A protein called epithalamin is located in the pineal gland of animals and is of interest due to its proposed anti-aging characteristics. Past research investigations have suggested that epithalamin may improve the maximum life span in animals, reduce levels of free radicals, and change catalase activity to avoid tissue damage. Epithalamin studies reportedly reduced mortality by 52% in fruit flies, 52% in normal rats, and 27% in mice genetically predisposed to specific cancers and cardiovascular diseases.
Extensive animal studies have purported its potential as a growth- and division-inhibiting regulator of cellular metabolism. Specifically,
Epitalon may promote longer-term cell viability in culture. Studies suggest that Epithalon's potential on telomeres is likely responsible for its potential to prolong cell life.
In mice and rats, Epithalon appeared to have the same impact as epithalamin. It has also suggested interesting impact within context of cancer research, lowering spontaneous breast tumors in mice prone to them and reducing the incidence of intestinal tumors in rats.
Epithalon Peptide and Longevity
Epithalon has been speculated in studies to do more than only reactivate telomerase and lengthen the life of cells; it has also been hypothesized to protect neurons from injury, improve the function of the intestinal mucosa, and decrease the rate of DNA mutation. That is to say, Epithalon may possibly increase not only longevity but also health span (the number of years lived without significant illness or impairment).
Epithalon Peptide- Mechanism of Action
How exactly Epithalon exerts its far-reaching impacts remains unclear. Research suggests that neither caloric intake nor total body mass may be affected noticeably. However, data suggests that introducing it in mouse models may have reduced the number of chromosomal aberrations. It would purport that Epithalon may offer more than one kind of DNA protection. Epitalon's potential to prevent other DNA damage is less well understood. At the same time, it is speculated to do so by activating telomerase and, therefore, preventing the degradation of telomeres (the end caps of DNA strands). Although its regulation of free radicals provides some insight, it is insufficient to explain the breadth of Epithalon's actions.
Studies in mice are being conducted to determine the peptide's long-term potential, and research into Epithalon's DNA-protecting properties is underway. Epithalon seems create more widespread impact than other substances studied within the context of reducing age-related decline in rodents. This information might be useful in determining how exactly Epithalon works.
What are Telomeres?
Telomeres are protective sequences of repeating nucleotides located at the ends of linear chromosomes. Telomeres are originally about 11,000 DNA bases long but may shorten with aging potentially down to as few as 4,000. Telomeres degrade at a higher pace in males than in females, which is an interesting ancillary finding.
Telomeres are a kind of selfless defense mechanism that prevents DNA damage. Telomeres can be sacrificed during DNA replication (copying) without harming any genes since they do not code for anything. This is essential due to the inherent flaws in DNA replication. Naturally, telomeres lose their protective function if they grow too short. There are systems inside cells that can detect this. When a telomere grows too short, the cell either becomes dormant or dies.
Epithalon Peptide and Telomerase
Rebuilding telomeres using an enzyme called telomerase reverse transcriptase (telomerase) delays cellular aging at the molecular level. Unfortunately, telomerase is not foolproof, and hence, aging still takes place even when this enzyme is present.
Research in 1998 suggested that artificially enhancing telomerase activity might not only lengthen the lifetime of somatic (skin) cells in culture but could potentially make them immortal. Gene therapy, metabolic suppression, and torpor/hibernation are only some methods explored since then to increase telomerase activity. None of these methods has been suggested to slow aging significantly, and they all have substantial downsides.
Epithalon's potential to affect telomerase activity was initially suggested in vitro somatic cells in 2003. Epithalon was hypothesized to induce telomerase synthesis in fibroblast cells with undetectable telomerase activity. The telomeres of every single cell appeared to become longer.
Beyond Telomerase with Epithalon Peptide
After falling out of favor for a while, the concept was brought back in 2016 when it was suggested that Epithalon may have had impacts beyond telomerase activation. This study also used cultured fibroblasts. It has been implied that Epithalon may also prevent senescent proteins like MMP-9 from building up. Senescent proteins are age-related proteins that tell cells to cease proliferating.
Epithalon has been hypothesized to decrease caspase-dependent apoptosis, in addition to its potential to inhibit MMP-9 synthesis. This is a major mechanism by which cells with shortened telomeres or other indicators of cellular aging are eliminated.
Investigations purport that Epithalon's potential for telomere length underlies its other functions. However, it is unclear whether the properties are the indirect consequence of Epithalon safeguarding telomeres or the direct outcome of some as-yet-unidentified function of Epithalon.
Epithalon Peptide and Aging
In addition to its potential impact on aging, Epithalon's actions on caspase are of interest in the context of several diseases. Neurodegenerative diseases like Alzheimer's and several autoimmune ailments have both been linked to elevated caspase activity. Developing a peptide that might regulate caspase activity may have far-reaching advantages.
References
[i] V. N. Anisimov, S. V. Mylnikov, T. I. Oparina, and V. K. Khavinson, "Effect of melatonin and pineal peptide preparation epithalamin on life span and free radical oxidation in Drosophila melanogaster," Mech. Ageing Dev., vol. 97, no. 2, pp. 81-91, Aug. 1997.
[ii] V. N. Anisimov, S. V. Mylnikov, and V. K. Khavinson, "Pineal peptide preparation epithalamin increases the lifespan of fruit flies, mice and rats," Mech. Ageing Dev., vol. 103, no. 2, pp. 123-132, Jun. 1998.
[iii] S. V. Rosenfeld, E. F. Togo, V. S. Mikheev, I. G. Popovich, V. K. Khavinson, and V. N. Anisimov, "Effect of epithalon on the incidence of chromosome aberrations in senescence-accelerated mice," Bull. Exp. Biol. Med., vol. 133, no. 3, pp. 274-276, Mar. 2002.
[iv] V. K. Khavinson, E. G. Rybakina, V. V. Malinin, I. Y. Pivanovich, S. N. Shanin, and E. A. Korneva, "Effects of short peptides on thymocyte blast transformation and signal transduction along the sphingomyelin pathway,"Bull. Exp. Biol. Med., vol. 133, no. 5, pp. 497-499, May 2002.
[v] V. K. Khavinson, N. M. Timofeeva, V. V. Malinin, L. A. Gordova, and A. A. Nikitina, "Effect of vilon and epithalon on activity of enzymes in epithelial and subepithelial layers in small intestine of old rats," Bull. Exp. Biol. Med., vol. 134, no. 6, pp. 562-564, Dec. 2002.
[vi] T. A. Dzhokhadze, T. Z. Buadze, M. N. Gaĭozishvili, M. A. Rogava, and T. A. Lazhava, "[Functional regulation of genome with peptide bioregulators by hypertrophic cardiomyopathy (by patients and relatives)],"Georgian Med. News, no. 225, pp. 94-97, Dec. 2013.
