{"id":5202,"date":"2022-10-11T00:00:00","date_gmt":"2022-10-11T00:00:00","guid":{"rendered":"https:\/\/salengei.com\/can-we-lengthen-telomeres\/"},"modified":"2022-10-11T00:00:00","modified_gmt":"2022-10-11T00:00:00","slug":"can-we-lengthen-telomeres","status":"publish","type":"post","link":"https:\/\/salengei.com\/en\/blog\/can-we-lengthen-telomeres\/","title":{"rendered":"Can we lengthen telomeres?"},"content":{"rendered":"

The last century has been characterized by an unprecedented increase in human life expectancy<\/strong> almost everywhere in the world.
\nThis demographic trend, however, has not been accompanied by the same extension in useful life and productivity, we are talking about quality of life.
\nToday, telomere length<\/strong> remains one of the most widely used biomarkers of aging in epidemiological and clinical studies.
\nIn recent years, this marker is also being increasingly used as a potential disruptor in personalized medicine. <\/p>\n

In today’s article we will dive a little into the topic of aging, telomeres and how simple but powerful actions can help us live longer and better.<\/p>\n<\/p>\n

\n\tWhat are telomeres?<\/strong><\/h1>\n

Telomeres are complexes consisting of tandem repeat DNA (sequential repeats are from TTAGGG) combined with associated proteins that play a key role in protecting chromosome ends and maintaining genome stability<\/strong>.
\nThese repeats prevent chromosomes from fusing together and DNA repair proteins from recognizing them as a double-strand break. <\/p>\n

\n

\n\t\tTelomeres shorten in parallel with aging<\/strong><\/h4>\n<\/blockquote>\n

They are considered a biological clock, as they shorten in parallel with aging<\/strong>.
\nIn addition, short telomeres are associated with several age-related diseases<\/strong>.
\nHowever, the variability in telomere shortening independent of chronological age suggests that it is a modifiable factor.
\nIn fact, it is regulated, among other things, by genetic damage, cell division, aging, oxidative stress, and inflammation, among other factors. <\/p>\n

One of the causes is that DNA polymerase incompletely replicates linear chromosomes, and that is why telomeric DNA shortens with repeated cell divisions until telomeres reach a critical length, at which point the cells enter senescence.<\/strong> That is why telomere length is an indicator of biological aging<\/strong>, and telomere dysfunction is related to age-related pathologies, such as cardiovascular diseases, Parkinson’s, Alzheimer’s and cancer.<\/p>\n<\/p>\n

\n\tWhy are they shortened?<\/strong><\/h1>\n

During the replication of linear chromosomes (these are found in most eukaryotic cells), the enzyme DNA polymerase replicates the ends of the DNA in a 5′ to 3′ direction using an RNA primer for initiation.
\nWhen this RNA primer is removed after DNA replication, the telomeric DNA sequence is lost from the ends.
\nFor this reason, in each cycle of somatic cell division, telomeres are shortened by 50 to 200 base pairs<\/strong> through incomplete synthesis of the lagging strand during DNA replication.
\nThis is due to the inability of DNA polymerase to fully replicate the 3′ end of the DNA strand, a phenomenon commonly referred to as “the final replication problem.” https:\/\/doi.org\/10.1038\/newbio239197a0<\/a><\/p>\n

Telomere length is epigenetically regulated by DNA methylation and histones.
\nWhen inflammation occurs and the accompanying proliferation of cells \u2013 especially during infections \u2013 it results in the loss of telomere repeats due to increased cell division.
\nThus, the plasma concentration of the inflammatory marker C-reactive protein is negatively correlated with telomere length<\/strong>. https:\/\/doi.org\/10.1210\/jc.2005-1814<\/a> <\/p>\n

In germ cells, stem cells, and many cancer cells, the enzyme telomerase reverse transcriptase adds a telomeric sequence to the ends of the newly synthesized DNA, maintaining telomere length.
\nWhen cells are not dividing and DNA is not replicating, the protein complex associated with telomere repeats called the refuge<\/strong> prevents unwanted telomere lengthening by restricting access to telomerase.
DOI: 10.1101\/gad.1346005<\/a> <\/p>\n

\n

\n\t\tInflammation produces oxidative stress<\/span><\/h4>\n<\/blockquote>\n

In addition, inflammation also produces oxidative stress<\/strong>.
\nWhen this oxidative stress is low-level, it can cause oxidative base modifications and single-strand breaks in DNA.
\nThis type of damage accumulates in telomeres since the G-rich telomeric sequence is more sensitive to oxidative damage.
\nDOI: https:\/\/doi.org\/10.1074\/jbc.274.2.962<\/a> <\/p>\n

The loss of protective telomere function due to the wear and tear of repeats makes chromosomes susceptible to fusing with other chromosomal ends and double-strand breaks, resulting in chromosomal rearrangements that affect genomic stability.
\nCritically short telomeres lose their epigenetic marks and are prone to recombinations.
\nDOI: https:\/\/doi.org\/10.1038\/ng1952<\/a> <\/p>\n

Telomere dysfunction is related to the development of age-related pathologies, as mentioned above, such as Parkinson’s disease, Alzheimer’s disease, cardiovascular diseases and cancer.<\/p>\n

\"\"<\/p>\n

\n\tWhat solutions are proposed?<\/strong><\/h1>\n

Telomere length has been shown to be associated with nutritional status<\/strong> in human and animal studies.
\nHealthy lifestyles and diets are positively correlated with telomere length.
\nChanges in diet and lifestyle can modulate telomerase activity in peripheral blood mononuclear cells, although it is unclear whether this translates into changes in telomere length. <\/p>\n<\/p>\n

\n\tTA-65<\/strong><\/h2>\n

The root of Astragalus membranaceus is able to increase the average length of telomeres and decrease the percentage of critically short telomeres and DNA damage.
\nRestoring telomerase activity in the mice studied, by reintroducing one copy of the Terc gene, rescues critically short telomeres and reverses chromosomal instability and cell and tissue defects associated with telomerase deficiency, including stem cell rescue, dysfunction and lifespan of the organism. <\/p>\n

The use of TA-65<\/a> results in telomerase-dependent short telomere elongation and rescue of associated DNA damage, demonstrating that TA-65’s mechanism of action is through the telomerase pathway.
\nDOI: 10.1111\/j.1474-9726.2011.00700.x<\/a> <\/p>\n

The findings also suggested that therapies aimed at reactivating telomerase and lengthening short telomeres with age could have significant anti-aging effects.
\nIn this sense, it has recently been shown that the enhanced activity of telomerase in mice that overexpress telomerase reverse transcriptase (TERT), is capable of delaying aging and prolonging the half-life by 40%, in addition to greater resistance to cancer. <\/p>\n

Thus, TERT overexpression improves the fitness of epithelial barriers, particularly the skin and gut, and produces a systemic delay in aging accompanied by an extension of median lifespan.
\nDOI: https:\/\/doi.org\/10.1016\/j.cell.2008.09.034<\/a> <\/p>\n<\/p>\n

\n\tVitamin D3<\/strong><\/h2>\n

The biologically active form of vitamin D, 1\u03b1,25-dihydroxyvitamin D3, possesses immunosuppressive properties.
\nThis is reflected in the inverse relationship between plasma vitamin D concentration and the inflammatory marker C-reactive protein. https:\/\/doi.org\/10.1210\/jc.2005-1814<\/a><\/p>\n

Telomere length is negatively correlated with plasma concentration of C-reactive protein.
\nThe addition of 1\u03b1,25 dihydroxyvitamin D3 to the cell culture medium reduces the expression of the proliferation factor granulocyte and macrocyte colony-stimulating factor that is important for the proliferation of all hematopoietic cell lineages and thus reduces lymphocyte proliferation.
\nIn addition, vitamin D also reduces the expression of the inflammation mediators interleukin-2 and interferon gamma. https:\/\/doi.org\/10.1073\/pnas.84.10.3385<\/a><\/p>\n<\/p>\n

\n\tOmega-3<\/strong><\/h2>\n

Plasma concentration of marine omega-3 fatty acids, decosahexaenoic acid and eicosapentaenoic acid, has been shown to be positively associated with a decrease in telomere length in study subjects over a period of 5 to 8 years.
DOI: 10.1001\/jama.2009.2008<\/p>\n

People who had a higher initial concentration of omega-3 fatty acids showed the maximal effect of omega-3 fatty acids on telomere wasting.
\nThe concentration of omega-3 fatty acids in plasma is associated with low pro-inflammatory markers and high anti-inflammatory markers. <\/p>\n

In mice, the diet enriched in marine omega-3 fatty acids improved the activities of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase and increased lifespan. https:\/\/doi.org\/10.1093\/jn\/131.10.2753<\/a><\/p>\n

Changes in anti-inflammatory and antioxidant properties induced by omega-3 fatty acids decrease cell turnover and oxidative DNA damage and may therefore reduce telomere shortening.<\/strong><\/p>\n

That is why from Salengei<\/strong> we do not hesitate to recommend MorEPA\u00ae Platinum<\/a>, whose pearls contain 1100 mg of omega-3, of which 764 mg are EPA and 236 mg of DHA.
\nIn addition, these pearls contain vitamin D3, which generates a synergistic action, enhancing the benefits. <\/p>\n

\"\"<\/p>\n<\/p>\n

\n\tConclusion<\/strong><\/h1>\n

Fortunately, science today allows us to measure, predict in a certain way and prevent aging.
\nTelomere length is proof of this and there is still much to be done to improve, but we also believe that the implementation of healthy routines and the incorporation of specific food supplements will help us live a fuller life with fewer diseases. <\/p>\n

Because at Salengei<\/strong> we believe that ageing is just that, right, living a longer, quality life. <\/p>\n

As you know, aging is one of our favorite topics and that is why we dedicate a lot of effort, hours of research and we are pleased to share the news with you.<\/p>\n","protected":false},"excerpt":{"rendered":"

In today’s article we will dive a little into the topic of aging, telomeres and how simple but powerful actions can help us live longer and better.<\/p>\n","protected":false},"author":3,"featured_media":2674,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[109],"tags":[],"class_list":["post-5202","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-antienvejecimiento"],"acf":[],"yoast_head":"\nCan we lengthen telomeres? - Salengei<\/title>\n<meta name=\"description\" content=\"In today's article we will dive a little into the topic of aging, telomeres and how simple but powerful actions can help us live longer and better.\" \/>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/salengei.com\/en\/blog\/can-we-lengthen-telomeres\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Can we lengthen telomeres? 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