What is this ingredient? Ergothioneine (EGT) is a unique sulfur‑containing amino‑thione obtained from the diet, especially from mushrooms and certain plant foods. Humans do not synthesize ergothioneine but selectively accumulate it via a specific transporter, OCTN1 (SLC22A4), which concentrates EGT in tissues exposed to high oxidative or inflammatory stress such as blood cells, brain, endothelium, liver, and kidneys [0,8]. Mechanistic studies show that ergothioneine is a potent antioxidant and cytoprotective molecule, scavenging reactive oxygen and singlet oxygen species, reducing oxidative DNA damage, and limiting mitochondrial injury in cell models [0,5,6,9].

Observational work in older adults finds that whole‑blood ergothioneine levels decline with age, and that people with mild cognitive impairment have significantly lower plasma EGT than age‑matched controls, suggesting that low ergothioneine status may be a risk factor for neurodegeneration and age‑related decline [1,3]. Recent human interventional data summarized in a 2024 review indicate that ergothioneine supplementation in older populations can improve aspects of cognition, memory, sleep quality, and neurodegeneration biomarkers, with a good safety profile at studied doses [3].

Why include it in this formula? The product “Ergothioneine+Spermidine - 60” combines ergothioneine with spermidine, clearly targeting cellular resilience, healthy aging, and brain and mitochondrial protection. Within this pairing, ergothioneine is the dedicated "cytoprotective antioxidant and stress‑buffer" pillar. By accumulating in high‑stress tissues and neutralizing ROS, EGT helps protect mitochondria, lipids, and DNA from chronic oxidative and inflammatory insults [0,5,6,9]. This is particularly relevant for long‑lived cells such as neurons and endothelial cells, where damage accumulates over decades.

Spermidine, in contrast, is primarily an autophagy‑activating polyamine that improves cellular cleanup and turnover. Used together, ergothioneine helps prevent and limit damage, while spermidine helps remove damaged components—two complementary strategies that align with modern concepts of longevity and cognitive resilience. In this way, EGT provides the redox‑stability backdrop that allows spermidine‑driven renewal processes to operate in a safer, less oxidatively stressed cellular environment.

References

• [0] Protective Effect of Ergothioneine against 7‑Ketocholesterol‑Induced Mitochondrial Damage in hCMEC/D3 Human Brain Endothelial Cells
• [1] Ergothioneine levels in an elderly population decrease with age and incidence of cognitive decline; a risk factor for neurodegeneration?
• [3] Ergothioneine for cognitive health, longevity and healthy ageing: where are we now?
• [5] L‑Ergothioneine scavenges superoxide and singlet oxygen and suppresses TNF‑α and MMP‑1 expression in UV‑irradiated human dermal fibroblasts
• [9] Protection against oxidative damage and cell death by the natural antioxidant ergothioneine

What is this ingredient? Spermidine is a naturally occurring polyamine found in all cells and in foods such as whole grains, legumes, some cheeses, and mushrooms. Inside cells, spermidine interacts with DNA, RNA, and proteins, and is best known for its ability to activate autophagy—the cell’s internal recycling and cleanup system. Mechanistic studies show that spermidine induces autophagy by inhibiting the acetyltransferase EP300 and modulating mTORC1 activity, leading to increased LC3 flux and reduced p62/SQSTM1, hallmarks of enhanced autophagy [0].

In animal models, lifelong spermidine supplementation extends lifespan by up to ~25%, reduces liver fibrosis and hepatocellular carcinoma, and improves cardiac function after myocardial infarction by promoting AMPK/mTOR‑mediated autophagic flux and reducing oxidative damage and inflammation [0,4]. Human cohort data from NHANES 2003–2014 indicate that higher dietary spermidine intake is associated with significantly lower cardiovascular and all‑cause mortality, even after adjustment for multiple confounders [9]. Emerging mechanistic work in human immune cells shows that spermidine can reverse B‑cell immunosenescence by restoring autophagy via eIF5A hypusination and TFEB translation [2].

Why include it in this formula? The product “Ergothioneine+Spermidine - 60” combines ergothioneine and spermidine, clearly targeting cellular resilience, healthy aging, and long‑term cardiometabolic and cognitive health. Within this duo, spermidine is the primary "autophagy and cellular housekeeping" pillar. By inducing autophagy and enhancing lysosomal clearance, spermidine supports removal of damaged mitochondria, misfolded proteins, and dysfunctional organelles—core processes that decline with age and contribute to cardiovascular, immune, and neurodegenerative risk [0,2,4,7].

Population data linking higher spermidine intake to reduced cardiovascular and all‑cause mortality [9], and Mendelian‑randomization work suggesting a protective role of higher spermidine levels against hypertension and adverse lipid profiles [1,6], align with this mechanistic picture. Ergothioneine, in turn, provides targeted antioxidant and cytoprotective support in high‑stress tissues. Used together, ergothioneine helps prevent and buffer oxidative and inflammatory damage, while spermidine enhances the cell’s ability to clear existing damage via autophagy, matching the product’s goal of supporting healthier aging at the cellular level rather than just masking symptoms.

References

• [0] Spermidine induces autophagy by inhibiting the acetyltransferase EP300
• [1] Protective effects of spermidine levels against cardiovascular risk factors: a bi-directional Mendelian randomization analysis
• [2] Polyamines control eIF5A hypusination, TFEB translation, and autophagy to reverse B cell senescence
• [4] Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway
• [7] Spermidine Suppresses Development of Experimental Abdominal Aortic Aneurysms
• [9] The association of dietary spermidine with all-cause mortality and CVD mortality: NHANES 2003–2014