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      Association of nutraceutical supplements with longer telomere length

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          Abstract

          Telomeres are nucleotide tandem repeats located at the tip of eukaryotic chromosomes that maintain genomic integrity. The gradual shortening of telomeres leads to cellular senescence and apoptosis, a key mechanism of aging and age-related chronic diseases. Epigenetic factors, such as nutrition, exercise and tobacco can affect the rate at which telomeres shorten and can modify the risk of developing chronic diseases. In this study, we evaluated the effects of a combination of nutraceutical supplements (NS) on telomere length (TL) in healthy volunteers with no medical history of any disease. Participants (n=47) were selected from healthy outpatients visiting a private clinic and were divided into the experimental group (n=16), that received the NS and the control group (n=31). We estimated the length of single telomeres in metaphase spread leukocytes, isolated from peripheral blood, using quantitative-fluorescent in situ hybridization (Q-FISH) analysis. The length of the whole telomere genome was significantly increased (P<0.05) for the mean, 1st quartile and median measurements in the experimental group. Similar findings were observed for short TL (20th percentile) (P<0.05) for the median and 3rd quartile measurements in the NS group, compared to the control group. The beneficial effects of the supplements on the length of short telomeres remained significant (P<0.05) following adjustment for age and sex. Telomeres were moderately longer in female patients compared to the male patients. On the whole, the findings of this study suggest that the administration of NS may be linked to sustaining the TL.

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          Most cited references48

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          The Epidemiology of Global Micronutrient Deficiencies

          Micronutrients are essential to sustain life and for optimal physiological function. Widespread global micronutrient deficiencies (MNDs) exist, with pregnant women and their children under 5 years at the highest risk. Iron, iodine, folate, vitamin A, and zinc deficiencies are the most widespread MNDs, and all these MNDs are common contributors to poor growth, intellectual impairments, perinatal complications, and increased risk of morbidity and mortality. Iron deficiency is the most common MND worldwide and leads to microcytic anemia, decreased capacity for work, as well as impaired immune and endocrine function. Iodine deficiency disorder is also widespread and results in goiter, mental retardation, or reduced cognitive function. Adequate zinc is necessary for optimal immune function, and deficiency is associated with an increased incidence of diarrhea and acute respiratory infections, major causes of death in those <5 years of age. Folic acid taken in early pregnancy can prevent neural tube defects. Folate is essential for DNA synthesis and repair, and deficiency results in macrocytic anemia. Vitamin A deficiency is the leading cause of blindness worldwide and also impairs immune function and cell differentiation. Single MNDs rarely occur alone; often, multiple MNDs coexist. The long-term consequences of MNDs are not only seen at the individual level but also have deleterious impacts on the economic development and human capital at the country level. Perhaps of greatest concern is the cycle of MNDs that persists over generations and the intergenerational consequences of MNDs that we are only beginning to understand. Prevention of MNDs is critical and traditionally has been accomplished through supplementation, fortification, and food-based approaches including diversification. It is widely accepted that intervention in the first 1,000 days is critical to break the cycle of malnutrition; however, a coordinated, sustainable commitment to scaling up nutrition at the global level is still needed. Understanding the epidemiology of MNDs is critical to understand what intervention strategies will work best under different conditions.
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            The shortest telomere, not average telomere length, is critical for cell viability and chromosome stability.

            Loss of telomere function can induce cell cycle arrest and apoptosis. To investigate the processes that trigger cellular responses to telomere dysfunction, we crossed mTR-/- G6 mice that have short telomeres with mice heterozygous for telomerase (mTR+/-) that have long telomeres. The phenotype of the telomerase null offspring was similar to that of the late generation parent, although only half of the chromosomes were short. Strikingly, spectral karyotyping (SKY) analysis revealed that loss of telomere function occurred preferentially on chromosomes with critically short telomeres. Our data indicate that, while average telomere length is measured in most studies, it is not the average but rather the shortest telomeres that constitute telomere dysfunction and limit cellular survival in the absence of telomerase.
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              Telomere diseases.

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                Author and article information

                Journal
                Int J Mol Med
                Int. J. Mol. Med
                IJMM
                International Journal of Molecular Medicine
                D.A. Spandidos
                1107-3756
                1791-244X
                July 2019
                10 May 2019
                10 May 2019
                : 44
                : 1
                : 218-226
                Affiliations
                [1 ]Metabolomic Medicine Clinic, Health Clinics for Autoimmune and Chronic Diseases, 10674 Athens
                [2 ]Laboratory of Toxicology, Medical School, University of Crete, 71003 Heraklion, Greece
                [3 ]Department of Clinical Pharmacy, University of Medicine and Pharmacy, Faculty of Pharmacy, Craiova 200349, Romania
                [4 ]Spin-Off Toxplus S.A., 71601 Heraklion, Greece
                [5 ]Department of Toxicology, University of Medicine and Pharmacy, Faculty of Pharmacy, Craiova 200349, Romania
                [6 ]Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas, 70013 Heraklion
                [7 ]Department of Hematology, University of Crete, School of Medicine
                [8 ]Laboratory of Anatomy-Histology-Embryology, Medical School, University of Crete, 71003 Heraklion
                [9 ]Laboratory of Forensic Medicine and Toxicology, School of Medicine, Aristotle University of Thessaloniki, 54124 Thessaloniki
                [10 ]Laboratory of Clinical Virology, School of Medicine, University of Crete, 71003 Heraklion, Greece
                Author notes
                Correspondence to: Professor Aristidis Tsatsakis, Laboratory of Toxicology, Medical School, University of Crete, 71003 Heraklion, Greece, E-mail: tsatsaka@ 123456uoc.gr
                [*]

                Contributed equally

                Article
                ijmm-44-01-0218
                10.3892/ijmm.2019.4191
                6559326
                31115552
                d885290e-e17d-45f8-893d-f2ab42564678
                Copyright: © Tsoukalas et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 29 March 2019
                : 02 May 2019
                Categories
                Articles

                telomere length,nutraceutical supplements,nutrition,telomerase activity,short telomere

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