreatic amylase and lipase.

If you are prescribed Tirzepatide for weight loss or diabetes, do not panic if your blood tests show higher pancreatic enzymes. The data shows this is a common side effect of the drug's mechanism but does not translate to actual pancreatitis. Routine monitoring is still advised, but the risk of clinical pancreatitis is no higher than with other standard treatments.

Switching antipsychotics to Aripiprazole results in significant weight reduction, but adding Aripiprazole to an existing regimen is not recommended due to increased risks of agitation and akathisia.

If you are gaining weight on your current antipsychotic, switching to Aripiprazole can lead to significant weight loss. However, do not simply add Aripiprazole to your current medication, as this can cause agitation and anxiety. Switching must be done carefully with your doctor, weighing the mental health stability against the metabolic benefits.