Browse the evidence

Exposure to environmental endocrine-disrupting chemicals (EDCs) is associated with adverse neurodevelopmental outcomes in children, including lower IQ, attention deficit, hyperactivity, and behavioral problems.

Reduce exposure to EDCs during pregnancy and childhood by avoiding plastic food storage, choosing natural personal care products, and filtering drinking water to protect developing brains.

Administration of recombinant human TSH (rTSH) significantly increases FDG PET detectability and lesion-to-background ratios in patients with well-differentiated thyroid carcinoma and negative radioiodine scans compared to TSH-suppressive therapy.

For patients with well-differentiated thyroid cancer who have detectable tumor markers but negative standard scans, using recombinant TSH (rTSH) before an FDG PET scan significantly improves the ability to find hidden disease compared to standard scans done while on thyroid hormone suppression. This method avoids the need to stop thyroid medication, which causes hypothyroidism.

Inhibition of liver-specific miR-122 using the antagomiR Miravirsen suppresses Hepatitis C Virus (HCV) replication.

Miravirsen is an antagomiR that targets miR-122 to treat Hepatitis C. This is a specialized medical treatment for a viral infection, distinct from general metabolic health advice.

Paternal obesity and poor nutrition can transmit metabolic disease risk to offspring through epigenetic modifications in sperm (DNA methylation and microRNA), affecting the health of the F1 and potentially F2 generations.

Men planning to have children should maintain a healthy weight and diet before conception. This can reduce the risk of passing on metabolic disease risks to their children via epigenetic mechanisms.

Specific gut bacteria, including Bacteroides fragilis (via Polysaccharide A) and Faecalibacterium prausnitzii, can enhance the efficacy of cancer immunotherapy (ICB) by modulating T-cell responses and reducing inflammation.

For cancer patients undergoing immunotherapy, maintaining gut health through a diverse, fiber-rich diet may support the efficacy of treatment. While specific NGPs like B. fragilis and F. prausnitzii show promise, they are not yet standard clinical interventions. Consult with oncology teams before making significant dietary changes.

High doses of n-3 omega fatty acids (1.8 g/day) may accelerate heart rate and increase the risk of ventricular tachycardia or fibrillation in patients with existing ventricular arrhythmias.

If you have a history of ventricular tachycardia or fibrillation, avoid high-dose fish oil supplements (1.8g/day or more) unless explicitly approved by your cardiologist, as they may worsen your condition.

Curcumin extends the lifespan of model organisms (C. elegans, D. melanogaster, yeast, and mice) by modulating longevity signaling pathways (IIS, mTOR, PKA, FOXO) and enhancing antioxidant defenses (Nrf2/HO-1, SOD).

Curcumin, the active compound in turmeric, appears to activate cellular stress-response pathways (like Nrf2 and FOXO) that are linked to longevity in animal studies. While human lifespan extension isn't proven, its anti-inflammatory and antioxidant properties may support healthy aging. Consider incorporating turmeric/curcumin as part of a diet rich in polyphenols, potentially with black pepper or lipids to enhance absorption, though it is not a magic bullet for longevity.

Lifestyle interventions do not significantly improve glucose tolerance, lipid profiles, or clinical reproductive outcomes (ovulation, pregnancy) in women with PCOS based on current evidence.

While lifestyle changes are beneficial for weight, insulin, and hormones in PCOS, they may not be enough to normalize glucose tolerance or lipid profiles. Women with these specific concerns may need additional pharmacological interventions alongside lifestyle changes. Additionally, current evidence does not support lifestyle changes as a standalone treatment for improving ovulation or pregnancy rates.

Arsenic exposure interferes with insulin signal transduction and glucose metabolism mechanisms, including the inhibition of insulin-stimulated glucose uptake and alteration of transcription factors like IUF-1 and PPARγ.

Laboratory studies show that arsenic can disrupt how cells process glucose and respond to insulin by interfering with key proteins and genes. However, these effects were observed at concentrations much higher than what most people encounter in drinking water, so the direct impact on human health remains uncertain.

Pyruvate cycling and the subsequent export of citrate and alpha-ketoglutarate from mitochondria to the cytosol serve as critical amplifying signals for glucose-stimulated insulin secretion in pancreatic beta-cells.

This finding highlights the complexity of insulin secretion. It suggests that supporting mitochondrial health and metabolic flexibility in beta-cells may be important for maintaining healthy insulin secretion, though direct dietary interventions for this specific pathway are not detailed in this review.

Overexpression of Nicotinamide Phosphoribosyltransferase (Nampt) extends the replicative lifespan of human vascular smooth muscle cells and fibroblasts by activating SIRT1 and promoting p53 degradation.

This research identifies Nampt (an enzyme that recycles NAD+) as a critical regulator of cellular aging in vascular cells. While this paper uses genetic overexpression in a lab setting, it suggests that maintaining or boosting NAD+ salvage pathways (potentially through precursors like Nicotinamide Riboside or Nicotinamide Mononucleotide) might support vascular health and delay cellular senescence. Current evidence is preclinical, so this is a mechanistic insight rather than a direct prescription.

In nonalcoholic fatty liver disease (NAFLD), lipotoxic hepatocytes release exosomes enriched with miR-192-5p, which activates pro-inflammatory M1 macrophages by inhibiting the Rictor/Akt/FoxO1 signaling pathway, thereby driving hepatic inflammation and disease progression.

This research highlights that liver fat accumulation (lipotoxicity) actively sends inflammatory signals to immune cells in the liver, worsening NAFLD. The primary actionable insight is that reducing hepatic fat (through caloric restriction, metabolic improvement, or specific dietary changes) may interrupt this exosomal miR-192-5p signaling, thereby reducing macrophage-driven inflammation and slowing disease progression.

Genetic variants in the IGF-IR and PI3KCB genes that result in lower free plasma IGF-I levels are associated with increased human longevity, specifically in individuals aged 85 and older.

This research suggests that longevity is linked to specific genetic variants that naturally keep IGF-I levels lower. There is no direct intervention protocol here, but it implies that maintaining metabolic health and avoiding excessive IGF-I elevation (e.g., through excessive caloric intake or supplementation) might align with natural longevity pathways. Focus on healthy aging rather than maximizing hormone levels.

GLP-1-based therapies may accelerate the progression of premalignant pancreatic lesions (PanINs) to pancreatic cancer in individuals with pre-existing dysplasia, acting as a growth factor rather than an initiator.

If you are taking a GLP-1 drug, be aware of the potential risk of pancreatic cancer, especially if you have a family history of pancreatic cancer or chronic pancreatitis. The paper suggests this risk is real and mechanistically plausible, not just a rare side effect.

The UCP3 C→T silent polymorphism in exon 3 is not significantly associated with metabolic rate or obesity in Pima Indians.

Testing for the UCP3 C→T polymorphism is unlikely to provide useful information for managing weight or metabolic rate in Pima Indians, as this specific variant shows no significant association with these outcomes.

Dietary restriction does not protect against all neurodegenerative conditions; specifically, it fails to protect and may accelerate disease progression in models of ALS caused by Cu/Zn-SOD mutations.

While DR is generally beneficial, it may not be suitable for everyone, particularly those with specific genetic mutations like Cu/Zn-SOD ALS, where it might worsen outcomes. Consultation with a physician is essential before adopting DR for neurodegenerative conditions.

miR-27a and miR-27b suppress adipocyte differentiation by targeting PPARγ, and lower miR-27a expression in obese mice may be necessary for adipocyte hypertrophy.

miR-27a and miR-27b suppress fat cell differentiation by targeting PPARγ. Lower levels of miR-27a in obese mice suggest that suppressing these miRNAs might promote fat cell growth, while mimicking them could potentially reduce lipid storage.

Cellular reprogramming to induced pluripotent stem cells (iPSCs) can model progeroid syndromes and reveal epigenetic defects associated with premature aging, offering a platform for screening epigenetic therapeutics.

iPSC technology allows scientists to study aging at a cellular level by creating stem cells from patients with premature aging syndromes. This helps identify potential drug targets but is not a treatment available to patients today.

Excessive nitric oxide production, particularly via inducible NOS (iNOS) during inflammation, is cytotoxic, promotes oxidative stress, and impairs mitochondrial function, leading to cell death and organ failure.

While NO is beneficial in normal amounts, chronic inflammation can lead to excessive NO production that damages cells. Managing inflammation through lifestyle and medical care helps prevent this harmful excess.

Curcumin, the active compound in turmeric, reduces amyloid-beta plaques and cognitive deficits in Alzheimer's disease models by directly binding to and clearing plaques, with bioavailability issues addressed by new formulations.

Turmeric contains curcumin, which has shown promise in reducing amyloid plaques in animal models. However, standard curcumin supplements have poor bioavailability. If considering supplements, look for advanced formulations designed to improve absorption, but note that human clinical trials are still ongoing. Dietary turmeric is a safe and low-cost addition to an anti-inflammatory diet.

IGF1 levels are positively associated with prostate cancer risk, while IGFBP3 levels are inversely associated, suggesting their potential as prognostic markers.

For men with prostate cancer, IGF1 and IGFBP3 levels may help predict outcomes. High IGF1 and low IGFBP3 are associated with worse prognosis.

In nonalcoholic fatty liver disease (NAFLD), the presence of hepatic cholesterol crystals within hepatocyte lipid droplets and the subsequent formation of Kupffer cell 'crown-like structures' around dead hepatocytes distinguish nonalcoholic steatohepatitis (NASH) from simple steatosis.

If you have fatty liver, simply reducing fat intake might not be enough if cholesterol crystallization is driving inflammation. The presence of cholesterol crystals and the resulting immune response (crown-like structures) are key markers of serious liver disease (NASH) versus simple fat accumulation. Managing this likely requires addressing the underlying metabolic drivers of cholesterol handling and inflammation, not just total fat intake.

Activation of the IL-4/STAT6 immune signaling pathway improves insulin sensitivity and glucose homeostasis by repressing hepatic PPARα-mediated fatty acid oxidation and reducing adipose tissue inflammation.

This research suggests that the type of immune response your body mounts matters for metabolic health. While chronic bacterial-type inflammation is linked to insulin resistance, specific immune pathways (like those triggered by allergies or parasitic responses) may actually improve how your body handles sugar and fat. This is a mechanistic finding in mice; it does not currently translate to a human treatment protocol.

Constitutive upregulation of the Nrf2 signaling pathway is a primary mechanism for extended healthspan and longevity in naturally long-lived species, acting as a master regulator of cytoprotection against oxidative stress, inflammation, and protein damage.

Focus on lifestyle factors that naturally activate the Nrf2 pathway, such as exercise and consuming phytochemicals found in plants (e.g., sulforaphane from broccoli, curcumin), rather than relying solely on antioxidant supplements. This supports the body's natural defense mechanisms against aging and disease.