Browse the evidence

Higher baseline expression of Cardiotrophin-1 (CT-1) in subcutaneous abdominal adipose tissue (scABD) protects men from the decline in insulin sensitivity typically caused by sustained overfeeding.

In lean men, higher baseline levels of the adipokine CT-1 in abdominal fat are associated with better preservation of insulin sensitivity during periods of overeating. This suggests that individual differences in adipose tissue biology may protect against diet-induced metabolic decline.

An acute increase in fibroblast growth factor 21 (FGF21) in response to low-protein overfeeding serves as a biomarker identifying individuals with a 'thrifty' metabolism who are susceptible to weight gain.

If you struggle with weight gain despite similar efforts to others, your body's hormonal response (specifically FGF21) to certain dietary stresses might be the cause. This isn't about willpower; it's a physiological 'thrifty' phenotype. Future testing may allow you to identify this susceptibility early, shifting focus from generic advice to targeted prevention.

Integrase Strand Transfer Inhibitor (INSTI) use was associated with a lower risk of progression from prediabetes to diabetes compared to Protease Inhibitor (PI)-based ART in a specific subset of participants, contrasting with some other observational studies.

This paper's finding that INSTIs might have a lower diabetes risk than PIs in a small group is not definitive. Do not change your medication based on this alone. Focus on the proven risk factors: manage your weight, waist circumference, and triglycerides through lifestyle changes, as these have a stronger and more consistent link to diabetes progression.

Insulin-lowering dietary strategies (calorie restriction, ketogenic/low-carbohydrate diets, and intermittent fasting) reduce systemic insulin and IGF-1 levels, which attenuates insulin-related growth signaling and reduces metastatic disease burden in preclinical animal models.

For metastatic cancer patients, insulin-lowering diets (like low-carb or intermittent fasting) are safe and feasible adjuncts to standard care. They improve metabolic markers (insulin, glucose) and may help control disease, but they are not yet proven to extend survival. Consult your oncology team to implement these strategies safely, ensuring they do not exacerbate weight loss or cachexia.

Low baseline triglyceride levels (<1.7 mmol/L) predict a more sustained and significant weight loss and glycemic response to gastric contractility modulation (GCM) therapy.

If considering GCM therapy, checking baseline triglycerides may help predict success. Patients with lower triglycerides are more likely to experience sustained weight loss and better glycemic control from the device.

GLP-1 receptor agonists (GLP-1 RAs) show promise as gerotherapeutic drugs by protecting against aging-related risk factors such as oxidative stress, cellular senescence, and inflammation, and may reverse brain aging and prevent sarcopenic obesity, although lifespan extension in humans is not yet reported.

If you are considering GLP-1 RAs for weight loss, discuss with your doctor their potential anti-aging benefits, such as reducing inflammation and protecting against cellular senescence. While they are not yet proven to extend lifespan in humans, they may offer significant healthspan benefits.

In individuals with type 2 diabetes and existing complications, a 5-day prolonged fasting-mimicking diet followed by a glucose load significantly reduces cellular resistance to dicarbonyl stress and increases oxidative stress markers, indicating heightened susceptibility to metabolic harm upon refeeding.

If you have Type 2 Diabetes with known complications (like kidney or nerve issues), extreme fasting followed by a large carbohydrate load may stress your cells more than it helps them. While fasting can improve insulin sensitivity in some, it appears to reduce your cells' ability to handle stress in this specific subgroup. Consult your doctor before attempting prolonged fasting, as your body may react with increased oxidative stress rather than metabolic improvement.

Fat loss during Ramadan fasting is significantly reduced or absent in females aged 36-70 years, unlike males and younger subjects.

Older women practicing Ramadan fasting may not see significant fat loss, though they will likely lose weight and lean mass. Focus on maintaining muscle through protein and strength training rather than expecting fat reduction.

Intermittent Energy Restriction (IER) does not provide superior improvements in cardiovascular risk markers (lipids, glucose, insulin, blood pressure) compared to Continuous Energy Restriction (CER) over the long term.

Do not expect IER to give you better blood work (cholesterol, blood sugar) than continuous calorie restriction. Any improvements in these markers are likely due to the weight loss itself, not the fasting pattern. Focus on achieving and maintaining a healthy weight through whichever method you can sustain.

Changes in lean mass do not significantly affect Resting Metabolic Rate (RMR) in the short term (16 weeks) for overweight/obese premenopausal women.

Do not rely on building muscle to significantly boost your resting metabolism for fat loss. While muscle is healthy and functional, its metabolic impact is small. Focus on creating a caloric deficit through diet and activity for effective fat loss.

Time-restricted eating combined with calorie restriction does not provide significant additional benefits for blood pressure, glucose profile, or lipid profile compared to calorie restriction alone.

Do not expect time-restricted eating to fix your blood pressure, blood sugar, or cholesterol if you are just counting calories. The benefits for these markers are not significantly better than just counting calories alone. Focus on the weight loss aspect of TRE.

Bariatric surgery significantly improves glycemic control (HbA1c reduction) in patients with metabolic syndrome, with effects sustained over 5 years.

For patients with metabolic syndrome and Type 2 Diabetes, bariatric surgery offers significant and sustained improvements in blood sugar control, often superior to medical management alone.

Bariatric surgery significantly improves blood pressure and lipid profiles in patients with and without metabolic syndrome.

Bariatric surgery leads to significant and sustained improvements in blood pressure and lipid profiles, reducing cardiovascular risk.

Serum HMW adiponectin levels do not significantly increase after 16 weeks of HIIT, but changes in adiponectin are strongly associated with changes in visceral adipose tissue (VAT) loss.

Don't expect HIIT to magically boost your adiponectin levels. However, if you lose visceral fat through HIIT, your adiponectin levels will likely improve as a result of that fat loss, not the exercise itself.

The effect of Tirzepatide on Fat-Free Mass (FFM) is inconclusive and potentially adverse, with some studies showing greater FFM loss compared to other anti-obesity drugs, particularly at higher doses.

While Tirzepatide is excellent for fat loss, patients should be aware that it may also cause a loss of lean muscle mass, potentially more than other similar drugs. To mitigate this, combining TZP treatment with resistance training and adequate protein intake is crucial, although clinical data on optimizing FFM preservation with TZP is currently lacking.

A lower omega-6 to omega-3 ratio (specifically 2.5:1) reduces rectal cell proliferation in patients with colorectal cancer, whereas a higher ratio (4:1) with the same omega-3 amount has no effect.

If you have colorectal cancer or are at high risk, aim for a very low omega-6 to omega-3 ratio of 2.5:1. This requires significantly reducing omega-6 oils (corn, soy, sunflower) and increasing omega-3 sources (fatty fish, flaxseed). Simply taking fish oil without reducing omega-6 may not provide the same protective benefits against cell proliferation.

Butyrate and propionate, produced by gut microbiota from dietary fiber, play a protective role against colorectal cancer (CRC) and metabolic syndrome by promoting apoptosis in cancer cells and improving insulin sensitivity.

To reduce your risk of colorectal cancer and metabolic syndrome, focus on eating a diet rich in diverse fibers (vegetables, fruits, whole grains, legumes). This feeds your gut bacteria to produce butyrate and propionate, which help protect colon cells and improve metabolic health. While supplements exist, whole food sources are preferred for overall health.

Sleep disruption is associated with an increased risk of certain cancers (colorectal, breast, prostate) and all-cause mortality, particularly in men.

For shift workers and those with chronic sleep disorders, maintaining sleep continuity and circadian alignment is critical for long-term health. Evidence links these disruptions to higher risks of colorectal, breast, and prostate cancers, as well as increased mortality, particularly in men. Prioritizing sleep hygiene and treating sleep disorders may mitigate these risks.

Obesity induces systemic oxidative stress and chronic low-grade inflammation through adipose tissue dysfunction, specifically via increased adipokine secretion (leptin, TNF-α, IL-6) and mitochondrial ROS production, which leads to endothelial dysfunction and insulin resistance.

Recognize that excess body fat, especially visceral fat, is biologically active and drives inflammation and metabolic issues. This is not just 'extra weight' but a source of hormones that disrupt your body's balance. Addressing obesity requires managing this hormonal output, not just counting calories.

Oxidative stress, generated by mitochondrial overproduction of superoxide due to glucose and free fatty acid overload, is the common pathogenic mechanism linking insulin resistance, beta-cell dysfunction, and endothelial dysfunction, thereby driving the progression from insulin resistance to type 2 diabetes and cardiovascular disease.

Focus on reducing cellular stress, not just blood sugar. This involves managing caloric intake and increasing physical activity to prevent the overload of glucose and fatty acids in cells, which generates damaging oxidative stress. This approach may help prevent both diabetes and cardiovascular disease by addressing the root cause of cellular dysfunction.

Propionate, a short-chain fatty acid produced from carbohydrate fermentation, can inhibit the conversion of acetate to cholesterol and fat, potentially reducing intra-abdominal tissue accretion and intrahepatocellular lipid content in overweight adults.

Foods that promote the production of propionate (a type of SCFA) in the gut may help manage body fat and liver fat levels. This suggests that the type of fiber you eat matters for metabolic health, not just total fiber intake.

Intravenous n-3 fatty acids (fish oil emulsions) reduce inflammation and improve outcomes in critically ill patients, including reduced infection rates and shorter hospital stays.

In hospital settings for critically ill patients, intravenous fish oil is used to modulate the severe inflammatory response. Evidence suggests it can help reduce infections and shorten the time patients spend in the hospital or on ventilators.

Plasma ghrelin exhibits a diurnal pattern with preprandial increases and postprandial decreases, peaking at 0200 h, suggesting ghrelin acts as a meal-initiation signal entrained to sleep and meal timing.

Your hunger hormone (ghrelin) naturally rises before meals and peaks in the early morning hours (around 2 AM). This rhythm suggests that late-night hunger is biologically driven. Aligning your last meal with this natural dip might help manage overnight cravings.

The association between short sleep duration and hypertension is not observed in adults aged 60 and older.

If you are over 60, the link between short sleep and high blood pressure may not be as strong as it is for younger adults. This might be due to other age-related factors like arterial stiffness or changes in sleep patterns.