Browse the evidence

Intermittent fasting preserves pancreatic beta-cell mass and improves glucose tolerance in obesity-induced diabetes by stimulating the autophagy-lysosome pathway.

Intermittent fasting may help preserve insulin-producing cells in obesity, but only if your cells can properly recycle waste (autophagy). If you have underlying cellular defects, fasting might stress your pancreas instead of helping it.

Intermittent fasting stimulates beta-cell regeneration markers (NEUROG3) in obesity-induced diabetes, but this effect is dependent on an intact autophagy-lysosome pathway.

Fasting may trigger regeneration signals in the pancreas during obesity, but this process is blocked if your cells cannot perform autophagy.

Women with Premenstrual Dysphoric Disorder (PMDD) exhibit more severe sleep disturbances and altered circadian hormone rhythms (specifically melatonin and cortisol) during the luteal phase compared to healthy women, including phase delays in melatonin and reduced melatonin amplitude.

If you have PMDD, your sleep issues are likely tied to a physiological resistance to melatonin and altered hormone rhythms during the week before your period. This is a recognized medical condition, not just 'stress'. Discussing chronotherapeutic treatments or hormone-regulating strategies with a healthcare provider may be more effective than standard sleep hygiene advice alone.

Single oral administration of Nicotinamide Mononucleotide (NMN) up to 500 mg is safe and well-tolerated in healthy men, causing no significant adverse clinical symptoms or changes in vital signs.

If you are a healthy man between 40 and 60, taking a single dose of NMN (up to 500mg) appears safe in the short term, with no observed negative effects on vital signs, liver enzymes, or general well-being. This does not prove long-term benefits, but it suggests the supplement is well-tolerated at these doses.

Oral administration of NMN (100-500 mg) leads to a dose-dependent increase in plasma levels of its metabolites, specifically N-methyl-2-pyridone-5-carboxamide (2Py) and N-methyl-4-pyridone-5-carboxamide (4Py), indicating successful metabolic conversion.

Taking NMN orally results in measurable levels of its metabolites in your blood, suggesting your body absorbs and processes it. Higher doses (500mg) produce more of these metabolites than lower doses (100mg).

Mitochondrial fusion in specific hypothalamic neurons (NPY/Agrp and POMC) regulates energy balance, where impaired fusion in these neurons can lead to resistance to diet-induced obesity or leptin resistance.

Mitochondrial health in the brain plays a role in how your body regulates hunger and stores fat. Disruptions in mitochondrial fusion in specific brain neurons may contribute to obesity and leptin resistance.

Fecal microbiota transplantation from healthy donors can improve glycemic control and insulin action in patients with type 2 diabetes.

Transplanting healthy gut bacteria can help some type 2 diabetes patients improve how their bodies handle sugar. While FMT is one way, you can try to cultivate a similar healthy microbiome through diet.

The 4.5-kb allele of the BclI restriction fragment length polymorphism at the glucocorticoid receptor (GRL) gene locus is associated with higher abdominal visceral fat (AVF) area, independent of total body fat mass.

If you have a family history of central obesity, your genetics may predispose you to storing fat viscerally, especially if you are lean. This is not a life sentence, but it means you must be vigilant about maintaining a healthy body fat percentage, as the genetic effect is most pronounced in leaner individuals. Focus on consistent physical activity and metabolic health rather than just scale weight.

The increase in overweight and obesity in Brazil is primarily driven by a 'contemporary Western lifestyle' characterized by dietary changes (increased consumption of fast food, processed foods, and dining out) and reduced physical activity due to urbanization and technological adoption.

To combat rising obesity, focus on structural changes: promote access to healthy foods, encourage active transportation, and limit the marketing of processed foods, rather than just telling individuals to 'eat less and move more'.

Reductions in physical activity, particularly occupational and domestic physical activity, due to technological adoption (appliances, transportation) and lifestyle changes (TV, computer use), contribute to obesity.

Incorporate more movement into your daily routine, not just structured exercise. Take the stairs, walk for transport, and do household chores actively to boost daily energy expenditure.

Exogenous administration of the peptide Spexin causes significant weight loss in rodents with diet-induced obesity by reducing caloric intake and inhibiting adipocyte uptake of long-chain fatty acids.

This research identifies Spexin, a peptide naturally produced by fat tissue, as a regulator of weight. In obese humans, Spexin levels are significantly lower than in lean individuals. In rodent models, restoring Spexin levels via injection reduced food intake and fat storage. While not yet a human therapy, it suggests that low Spexin may contribute to obesity and that restoring it could be a therapeutic strategy.

Dietary phytochemicals and macro/micronutrients modulate epigenetic mechanisms (DNA methylation, histone modification) to attenuate 'inflammaging' and promote healthy aging.

To support healthy aging and reduce chronic inflammation, prioritize a diet rich in plant-derived phytochemicals (found in vegetables, fruits, and plant juices) and balanced macro- and micronutrients. This dietary pattern helps regulate metabolic pathways and epigenetic gene expression, potentially protecting against age-related diseases.

Specific dietary components (e.g., folate, choline, vitamin B12) influence DNA methylation patterns by affecting the availability of methyl donors like S-adenosylmethionine (SAM).

Ensure adequate intake of folate, choline, and vitamin B12 through your diet to support healthy DNA methylation processes, which are linked to cardiovascular health and aging.

Caloric restriction and specific phytochemicals (e.g., resveratrol, tea catechins) can extend healthspan and modulate aging-related epigenetic marks.

Consider incorporating caloric restriction or consuming phytochemical-rich foods (like those found in tea and grapes) to potentially slow age-related epigenetic changes and support longevity.

There is no conclusive evidence linking non-nutritive sweetener consumption to chronic kidney disease in high-risk patients, although some individual studies show positive associations.

For individuals at high risk of chronic kidney disease, current systematic evidence does not show that artificially sweetened soda increases the risk. However, because some individual studies show positive associations, those with existing kidney conditions should consult their healthcare provider for personalized advice.

High dietary intake of omega-6 polyunsaturated fatty acids (specifically linoleic acid) is positively associated with an increased risk of breast cancer, particularly in individuals with specific genetic variants affecting omega-6 metabolism.

If you have a family history of breast cancer or genetic risks, consider reducing high-omega-6 oils (corn, soybean, sunflower) and increasing omega-3 sources. This may help mitigate risk, especially if you have genetic variants affecting fat metabolism.

Insulin-like Growth Factor-I (IGF-I) administration ameliorates liver fibrosis and NASH by inducing cellular senescence in hepatic stellate cells (HSCs), thereby inactivating them and limiting fibrosis progression.

IGF-I shows promise in animal studies for reversing liver scarring (fibrosis) by putting the scar-forming cells into a state of 'senescence' where they stop working. While not yet a standard human treatment, it represents a potential future therapy for advanced liver disease.

Mitochondrial dysfunction, specifically through ROS generation, mtDNA mutations, and altered redox homeostasis, is a primary driver of the aging process.

Focus on interventions that support mitochondrial health, such as exercise and dietary restriction, as these organelles are central to aging mechanisms. While specific protocols aren't detailed here, the paper highlights that boosting mitochondrial function (e.g., via exercise) can decrease markers of age-related diseases like Alzheimer's.

Administration of specific probiotic strains (primarily Lactobacillus and Bifidobacterium) reduces body weight and adipose tissue mass in diet-induced obese animal models through mechanisms involving SCFA production, gut barrier integrity, and immune modulation.

Specific probiotic strains (like Lactobacillus and Bifidobacterium) show promise in reducing fat mass in animal studies, but human results are inconsistent. Do not rely on probiotics as a primary weight loss strategy. They may offer modest metabolic support when combined with a healthy diet, but they are not a standalone solution for obesity.

Probiotics can improve gut barrier integrity and reduce metabolic endotoxemia (LPS translocation) in obese models, thereby lowering systemic inflammation.

A healthy gut lining helps prevent inflammation, which is linked to obesity. Probiotics may help strengthen this barrier, but the most effective way to support gut health is through a diet rich in fiber and fermented foods.

Male recreational strength trainers using anabolic-androgenic steroids (AAS) exhibit significantly higher rates of substance dependence disorder, anxiety disorders, and recent cocaine use compared to non-users, despite being primarily motivated by aesthetic and performance goals.

If you are a recreational lifter using steroids, be aware that your risk for anxiety, substance dependence, and cocaine use is significantly higher than non-users. Most users are not pros but regular gym-goers. Disclosing this to your doctor is crucial for managing side effects like high blood pressure or lipid issues, even if you feel safe. The motivation is usually aesthetics, not professional competition.

AAS users engage in extensive polypharmacy (averaging 11.1 agents/year) to mitigate adverse effects such as gynecomastia, testicular atrophy, and sexual dysfunction, using agents like tamoxifen, clomiphene, and PDE5 inhibitors.

If you are using AAS, you are likely also using other drugs to manage side effects like gynecomastia or low testosterone. This polypharmacy increases health risks. Be aware of what you are taking and why. Regular blood work is essential to monitor the impact of these combined substances.

Combined diet and exercise interventions during pregnancy do not significantly reduce the risk of developing gestational diabetes mellitus (GDM) compared to standard care alone, although they may reduce the risk of preterm birth.

Current evidence does not support combined diet and exercise interventions as a reliable method for preventing gestational diabetes. However, these interventions are still recommended because they reduce the risk of preterm birth and improve maternal health behaviors. Pregnant women should engage in light-to-moderate exercise and healthy eating for overall pregnancy health, not solely for GDM prevention.

Black tea theaflavins (TF-1, TF-2, TF-3) reduce hepatic lipid accumulation and fatty acid synthesis while stimulating fatty acid oxidation in human hepatocytes (HepG2) and high-fat diet-fed rats by activating AMPK via the LKB1 and ROS pathways.

Black tea contains theaflavins, which appear to help reduce liver fat and improve lipid metabolism by activating AMPK, a key energy sensor. While this study used high concentrations in cells and rats, drinking black tea as part of a healthy diet may offer metabolic benefits, particularly for those with fatty liver or obesity risk, though it is not a substitute for medical treatment.