Browse the evidence

Co-ingesting cluster dextrin (CDX) with protein after resistance exercise does not increase myofibrillar protein synthesis or total amino acid availability compared to glucose, despite enhancing intramuscular mTORC1 signaling.

If you are eating protein after resistance training, switching from glucose to cluster dextrin will not help you build more muscle. While CDX might trigger slightly higher signaling markers (mTORC1), it does not translate to actual muscle protein synthesis gains compared to regular glucose. Stick to what works and costs less.

Personalized diet advice based on single or few continuous glucose monitor (CGM) measurements of duplicate meals is unreliable in adults without diabetes because within-subject glycemic variability for identical meals is similar to variability for different meals.

Do not make permanent dietary changes based on a single CGM reading of one meal. Your body's response to the exact same meal can vary significantly from day to day due to factors like sleep, stress, and activity. If you use a CGM, look for broad patterns over weeks (e.g., 'plant-based diets generally lower my glucose') rather than trying to identify specific 'bad' foods based on one spike. Reliable personalization requires aggregating many repeated measurements, not just one or two.

A small change approach (SCA) consisting of a 2000-step daily increase and 100 kcal daily reduction does not prevent long-term weight gain in adults with overweight or obesity compared to monitoring alone over 2-3 years.

If you have overweight or obesity, simply adding 2000 steps and cutting 100 calories a day is unlikely to keep your weight off in the long run (2+ years). While you might see some benefit for the first year, it eventually fades to being no better than just having your weight checked regularly. For long-term management, you likely need more than just these small, isolated changes.

Genetic deletion or specific knockdown of the mitochondrial protein MCJ (DnaJC15) in brown adipose tissue promotes thermogenesis and protects against diet-induced obesity through a UCP1-independent mechanism mediated by eIF2α signaling.

This research suggests that targeting the MCJ protein in fat cells could help the body burn more energy and resist weight gain, even without relying on the classic 'uncoupling' protein UCP1. While this is currently a genetic finding in mice, it points to potential future therapies for obesity that enhance metabolic rate through mitochondrial stress responses.

Biliopancreatic diversion with duodenal switch (BPD/DS) and its variants (SADI, TB) provide superior weight loss compared to Sleeve Gastrectomy (SG) and Roux-en-Y Gastric Bypass (RYGB) in extreme obesity, but at the cost of higher early complication rates and malnutrition risk.

For extreme obesity, malabsorptive surgeries like BPD/DS or SADI provide the best weight loss (38%+), significantly better than SG (23%) or RYGB (26%). However, these come with higher early complication rates (12.9% vs 4-8%). SG is safer but less effective for weight loss, making it a good option for older/younger patients or as a first step.

Resmetirom, a thyroid hormone receptor beta (THRβ) agonist, is the first FDA-approved drug specifically for MASH, demonstrating significant improvement in both steatohepatitis and fibrosis in patients with advanced liver fibrosis.

Resmetirom is the first FDA-approved drug specifically for MASH. It works by targeting thyroid hormone receptors in the liver to reduce fat and inflammation. It is particularly effective for patients with advanced fibrosis, but note that about 70% of patients may not respond. It is a valuable option for those who do not respond to GLP-1RAs or SGLT2-is, or who need liver-specific treatment.

Significant inequities exist in access to bariatric surgery in Australia, with lower rates in public hospitals, rural areas, and among males, despite similar or higher obesity prevalence in these groups.

Access to bariatric surgery in Australia is uneven, with rural residents, men, and those without private healthcare facing significant barriers. If you live in a rural area or are a man, be proactive in seeking information and support to overcome these barriers. Explore public sector options and discuss your specific situation with a healthcare provider.

Incretin therapies are associated with gastrointestinal side effects and potential risks of gallstone disease and pancreatitis, requiring careful patient selection and monitoring, particularly in those with a history of these conditions.

While incretin therapies are effective for MASH, patients should be aware of common side effects like nausea and potential risks like gallstones or pancreatitis. These risks can be managed with slow dose titration, dietary adjustments, and regular monitoring, making the therapy safe for most patients when used appropriately.

Higher plasma levels of the specific nephronectin (NPNT) splice isoform, driven by increased body fat mass, causally increase the risk of severe COVID-19 and hospitalization.

If you have higher body fat mass, your body produces more of a specific protein called NPNT (specifically a splice isoform), which increases your risk of severe COVID-19. Reducing body fat mass and increasing fat-free mass through diet and exercise can lower these NPNT levels, thereby reducing your risk of severe outcomes from COVID-19.

A 12-month behavioral weight maintenance intervention following weight loss fails to provide long-term metabolic or weight benefits beyond the intervention period, as benefits disappear after the maintenance phase ends.

A one-year maintenance program after weight loss will not prevent long-term weight regain or metabolic decline once you stop the program. To maintain results, you likely need a strategy of repeated short-term interventions or continuous lifestyle management, as a single fixed-duration maintenance phase is insufficient for long-term success.

Lower adipose NPR-C mRNA expression and higher NPR-A mRNA expression after weight loss predict better long-term weight maintenance and improved insulin sensitivity, independent of the weight maintenance intervention.

Your body's molecular response to weight loss (specifically the ANP system in fat tissue) may predict how well you maintain your weight and insulin sensitivity long-term. While you cannot change this directly, it suggests that personalized monitoring might be needed for those with less favorable molecular profiles.

Higher AMY1 gene copy number does not significantly modify the risk of cardiovascular disease or mortality associated with starch intake.

You do not need to test your AMY1 gene copy number to determine your starch intake. Standard moderate starch intake recommendations likely apply to you regardless of your genetic makeup regarding amylase.

Switching from a healthy low-fat diet to a healthy low-carbohydrate diet (or vice versa) after 6 months of weight loss does not result in renewed or accelerated weight loss compared to continuing the initial diet.

If you hit a weight loss plateau after 6 months, simply switching from a low-fat diet to a low-carb diet (or vice versa) is unlikely to restart weight loss. The body's physiological response to weight loss (slower metabolism, increased hunger) persists regardless of the specific macronutrient composition of a 'healthy' diet. Focus on maintaining the deficit and behavioral adherence rather than expecting a diet switch to magically overcome the plateau.

Setmelanotide, an MC4R agonist, significantly reduces hunger and improves health-related quality of life in patients with POMC deficiency, LEPR deficiency, and Bardet-Biedl syndrome (BBS).

If you or your child has a confirmed diagnosis of POMC, LEPR, or BBS-related obesity, standard diet and exercise plans are unlikely to resolve the insatiable hunger (hyperphagia) because they don't fix the underlying genetic signaling error. Setmelanotide is an approved targeted therapy that directly addresses this mechanism, significantly reducing hunger scores and improving quality of life in clinical trials. Consult a specialist in rare metabolic disorders to determine eligibility.

Leptin replacement therapy is effective for reducing hunger and weight in patients with congenital leptin deficiency (homozygous LEP variants) but is ineffective in patients with defects downstream of the leptin receptor (e.g., POMC, PC1/3, MC4R deficiencies).

Leptin injections are highly effective for the rare condition of congenital leptin deficiency, significantly reducing hunger and weight. However, they are useless for patients with other genetic causes of obesity (like POMC or MC4R defects) because the body's ability to respond to leptin is broken downstream. Genetic testing is essential before considering this therapy.

BMI is an inadequate measure of obesity because it does not distinguish between lean muscle mass and adipose tissue, leading to misclassification of metabolic health.

Don't rely on BMI alone. If you have a normal BMI but feel unwell, ask about waist circumference and metabolic health. If you have a high BMI but are muscular, focus on metabolic markers rather than just weight.

Repeated or substantial weight loss (≥5 kg, especially >10 kg or ≥3 episodes) is associated with significantly increased all-cause and cardiovascular mortality in men, but not in women.

If you are a man, be cautious about repeated, large weight loss cycles (especially >10kg or 3+ times). This study links such patterns to higher heart and overall mortality risk. Women in this study did not show the same risk. Focus on maintaining a stable, healthy weight rather than repeated drastic losses, and consult a doctor if weight loss is unintentional.

Repeated weight loss (≥3 episodes of ≥5 kg) is associated with increased all-cause and cardiovascular mortality, regardless of the total amount lost in a single episode.

If you have lost weight 3 or more times (even if each time was 5kg), your risk of heart disease and early death may be higher than if you had never lost weight. Try to maintain a stable weight rather than cycling up and down.

Activation of the Area Postrema (AP) by GLP-1R agonists induces aversion (nausea) but is not necessary for appetite suppression, which is mediated by other brainstem regions like the Nucleus Tractus Solitarius (NTS).

Current GLP-1 drugs cause nausea by activating the Area Postrema in the brain, but weight loss is achieved by activating other brainstem areas (NTS). This separation suggests future drugs could be designed to minimize nausea while maintaining weight loss benefits.

Bariatric surgery (RYGB, VSG) and GLP-1R agonists share common neural targets in the brainstem (NTS, lPBN, CeA) and hypothalamus, suggesting overlapping mechanisms of action despite different peripheral origins.

Bariatric surgery and GLP-1 medications both work by activating specific brain pathways that reduce hunger and food intake. This shared mechanism explains why both are effective for severe obesity, even though one is surgical and the other is pharmacological.

Inhibiting Gs signaling specifically in K cells reduces plasma GIP levels and worsens glucose tolerance after refeeding.

This finding highlights that the natural Gs-mediated signaling in gut K cells is essential for maintaining normal blood sugar levels after eating. Disrupting this specific pathway impairs the body's ability to manage glucose spikes.

Diet and lifestyle interventions alone are insufficient for long-term obesity management, as they typically result in only ~3% sustained weight loss at 5 years and fail to reverse population-level obesity trends.

Do not rely on short-term diet and exercise programs for long-term weight control. The average outcome is minimal sustained loss (~3%). Recognize obesity as a chronic condition requiring long-term, multidisciplinary support (medical, behavioral, environmental) rather than a finite 'program' you complete.

Elevated plasma levels of COL6A3-derived endotrophin, driven by increased body mass index (BMI), causally mediate an increased risk of coronary artery disease (CAD).

This research highlights that high body fat increases a specific protein fragment called endotrophin, which directly contributes to heart disease risk. The good news is that reducing body fat lowers these levels, suggesting that weight management strategies are effective not just for general health, but specifically for mitigating this biological pathway to heart disease.

Consuming a high-protein breakfast (34g) versus a low-protein breakfast (6g) for 12 weeks increases subjective satiety but does not result in significant changes in body composition (fat mass, lean mass, weight) or cardiometabolic health markers in young women with overweight.

Eating a high-protein breakfast (around 34g) will likely make you feel fuller throughout the morning compared to a low-protein breakfast. However, if your goal is weight loss or improved blood markers, simply switching to a high-protein breakfast without other changes (like reducing overall calories or increasing exercise) is unlikely to produce results in young overweight women. The increased satiety did not lead to a significant reduction in daily energy intake or body fat in this study.