Browse the evidence

Heritability of longevity increases with age, reaching its highest levels in centenarians, suggesting that genetic factors become more dominant in determining survival at extreme ages.

While lifestyle matters for everyone, genetic factors play an increasingly important role in who survives to extreme old age (100+). This suggests that for those aiming for extreme longevity, genetic predisposition is a significant, albeit non-modifiable, factor.

A composite panel of seven circulating senescence-associated secretory phenotype (SASP) proteins (GDF15, FAS, OPN, TNFR1, ACTIVIN A, CCL3, and IL-15) serves as a superior biomarker for predicting adverse postoperative outcomes and biological age compared to chronological age or single-protein markers.

This research suggests that measuring a specific set of 7 proteins in the blood (GDF15, FAS, OPN, TNFR1, ACTIVIN A, CCL3, and IL-15) can provide a more accurate assessment of biological age and surgical risk than chronological age. For older adults, this panel may help identify those at higher risk for complications after surgery, potentially guiding pre-operative care and post-operative monitoring.

High levels of sedentary behavior are NOT associated with an increased risk of breast, rectal, ovarian, prostate, stomach, esophageal, testicular, renal cell, or non-Hodgkin lymphoma cancers.

While high sedentary behavior is linked to colon, endometrial, and lung cancers, it does not appear to increase the risk of breast, prostate, ovarian, or other cancers. However, reducing sedentary time is still beneficial for overall health and may help mitigate the risks for the cancers that are associated with it.

Semi-supercentenarians (aged 105+) exhibit a significantly lower epigenetic age (approx. 8.6 years younger) than expected based on their chronological age.

For individuals reaching extreme old age (105+), biological age may lag significantly behind chronological age. This suggests that some individuals possess genetic or epigenetic traits that slow down the molecular processes of aging. While this is not an intervention, it underscores the importance of biological age metrics in assessing health in the very elderly, as they may be biologically younger than their birth year suggests.

Earmarking (hypothecating) health tax revenues for specific health objectives increases public support for the tax and political sustainability, whereas using revenues for general fiscal purposes leaves the tax vulnerable to lobbying and repeal.

To ensure health taxes survive political pressure, governments must earmark the revenue for specific health-related spending, such as subsidizing healthy foods or targeting child obesity. This builds public support and protects the tax from industry lobbying that often leads to repeal when revenues go into the general fund.

HMB supplementation does not improve strength, body composition, or performance in experienced, resistance-trained athletes.

If you have been lifting consistently for years, HMB will not help you get stronger or build more muscle. Save your money.

Physiological aging in humans is characterized by the accumulation of unrepaired DNA double-strand breaks (DSBs) in hematopoietic stem and progenitor cells, driven by a decline in DSB repair capacity rather than telomere shortening.

Your body's ability to repair DNA damage declines with age, leading to accumulated genetic errors in blood stem cells. However, this process is not fixed; individuals with healthy lifestyles maintain higher repair efficiency and lower damage levels even in their 70s. Focus on lifestyle factors that support cellular repair mechanisms rather than accepting damage as inevitable.

Knockdown of fibrillarin reduces nucleolar size and extends lifespan in wild-type C. elegans.

Reducing the expression of the nucleolar protein fibrillarin extends lifespan in C. elegans. This suggests that inhibiting specific aspects of ribosome production can promote longevity.

Mitochondrial dysfunction is not sufficient to cause aging or limit lifespan in animals, as evidenced by mutants with severe defects living normal or extended lives.

Focus on overall metabolic health rather than trying to eliminate all mitochondrial stress. Some level of mitochondrial stress (e.g., from exercise) may trigger protective mechanisms that support longevity, whereas severe dysfunction without adaptive responses is harmful.

Genetically predicted leisure television watching causally increases the risk of COVID-19 hospitalization and disease severity.

Reduce time spent watching television, as it is causally linked to higher risks of COVID-19 hospitalization and severity. This risk is mediated by metabolic factors like obesity and smoking, so replacing TV time with physical activity may mitigate these risks.

Conventional wastewater treatment plants are ineffective at removing many endocrine-disrupting compounds, leading to their presence in surface water and drinking water supplies.

If concerned about EDCs, consider using water filters certified to remove specific contaminants like BPA or pesticides, as standard municipal treatment may not remove them. Check local water quality reports for emerging contaminants.

High preoperative intramuscular adipose tissue content (IMAC) and low psoas muscle mass index (PMI) are independent risk factors for increased mortality after living donor liver transplantation.

For patients with liver disease or undergoing major surgery, muscle quality matters as much as muscle size. Intramuscular fat (steatosis) is a hidden risk factor that increases mortality. While you cannot easily change muscle quality at home, understanding that 'empty' muscle (low quality) is dangerous highlights the importance of comprehensive nutritional therapy and rehabilitation before surgery, not just weight loss or strength training.

Vagal afferent signaling regarding food intake is primarily driven by mechanoreceptors (IGLEs) sensing intestinal stretch, rather than chemoreceptors sensing gut peptides like GLP-1.

When taking GLP-1 medications, part of the weight loss comes from the physical feeling of fullness (stretch) in your stomach and intestines, not just a chemical signal. This is why you feel full faster and stay full longer. The drug enhances these mechanical signals to your brain.

Financial conflicts of interest are prevalent among members of clinical practice guideline panels, with a significantly higher prevalence in non-government sponsored guidelines compared to government sponsored ones.

When evaluating clinical guidelines, check the funding source and panel disclosures. Non-government sponsored guidelines have a 69% rate of financial conflicts of interest, compared to 16% for government-sponsored ones. Prioritize guidelines with transparent, government or non-profit backing to minimize bias.

Current standard laboratory nucleic acid amplification tests (NAATs) are more accurate and cost-effective than rapid point-of-care tests (POCTs) for detecting genital chlamydia infection.

For chlamydia testing, laboratory-based nucleic acid amplification tests (NAATs) remain the gold standard because they are more accurate and cost-effective than rapid point-of-care tests. While rapid tests provide faster results, they miss more infections and cost more to the healthcare system. Providers should prioritize NAATs for diagnostic accuracy, though rapid tests may be considered in specific contexts where they significantly increase testing uptake.

Epigenetic aging initiates early in life upon the loss of pluripotency during differentiation, and the epigenetic age of a tissue is largely determined by the composition of stem cells versus differentiated cells.

Epigenetic aging begins when cells lose their stem-like pluripotency and start differentiating. The overall epigenetic age of a tissue reflects the balance of young stem cells and older differentiated cells. Maintaining a healthy stem cell pool may help keep tissue-level epigenetic age lower.

Exercise training fails to significantly increase aerobic capacity in p53-deficient mice, indicating p53 is necessary for the adaptive response to endurance training.

Not everyone adapts to endurance training with the same magnitude of mitochondrial improvement. If your genetic makeup (specifically p53 function) is suboptimal, your aerobic capacity may not improve significantly with standard training protocols, regardless of effort.

Cardiolipin oxidation is a primary event in the release of cytochrome c and increased permeability of the mitochondrial membrane to apoptosis factors.

Maintain mitochondrial health to prevent cardiolipin oxidation, which is a key step in apoptosis and aging.

Alpha-tocopherol (Vitamin E) supplementation is ineffective in preventing ethanol-induced muscle lesions or restoring protein synthesis rates in alcoholics.

Taking Vitamin E supplements will not protect your muscles from the damage caused by alcohol. Studies show it fails to prevent the reduction in protein synthesis or other lesions caused by ethanol. The only way to prevent this specific damage is to stop drinking.

Voluntary industry self-regulation and public-private partnerships are ineffective at reducing non-communicable disease (NCD) risk exposure and often serve to delay or prevent stricter statutory regulation.

Do not rely on voluntary industry pledges or 'healthy' marketing claims to manage NCD risk. These measures have been evaluated and found ineffective. Effective risk reduction requires statutory regulation, such as taxation, marketing restrictions, and clear labeling, enforced by public authorities rather than left to industry self-interest.

The differential expression of immunity-related genes during aging is linked to the rate of aging, where long-lived organisms exhibit enhanced resistance to pathogens.

Genetic factors that enhance immune response in model organisms are associated with extended lifespan, suggesting a conserved link between immune fitness and longevity.

Blocking the expression of immune-related genes can prevent lifespan extension in long-lived nematodes, indicating a positive effect of the immune response on longevity.

In model organisms, the immune system is not just for fighting infection but is actively required for extended lifespan, suggesting a trade-off between immune activation and aging.

The accumulation of senescent cells in tissues drives organ degeneration and aging phenotypes, and their clearance extends lifespan and improves homeostasis in mammalian models.

Focus on maintaining immune system health and reducing chronic stressors that induce senescence. While direct 'senolytic' interventions are emerging, lifestyle factors that reduce cellular stress (exercise, balanced nutrition) may help manage senescent cell burden.