Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial

Kiecolt‐Glaser, Janice K.; Epel, Elissa S.; Belury, Martha A.; Andridge, Rebecca; Lin, Jue; Glaser, Ronald; Malarkey, William B.; Hwang, Beom Seuk; Blackburn, Elizabeth H.

doi:10.1016/j.bbi.2012.09.004

Cited by 229 publications

(191 citation statements)

References 67 publications

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“…This did not appear to be telomerase-mediated, at least as measured at the two timepoints. The greater the improvements in the ratio the greater the reductions in oxidative stress and inflammation, two factors that may be key mechanisms of telomeric shortening (30).…”

Section: The Promise Of Interventionsmentioning

confidence: 99%

How “Reversible” Is Telomeric Aging?

Epel

2012

Cancer Prevention Research

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A critical question in human health is the malleability of telomere length. Telomere length, sampled at one point during adult life, is predictive of certain types of cancer and other immune and metabolicrelated diseases. We now know from basic studies that the telomere/telomerase maintenance system plays a causal role in accelerating biologic aging and promoting disease processes. One can develop short telomeres for a multitude of reasons. Historical factors such as genetics, prenatal conditions, and early adversity, contribute to adult telomere length; however, current stress and lifestyle are also associated. If these modifiable predictors are causal factors in telomere shortening, there is a tremendous opportunity to improve maintenance and possibly even lengthen telomeres with behavioral interventions. This minireview discusses our current understanding of telomere lengthening and questions facing the field. Several small-scale stress reduction/wellness studies show promising findings, suggesting that cell aging can be slowed or reversed in vivo over short periods. Moreover, possible mechanisms are discussed, that take into account actual telomeric lengthening, such as that which occurs through telomerase-mediated elongation, or mechanisms resulting in "pseudo-telomeric lengthening" as might occur from changes in cell type distribution. There is a strong need for more translational clinical to bench research to address mechanistic questions in experimental models. In addition, well-designed intervention research that examines both telomeres and potential mediators of change can further enhance our understanding of malleability, mechanism, and clinical implications of telomere lengthening. Cancer Prev Res; 5(10); 1163-8. Ó2012 AACR.A rapidly growing body of research suggests that one snapshot measure of leukocyte telomere length is predictive of age-related physiologic decline, onset of diseases of aging, such as cancer and dementia, and early mortality (1-3). Thus, it is not surprising that when people learn about telomeres, one of the most common questions is "Can telomeres be lengthened?" The answer is not so simple. While the quick answer is "yes," it is one that requires qualification and explanation. Here, we review what is known so far about telomere lengthening in humans, with respect to stress reduction interventions in particular, and address important questions to understand the mechanisms of apparent telomere lengthening. Telomeres Shorten . . . and LengthenTelomeres tend to shorten slowly over years of aging but are active and dynamic, especially when examined over short periods. In the early studies of telomeres in single-celled organisms called protozoa, Blackburn and Greider observed, "telomeres are dynamic structures in vivo, being acted on by shortening and lengthening activities" (4). They discovered telomerase, an intracellular enzyme that has an RNA reverse transcriptase component that lengthens telomeres. Telomerase-mediated elongation of telomeres occurs through de novo synthes...

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Section: The Promise Of Interventionsmentioning

confidence: 99%

How “Reversible” Is Telomeric Aging?

Epel

2012

Cancer Prevention Research

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“…Accordingly, a high total ω-6/ω-3 PUFA ratio is associated with increased sensitivity to antigens by promoting inflammation (e.g., Calder, 2007Calder, , 2009Romieu et al, 2008). In mammals, a ratio above 3 is considered to induce not only inflammation, but also pro-oxidant production, thereby potentially further increasing oxidative stress in urban-dwelling animals (Simopoulos, 2002;Kiecolt-Glasera et al, 2013). Because the immune system responds to pollution (Romieu et al, 2008;Isaksson, 2015, and references therein), the dietary FA composition, and resultant FA compositions of blood and tissues (Austin, 1993;Pierce et al, 2005;McCue et al, 2009;BenHamo et al, 2011), can play a significant role on birds' health in the urban environment.…”

Section: Introductionmentioning

confidence: 99%

Species-Dependent Effects of the Urban Environment on Fatty Acid Composition and Oxidative Stress in Birds

et al. 2017

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Ecological impacts of urbanization include the loss of biodiversity and changes in species composition and population densities. However, how the urban environment affects fundamental physiological parameters is largely unknown. Here, we investigated physiological components related to health and nutrition, namely, plasma fatty acids (FA) and lipid peroxidation at inter-habitat and interspecific levels. Specifically, we compared four passerine bird species-the great tit (Parus major), the blue tit (Cyanistes caeruleus), the house sparrow (Passer domesticus), and the tree sparrow (P. montanus)-from urban and rural environments. Significant interactions between species and habitat were revealed for the majority of the FAs. Interestingly, the observed inter-habitat variation in FAs was frequently in opposite directions when comparing species from the two families (tits, Paridae; sparrows, Passeridae). These patterns suggest that sparrows and tits feed on different food sources, or modulate their FA metabolism differently, across the urban-rural gradient. By using canonical discriminant analyses (CDA), we further demonstrated species-specific signals in FA composition, with misclassification of species being <1% within habitats and <7% between habitats. Finally, the urban-rural FA differences between species and families were manifested in two indices of health. Firstly, urban blue tits had a higher total ω-6/ω-3 polyunsaturated FA ratio than rural conspecifics, which is believed to increase inflammatory responses. Secondly, urban sparrows of both species showed higher lipid peroxidation indices (indicating a higher susceptibility to lipid peroxidation if exposed to pro-oxidants), and consequently, a higher level of lipid peroxidation compared to their rural conspecifics. Collectively, the speciesand habitat-specific differences in plasma FA composition, which are linked to nutrition and metabolism, suggest that the urban environment affect tits and sparrows primarily via two different pathways-inflammation and oxidative stress, respectively,-with potential consequences for the health of urban populations.

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“…Adequate intake of omega-3 fatty acid supplements, to improve the balance of omega-3s to omega-6s, may slow a key biological process linked to aging. Among overweight middle-aged and older adults who took omega-3 supplements for 4 months, the ratio of their fatty acid consumption was altered in a way that helped preserve white blood cell telomeres, which normally shorten during the aging process (Kiecolt-Glaser et al 2013). The improved omega ratio also resulted in reduced oxidative stress, caused by free radicals in the blood by about 15% compared to those in the placebo group.…”

Section: Healthy Agingmentioning

confidence: 79%