Browse the evidence

Resistance training induces an acute and chronic expansion of the satellite cell (SC) pool in skeletal muscle, but this expansion does not result in a detectable increase in myonuclear content during the first 10 weeks of training in young, previously trained men.

If you are a young, previously trained man, expect your satellite cells to increase in number during the first few months of resistance training, but do not expect this to immediately translate into more muscle nuclei. Your muscle is likely adapting through increased protein synthesis and repair mechanisms rather than structural nuclear addition at this stage. Focus on consistent training; the nuclei may add up if you train long enough or intensely enough to exceed current transcriptional capacity.

Ethnic disparities in Type 2 Diabetes are influenced by genetic variations regulating lipid and amino acid metabolism, leading to distinct metabolic signatures and drug responses across populations.

Your ethnic background influences how your body metabolizes nutrients and responds to medications for Type 2 Diabetes. This is due to genetic variations affecting lipid and amino acid metabolism. Discuss your specific metabolic profile with your healthcare provider to tailor dietary and therapeutic strategies, as personalized approaches are more likely to succeed than generic ones.

High variability in bodyweight is associated with an increased risk of incident atrial fibrillation in patients with type 2 diabetes mellitus, independent of baseline BMI and overall weight change direction.

If you have type 2 diabetes, avoid extreme weight cycling. Whether you are trying to lose weight or maintain it, try to do so gradually. Large swings in body weight (e.g., losing 10% and regaining it quickly) are linked to a higher risk of atrial fibrillation. Focus on stable, sustainable weight management rather than rapid, drastic changes.

Current dietary assessment methods for UPF intake are limited and require improvement, including better classification algorithms and exposure assessment tools.

Be aware that current estimates of UPF intake may be inaccurate due to limitations in dietary assessment tools. Future research aims to improve these methods, which will lead to better public health guidance.

In older adults, satellite cells that are physically incarcerated by thickened laminin in the extracellular matrix exhibit significantly reduced activation in response to resistance exercise compared to non-incarcerated satellite cells.

If you are older and feel your muscles aren't responding to exercise as well as they used to, it may be due to structural changes in the muscle tissue (thickening of the outer layer around muscle stem cells) that 'trap' them. The good news is that consistent resistance training over several months can reverse this trapping process, allowing your muscle stem cells to activate properly again and support muscle growth.

Higher plasma levels of the gut microbiome-derived metabolite Trimethylamine-N-oxide (TMAO) are associated with a significantly higher risk of incident atherosclerotic cardiovascular disease (ASCVD) in a diverse, community-based population free of prior cardiovascular disease.

This study suggests that higher levels of TMAO, a byproduct of gut bacteria processing nutrients like red meat and eggs, are linked to a higher risk of heart disease. While it doesn't tell you to eliminate these foods, it highlights the importance of your gut health and kidney function. If you have risk factors for heart disease, discussing your diet and TMAO levels with your doctor might be worthwhile, especially if you have reduced kidney function.

Muscle typology (determined by muscle carnosine levels) does not explain inter-individual variability in resistance training-induced increases in muscle volume, maximal dynamic strength, or fiber cross-sectional area when training is performed to failure at 60% 1RM.

If you are new to resistance training, your muscle fiber type (whether you are naturally 'fast' or 'slow') does not determine how much muscle or strength you will gain. As long as you train to failure with a moderate load (around 60% of your max), you will see similar improvements regardless of your genetics. Focus on consistency and effort rather than trying to tailor your program to your fiber type.

Timing of creatine ingestion (pre- vs. post-exercise) does not significantly influence gains in muscle mass or strength compared to resistance training alone.

Take your creatine whenever is most convenient for you. Whether you take it before or after your workout makes no measurable difference to your muscle growth or strength gains. Focus on taking it consistently every day rather than stressing about the exact timing.

Using velocity loss (VL) thresholds to prescribe or monitor resistance training volume for free-weight back squats is flawed and should not be used because the relationship between velocity loss and repetitions completed to failure lacks stability and predictive validity across sessions.

Do not use velocity loss thresholds to determine how many reps to perform in free-weight back squats. The relationship between how fast you move and how many reps you can do is too unstable from session to session to be useful for programming. Stick to traditional methods like RPE or fixed rep ranges.

Current precision nutrition tools based on Polygenic Risk Scores (PRS) have limited predictive power because they often fail to account for gene-environment interactions.

Do not rely solely on genetic testing for dietary advice. Current genetic risk scores are incomplete because they ignore your lifestyle. For accurate precision nutrition, genetic data must be combined with environmental factors like diet and activity.

Using the Glycemic Index (GI) as a primary indicator for carbohydrate quality fails to improve diet quality or Dietary Guidelines adherence because it ignores nutrient density and food context.

Stop using Glycemic Index (GI) labels or lists to guide your daily food choices. The GI ignores nutrient density and doesn't predict how your body reacts to mixed meals. Instead, focus on the Dietary Guidelines for Americans: eat nutrient-dense foods (vegetables, fruits, whole grains, legumes) in appropriate portions. This approach is more reliable for health than chasing low GI numbers.

In patients with type 2 diabetes and recent acute coronary syndrome, a body weight loss of 5% or more is independently associated with a significantly higher risk of all-cause mortality and cardiovascular events.

If you have diabetes and a history of heart issues, losing more than 5% of your body weight without trying is a medical emergency. It often signals worsening heart failure, kidney disease, or other serious conditions. Do not view this weight loss as a success; consult your doctor immediately to investigate the cause.

In patients with type 2 diabetes and recent acute coronary syndrome, a higher baseline Body Mass Index (BMI > 30 kg/m2) is associated with a lower risk of primary cardiovascular outcomes compared to those with a BMI of 26-30 kg/m2.

If you have diabetes and recent heart issues, having a higher BMI (over 30) might actually protect you from cardiovascular events compared to being 'normal' weight. Do not attempt aggressive weight loss unless advised by your doctor, as maintaining your current weight may be beneficial for your heart.

Acute exercise (both HIIT and MICT) results in more phosphosite down-regulation than up-regulation, suggesting that acute exercise involves the inhibition of kinase activity and/or activation of phosphatases.

Exercise doesn't just turn things on; it also turns things off. This balance is crucial for adaptation. Don't assume more activation is always better; regulation (inhibition) is part of the process.

Standard RNA-seq normalization strategies that ignore global changes in total RNA content during resistance training produce counterintuitive, biologically invalid results by failing to account for increased ribosomal biogenesis and tissue mass.

If you are analyzing muscle gene expression after resistance training, do not use standard normalization methods that assume total RNA remains constant. You must account for the increase in total RNA (ribosomal biogenesis) caused by muscle growth, or your results will be biologically invalid and counterintuitive.

Tirzepatide has surpassed semaglutide as the most commonly prescribed first-time GLP-1 RA medication in the US as of September 2025.

Tirzepatide is now the most frequently prescribed first-time GLP-1 medication in the US, overtaking semaglutide. This reflects changing prescribing preferences among physicians.

Lean individuals with Metabolic Dysfunction-Associated Fatty Liver Disease (lean-MAFLD) face a significantly higher risk of liver-related mortality compared to overweight or obese MAFLD patients, despite having equivalent metabolic profiles and similar risks for extrahepatic mortality.

If you are lean but have been diagnosed with fatty liver (MAFLD), do not assume you are safe because you are thin. Your risk of liver-related death is actually higher than that of obese patients with the same condition. Standard weight loss advice, especially rapid loss via drugs, can be dangerous for you because it strips away muscle, which your liver needs. Focus on metabolic health markers (blood pressure, glucose, lipids) and consult your doctor about treatments that preserve muscle mass rather than just focusing on weight loss.

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.

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.

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.

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.

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.