Browse the evidence

There is no significant association between fast food consumption or TV viewing and body mass index in adult men aged 20-45.

For men, fast food consumption and TV viewing were not significantly linked to body weight in this study. Other factors may be more relevant for weight management in men.

Leptin replacement therapy in adults with genetically confirmed leptin deficiency causes profound weight loss, resolution of type 2 diabetes, and recovery of hypogonadism.

If you have a rare genetic condition causing leptin deficiency, leptin replacement therapy can reverse morbid obesity, diabetes, and hypogonadism. However, this does not apply to the vast majority of people with common obesity, who typically have high leptin levels but are resistant to its effects. This treatment is not a general weight-loss solution for the general population.

Weight loss in obese humans significantly increases fasting plasma ghrelin levels, reversing the suppression typically seen in obesity.

When you lose weight, your body naturally produces more ghrelin, the 'hunger hormone.' This study confirms that this increase is a direct result of losing weight and correlates with how much weight you lose. Expect increased hunger as a biological response to your new, lower body weight, not as a personal failing.

Gut microbiota metabolize tryptophan into indole-3-propionate (IPA) and indole-3-aldehyde, which have antioxidant and anti-inflammatory properties, potentially protecting against neuronal damage and ischemia.

Your gut bacteria break down tryptophan into compounds that protect your brain from damage and inflammation. Eating a diet rich in tryptophan (found in turkey, eggs, seeds) supports this process, but the exact benefits depend on your unique gut bacteria.

Antagonism of the growth hormone secretagogue receptor (GHS-R) using specific peptide antagonists reduces food intake, decreases body weight gain, and improves glycaemic control in obese mouse models.

This research suggests that blocking the ghrelin receptor (GHS-R) can reduce food intake and body weight gain in obese individuals. While this specific study used mouse models and peptide antagonists, it supports the biological plausibility that ghrelin signaling plays a key role in obesity and that targeting this pathway could be a valid strategy for weight management and improving blood sugar control.

Dietary supplementation with carotenoids (specifically β-cryptoxanthin and astaxanthin) prevents and reverses NASH progression by regulating macrophage/Kupffer cell polarization toward the anti-inflammatory M2 phenotype.

Current research indicates that specific carotenoids, β-cryptoxanthin and astaxanthin, can reverse NASH in mouse models by shifting liver immune cells (Kupffer cells) from a pro-inflammatory state (M1) to a healing state (M2). However, the authors explicitly state there is currently no evidence that these carotenoids exhibit beneficial effects in human patients. Until human trials are conducted, these should be viewed as promising experimental mechanisms rather than established treatments.

Antibiotic exposure, particularly in infancy, is associated with long-term reduction in bacterial diversity and increased risk of weight gain and obesity.

If you or your child must take antibiotics, be aware it may impact weight and gut health long-term. Post-treatment, focus on prebiotic fibers to help restore bacterial diversity.

Upregulation of SIRT1 activity via STACs or NAD+ boosters (NR, NMN) protects against cardiovascular aging phenotypes including endothelial dysfunction, atherosclerosis, and ischemia-reperfusion injury by modulating transcription factors and antioxidant pathways.

Current research suggests that maintaining NAD+ levels and sirtuin activity may support cardiovascular health and delay age-related decline. While human trials are ongoing, strategies that naturally support NAD+ (like exercise and lean diets) are supported by this mechanism. Be cautious of unproven high-dose supplements, as excessive SIRT1 activation in certain contexts (like high-fat diets) may have adverse effects on lipid metabolism.

SIRT1 plays a complex, context-dependent role in atherosclerosis where tissue-specific overexpression can be protective, but whole-body overexpression in the context of high-fat diets may exacerbate the disease.

Do not assume that boosting SIRT1 (e.g., via high-dose resveratrol or NMN) is always beneficial for heart health, especially if you have existing metabolic issues like high cholesterol or obesity. The paper warns that whole-body SIRT1 activation can worsen lipid profiles in high-fat diet contexts. Consult a physician before using sirtuin activators if you have metabolic syndrome.

NAD+ boosters (specifically NMN and NR) and SIRT1 activators (like resveratrol) improve angiogenesis and endothelial function in aging models by restoring the NAD+-SIRT1 axis.

Aging is associated with reduced blood flow and capillary density. This research suggests that boosting NAD+ (via precursors like NMN or NR) or activating SIRT1 (via exercise or STACs) may help restore blood vessel growth and function. This could potentially improve endurance and mobility in older adults, though human clinical results are still pending.

General obesity is associated with significantly elevated serum levels of both pro-inflammatory (IL-5, IL-12, IL-13, IFN-γ, TNF-α) and anti-inflammatory (IL-10) cytokines compared to non-obese individuals.

Obesity is linked to higher levels of various inflammatory markers in your blood, including both 'bad' (pro-inflammatory) and 'good' (anti-inflammatory) cytokines. This suggests a complex immune state rather than just simple inflammation.

Obesity is associated with reduced muscle quality (strength normalized to muscle mass) in some studies, but this finding is inconsistent and likely confounded by methodological differences in measuring muscle size and neural activation.

Don't assume your muscles are 'bad' just because you're obese. Research shows that when you measure muscle accurately and account for how your nervous system works, obese muscles can be just as effective as non-obese muscles. The 'weakness' is often due to how much weight you carry and how your nervous system activates muscles, not the muscle tissue itself.

Long sleep duration (9+ hours) is strongly associated with increased mortality risk, but this association is largely explained by confounding factors such as depression, antidepressant use, and low socioeconomic status rather than being a direct causal effect of sleep length itself.

If you consistently sleep 9+ hours, do not panic about mortality risk. Instead, investigate potential underlying causes such as depression, medication use (antidepressants/benzodiazepines), or socioeconomic stress. Treating these underlying factors is likely more impactful for your health than trying to restrict your sleep duration.

Beta cell dedifferentiation, where beta cells lose their identity and insulin production capability without dying, contributes to beta cell deficit in T2D.

In T2D, some beta cells may not be dead but 'silenced' (dedifferentiated). Restoring blood glucose levels might allow them to regain function, offering a potential therapeutic target.

An increase in the number of close friends is significantly associated with a 29% decrease in mortality risk among older men (aged 65+), whereas an increase in the overall social network index was not significantly associated with mortality in men under 65.

For older men, actively increasing the number of close friends can significantly reduce mortality risk. Focus on maintaining and nurturing close friendships rather than just broad social network size. Regular contact with close friends is a key protective factor.

Pharmacological interventions targeting aging pathways (e.g., rapamycin, metformin, resveratrol) show potential to decelerate vascular aging but are limited by side effects and are not yet recommended for healthy individuals.

Do not use anti-aging drugs like rapamycin or metformin for healthy aging without medical supervision. Focus on lifestyle changes first, as they are safer and more effective. Pharmacological options are currently reserved for specific medical conditions.

Wearable activity trackers have small or non-significant effects on physiological markers (blood pressure, cholesterol, glycosylated haemoglobin) and psychosocial outcomes (quality of life, pain).

While using a wearable activity tracker will likely increase your physical activity and help with weight loss, do not expect it to significantly lower your blood pressure, cholesterol, or blood sugar on its own. Similarly, improvements in quality of life or pain reduction are not guaranteed. The primary benefit is increased movement.

Orthorexia nervosa is a pathological fixation on healthy food that leads to nutritional deficiencies, medical complications, and poor quality of life, distinguishable from anorexia by its motivation (health/purity vs. weight loss) and from OCD by its ego-syntonic nature.

If you find yourself spending hours scrutinizing food labels, avoiding entire food groups due to 'purity' concerns, or feeling intense guilt when eating 'impure' foods, this may be orthorexia. Unlike healthy eating, it causes distress, social isolation, and potential medical issues. Seek help from a multidisciplinary team (therapist, dietitian, physician) if your diet is restricting your life.

Obesity reduces oocyte quality and maturity, leading to lower fertilization rates and increased miscarriage, independent of the number of follicles developed.

If you are obese, your eggs may be less mature and fertilize less efficiently, even if you produce many follicles during IVF. This increases the risk of miscarriage. Losing weight before IVF can improve egg quality and increase your chances of a successful pregnancy.

Dietary flavonoids exert anti-obesity and anti-diabetic effects by modulating multiple molecular targets, including the activation of AMPK and GLUT4 translocation to improve glucose uptake, and the inhibition of inflammatory cytokines (TNF-α, IL-6) and lipid synthesis enzymes (SREBP-1c, HMG-CoA) to reduce fat accumulation.

Incorporate flavonoid-rich foods like berries, tea, citrus fruits, and soy into your diet. These compounds may help manage blood sugar and weight by improving insulin sensitivity and reducing inflammation, though specific dosages and long-term human effects require more clinical research.

There is limited or insufficient data to show that preventing type 2 diabetes through lifestyle changes results in a lower risk of cardiovascular and microvascular complications.

While preventing diabetes is a huge health win, current evidence does not yet prove that it automatically reduces your risk of heart disease or other complications. You should still manage other risk factors like blood pressure and cholesterol.

Women require less CPAP pressure than men for treating OSA of similar severity, but face challenges with adherence and appropriate screening tools.

If you are a woman using CPAP for sleep apnea, ensure your pressure settings are titrated specifically for you. Women often require lower pressures than men for the same severity of apnea. If you are experiencing discomfort or high pressure settings, discuss a re-titration with your sleep specialist.

Weakness (low grip strength) predicts mortality in older men, but the association with mortality is inconsistent and weaker in women compared to mobility impairment.

For older men, low grip strength is a significant warning sign for increased mortality risk. For women, the link is weaker and less consistent. Regular strength testing is a valuable tool for assessing long-term health risks, especially in men.

Elafibranor (PPAR alpha/delta agonist) and Obeticholic Acid (FXR ligand) show promise in resolving NASH and improving fibrosis in clinical trials.

Elafibranor and Obeticholic Acid are emerging pharmacological treatments showing improvement in NASH and fibrosis in trials. They are not yet universally approved for NASH but are in Phase 3 testing.