Episode Notes:
In recent years, telomeres have garnered a lot of interest for their potential involvement in aging mechanisms. In fact, there are many scientists that believe aging, disease development, and overall health can all be linked to telomere length and the rate of telomere shortening.
Similar to aglets at the end of shoelaces, telomeres are protective caps on the ends of DNA strands contained within chromosomes. The result of damage and inevitable telomere shortening over time, is the vulnerability for genomic instability, programmed cell death, and biological aging.
In this episode, we’re going to address the mechanisms of telomere shortening and its implications on health and aging. We will also discuss the role of lifestyle factors on rates of shortening, including stress, exercise, sleep, and more. Finally, we will provide five actionable tips for improving your telomere health!
Age is just a number. Keep your telomeres healthy and you may be around for a long time.
TOPICS:
[1:43] What are telomeres?
[3:59] Telomere shortening
[5:40] Implications: Aging and disease
[7:50] Lifestyle factors influencing telomere health
[13:50] 5 ways to improve telomere health
What Are Telomeres?
In recent years, telomeres have garnered a lot of interest for their potential involvement in aging mechanisms. In fact, there are many scientists that believe aging, disease development, and overall health can all be linked to telomere health and function. Adding in the current pandemic and large body of data that has correlated various comorbidities and measures of poor health with worse COVID outcomes, it is important that we try to understand all the mechanisms of human health.
So what’s the bottom line?
Telomeres are possibly a strong indicator of human health and aging.
1. What are telomeres?
2. Implications of telomere shortening
3. Lifestyle factors and telomere health
What are telomeres?
If you don’t remember the fundamentals from biology class, bear with me and I will try to simplify this as much as possible. As we know, living organisms are composed of cells. Within each cell are different components, including the nuclei, mitochondria, cytoplasm, and more. We’re focused on the nucleus.
Inside of the nuclei of human cells are chromosomes with contain our genetic code, or DNA, which essentially functions as our most fundamental programming [1,2]. Each chromosome forms a unique ‘X’ shape in which the ‘arms’ extending outwards are actually DNA strands. And that leads us the telomeres, which are specialized structures that create a protective cap at the end of each DNA strand [1,3].
So what is a telomere? Well, it is actually formed from repeated genetic code that is added onto the end of the DNA strand. The telomeres – taking the standard form of base pairs – are not essential; they are extra. Therefore, telomeres do not contribute to cellular functionality or gene expression.
So what purpose do they serve and why are they important? I think the best way to address these questions is with an analogy.
Think of the DNA strands on your chromosomes like a shoelace. When a shoelace is brand new or well-maintained, it features a hard plastic coating at the end, called an aglet. As I am sure we have all experienced, few things are as annoying as shoelaces without an aglet, because they help to protect from fraying, unraveling, and damage to the shoelace.
But over time, aglets accrue damage through usual wear and tear, or perhaps a traumatic injury may cause it to completely break (or if you are me, you play with it too much and eventually rip it off). And what is the result? The shoelace becomes damaged, it no longer functions properly, and in many cases, the shoelaces are thrown away.
It turns out that telomeres are very similar to aglets. If they are shortened beyond a particular threshold, they fail to sufficiently protect DNA strands. As you might expect, exposed DNA can become damaged which may lead to serious health issues. Specifically, research indicates that shortened telomeres promote biological aging (referred to as senescence), programmed cell death (referred to as apoptosis), and genome instability (which is the vulnerability of genetic code to be damaged and altered) [4, 5].
Alright, so we know that telomeres are protective caps on our chromosomes and that they shorten over time. So, the next question, what shortens telomeres?
Unfortunately for those who want to live forever, telomere shortening is an inevitable part of the natural aging process [6]. Every time cell division occurs – which is very frequently – a chromosome must be replicated. However, during replication, it is impossible for telomeres to replicate the entire DNA strand. Therefore, a few base pairs from the telomere are lost with each division.
Because the telomere is composed of additional genetic code, this loss of base pairs does not influence cellular functionality or gene expression. But, as they are gradually shortened throughout life, they must eventually reach a breaking point, referred to as ‘telomeric brink.’ Research has found that reaching this point is correlated with a high risk of imminent death [7].
Therefore, dying of old age may actually be akin to dying of shortened telomeres.
So if we want to live longer and delay the inevitable, our best hope may be to slow down the rate of telomere shortening. Currently, scientific research is mounting evidence that genetic, epigenetic, and lifestyle factors may strongly influence the rate of telomere shortening [4]. And that’s what we are going to talk about next.
But first, just a reminder that if you are unfamiliar with the differences between genetics and epigenetics, I recommend that you check out episode 020!
Implications of telomere shortening
Let’s start this section off with some math for context. Research shows that human telomeres typically fall within a range of 5-15kb (kilobase), with 5kb corresponding to the telomeric brink [7-10]. For reference, a kilobase is a unit of measurement equal to 1000 base pairs of DNA. Therefore, humans may have up to 15,000 base pairs in their telomeres, although the average length at birth is closer to 10,000 base pairs.
As mentioned previously, what is most important is the rate of telomere shortening. It turns out that telomere shortening in humans averages around 70 base pairs per year [10]. Based on this rate, a human born with 10,000 base pairs would have a life expectancy of about 71 years (5,000 base pairs lost until telomeric brink divided by 70 base pairs lost per year). Meanwhile, someone with 15,000 base pairs at birth would have double the life expectancy, about 143 years, because they would need to lose 10,000 base pairs until the telomeric brink.
This is where it gets interesting. Mice are born with telomere lengths around 50kb! Yes, mice have telomeres that are up to five times as long as humans, yet they have drastically shorter life spans. Again, the key is the rate of shortening. In fact, telomere shortening in mice is around 100 times faster than in humans, around 7,000 base pairs per year! [10]
In the quest to optimize longevity and age gracefully, it may come down to maintaining telomere length that is equal to or longer than the average length in a given age demographic. Research enhances this notion, showing that increasing prevalence of age-related diseases and premature death are more frequently observed in individuals with telomeres that are shorter than average for their specific age group, and not necessarily a standard telomere length [4].
As we have seen, rates of telomere shortening strongly indicate rates of biological aging. But the impact of telomere shortening on disease onset may be just as significant, if not more.
Age-related diseases such as coronary heart disease and heart failure [11-14], cancer [15-18], diabetes [19], and osteoporosis [20] have all been associated with accelerated telomere shortening. And as always, you can find links to scientific studies – all 45 in this episode alone – on learniiperform.com.
Even with increasing bodies of evidence relating accelerated telomere shortening with negative health outcomes, potential implications are not yet fully understood, although expected to be substantial [17, 21, 22]. But what we do know, according to scientific literature, is that telomere health – both the telomere length and rate of shortening – is very important for overall health!
Lifestyle Factors and Telomere Health
To review, we can conclude that if you can slow down the rate of telomere shortening, it is more likely that you will increase longevity and reduce disease risk. The million dollar question: what lifestyle factors influence telomere shortening?
We are going to cover five different factors: stress, exercise, sleep, fasting, and omega-3s.
But please remember that scientific research is ongoing and evolving. Although these provide great promise, researchers are still seeking to understand the mechanisms behind telomere shortening and human aging. Unfortunately, I cannot promise that you will live forever, sorry.
Stress
Increased levels of both biological and psychological stress have been consistently associated with accelerated telomere shortening [4]. More precisely, literature points that oxidative stress induced through various factors – genetic, epigenetic, and environmental – appears to be the most significant contributor [8, 9].
What might these factors entail? The most commonly addressed in literature include smoking [23, 24], obesity [23, 25], lack of exercise [26], socioeconomic status [27], and subtelomeric DNA methylation and epigenetics [28, 29].
You know what they say: “stress ages you,” and this may be completely true. Let’s consider some alarming studies.
In 2004, a study comparing mothers caring for chronically ill children and mothers caring for healthy children found that the accelerated aging due to perceived stress was up to 17 years [5, 30]. In 2019, a study of 80,000 adults correlated socioeconomic status to shorter telomere lengths [27]. This considered neighborhood socioeconomic status as well as education-based status.
Exercise
Once again, our good friend exercise comes up in discussion as being important to health and longevity. Although research is ongoing, there is strong evidence that exercise may have protective and restorative effects on health [31].
Let’s start with some powerful data from a 2017 study. A randomized sample of close to 6,000 U.S. adults was assessed for telomere length and self-reported physical activity levels [32]. The results: the biological age of highly active adults (men and women) was, on average, nine years younger than sedentary adults.
Another interesting study from 2008 using over 2,000 twin volunteers demonstrated that active individuals have significantly longer telomeres than non-exercisers, after accounting for age and sex [33]. For more studies that have associated physical activity with longer telomeres, I encourage you to seek out the references on my website or search on PubMed [5, 34, 35].
Sleep
One key reason that sleep may be so important is that oxidative stress accumulates in sleep-deprived individuals [36]. For a whole episode on the dangers of sleep deprivation, I encourage you to listen to Learn II Perform episode 005.
A study in 2011 on women under 50 found that those who slept six hours or less per night experienced the equivalent telomere shortening of nine years when compared to a group that slept nine hours or more each night [5, 37]. While nine or more hours a night may be unrealistic for most, this still serves of strong evidence that sleep may have a significant influence on telomere health.
In 2012, a study found that men who averaged five hours or less each night, compared to men sleeping seven hours or more, had telomeres shortened by 6% [5, 38]. Again, this is a statistically significant result that further promotes the need for sufficient sleep.
Fasting
Fasting, or time-restricted feeding, has been strongly linked to increased longevity and protection against age-related diseases. Two key pathways come into play, mechanistic Target of Rapamycin (or mTOR) and autophagy [39]. For those unfamiliar with these, I urge you to check out episode 006 on fasting for a complete review, because I will not go into detail in this episode.
But basically, when feeding, mTOR is activated, a process that regulates cell growth and proliferation. Constant feeding promotes constant mTOR activation. More mTOR means an increased rate of cell division, and therefore, shorter telomeres. Alternatively, fasting suppresses the mTOR pathway, reducing the rate of cell division. In addition, fasting-induced autophagy removes dead and senescent cells.
The idea is that eating less frequently will reduce the rate of cellular divisions, and thus reduce the rate of telomere shortening. Scientific literature is lacking in this area, but let’s look at what has been studied.
In a 2019 study on planarians (a type of flatworm), it was found that a greater prevalence of stem cells with long telomeres may have resulted from fasting-induced mTOR down-regulation [40]. Additionally, the researchers found that the maximum telomere length was actually greater after this down-regulation.
Similar results came from a 2020 study that was also performed with fasted planarians [41]. They discovered that fasting may rejuvenate stem cells, meanwhile the frequency of longer telomeres and the maximum telomere length in stem cells both increased with fasting.
Omega 3s
Finally, we will close off with Omega-3s. While nutrition is certainly a key contributor to health, substantial evidence points directly at omega-3s.
Two different studies associated reduced rates of telomere shortening with omega-3 supplementation, attributed to the reduction in oxidative stress and inflammation, and improvements in omega 6:3 ratios [42, 43].
With average omega-3 consumption drastically below recommended levels and a high prevalence of omega-6 fatty acids in processed foods and the Standard American Diet, omega-3 supplementation may be one of the easiest tools to implement in pursuit of improved telomere health [44, 45].
So What Can You Do
Since I have not measured my own telomeres, I do not have much to add in terms of personal experience. As far as my own efforts to optimize telomere health, it is simply part of my holistic approach to human optimization. The pieces of advice mentioned here align directly with my own efforts at maximizing longevity and vitality.
But before reviewing some actionable steps, there is one more valuable piece of information worth covering. Although telomere shortening is more or less unavoidable, there is a potential mechanism to prevent and/or reverse telomere shortening. This is done through the activation of a special enzyme called telomerase, which adds base pairs back onto telomeres [5].
At this time, large amounts of research are undergoing to determine how we may be able to activate telomerase, but it appears to be something to look forward to in the future. For now, evidence suggests that telomerase activation is often inhibited by biological and psychological stress [5]. Therefore, by reducing stress in your life, you may be able to better activate telomerase to preserve and potentially grow your telomeres!
With that, here are five actionable ways to improve telomere health:
1. Reduce Stress
As best as you can, try to reduce or manage your stress. Some examples of stress-relieving activities include meditation, spending time in nature, spending time with loved ones, journaling, reading, writing in a gratitude journal, exercising, and many other things. Make your health and wellbeing a priority.
2. Exercise regularly
No surprise here. Try to exercise regularly, ideally between 90 and 150 minutes of moderate-to-high intensity each week.
3. Improve your sleep
Both sleep quantity and quality are critical. Focus on consistent sleep/wake timing, reducing light and screen exposure before bed, and aiming for at least 7 hours a night. For a comprehensive set of sleep recommendations, refer to Learn II Perform episode 005!
4. Try intermittent fasting
Experiment with some form of regular intermittent fasting to suppress the mTOR pathway and activate autophagy.
5. Supplement with Omega-3s
I frequently recommend omega-3 supplementation for a variety of reasons, and this adds to the reasoning. Unless your diet is very high in seafood and very low in processed foods, nut, seed and plant oils, you could probably benefit from Omega-3 supplementation.
And that’s a great place to start. Just remember, age is just a number. You have more control over your health and your longevity than you may think. It is never too late to take control of your health. Keep your telomeres healthy and they will keep you healthy!
As Hugh Hefner once said, “I truly believe that age – if you’re healthy – age is just a number” [46].
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References
[1] Pathak I, Bordoni B. Genetics, Chromosomes. [Updated 2021 Feb 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557784/
[2] Stewart F. (2010). The anatomy of a chromosome. The Ulster medical journal, 79(3), 110–113. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284714/
[3] Saretzki G. (2018). Telomeres, Telomerase and Ageing. Sub-cellular biochemistry, 90, 221–308. https://doi.org/10.1007/978-981-13-2835-0_9
[4] Shammas M. A. (2011). Telomeres, lifestyle, cancer, and aging. Current opinion in clinical nutrition and metabolic care, 14(1), 28–34. https://doi.org/10.1097/MCO.0b013e32834121b1
[5] Starkweather, A. R., Alhaeeri, A. A., Montpetit, A., Brumelle, J., Filler, K., Montpetit, M., Mohanraj, L., Lyon, D. E., & Jackson-Cook, C. K. (2014). An integrative review of factors associated with telomere length and implications for biobehavioral research. Nursing research, 63(1), 36–50. https://doi.org/10.1097/NNR.0000000000000009
[6] Andrews, N. P., Fujii, H., Goronzy, J. J., & Weyand, C. M. (2010). Telomeres and immunological diseases of aging. Gerontology, 56(4), 390–403. https://doi.org/10.1159/000268620
[7] Steenstrup, T., Kark, J. D., Verhulst, S., Thinggaard, M., Hjelmborg, J., Dalgård, C., Kyvik, K. O., Christiansen, L., Mangino, M., Spector, T. D., Petersen, I., Kimura, M., Benetos, A., Labat, C., Sinnreich, R., Hwang, S. J., Levy, D., Hunt, S. C., Fitzpatrick, A. L., Chen, W., … Aviv, A. (2017). Telomeres and the natural lifespan limit in humans. Aging, 9(4), 1130–1142. https://doi.org/10.18632/aging.101216
[8] Srinivas, N., Rachakonda, S., & Kumar, R. (2020). Telomeres and Telomere Length: A General Overview. Cancers, 12(3), 558. https://doi.org/10.3390/cancers12030558
[9] Fouquerel, E., Lormand, J., Bose, A., Lee, H.-T., Kim, G. S., Li, J., Sobol, R. W., Freudenthal, B. D., Myong, S., & Opresko, P. L. (2016). Oxidative guanine base damage regulates human telomerase activity. Nature Structural & Molecular Biology, 23(12), 1092–1100. https://doi.org/10.1038/nsmb.3319
[10] Whittemore, K., Vera, E., Martínez-Nevado, E., Sanpera, C., & Blasco, M. A. (2019). Telomere shortening rate predicts species life span. Proceedings of the National Academy of Sciences, 116(30), 15122–15127. https://doi.org/10.1073/pnas.1902452116
[11] Fitzpatrick, A. L., Kronmal, R. A., Gardner, J. P., Psaty, B. M., Jenny, N. S., Tracy, R. P., Walston, J., Kimura, M., & Aviv, A. (2007). Leukocyte telomere length and cardiovascular disease in the cardiovascular health study. American journal of epidemiology, 165(1), 14–21. https://doi.org/10.1093/aje/kwj346
[12] Brouilette, S. W., Moore, J. S., McMahon, A. D., Thompson, J. R., Ford, I., Shepherd, J., Packard, C. J., Samani, N. J., & West of Scotland Coronary Prevention Study Group (2007). Telomere length, risk of coronary heart disease, and statin treatment in the West of Scotland Primary Prevention Study: a nested case-control study. Lancet (London, England), 369(9556), 107–114. https://doi.org/10.1016/S0140-6736(07)60071-3
[13] Zee, R. Y., Michaud, S. E., Germer, S., & Ridker, P. M. (2009). Association of shorter mean telomere length with risk of incident myocardial infarction: a prospective, nested case-control approach. Clinica chimica acta; international journal of clinical chemistry, 403(1-2), 139–141. https://doi.org/10.1016/j.cca.2009.02.004
[14] van der Harst, P., van der Steege, G., de Boer, R. A., Voors, A. A., Hall, A. S., Mulder, M. J., van Gilst, W. H., van Veldhuisen, D. J., & MERIT-HF Study Group (2007). Telomere length of circulating leukocytes is decreased in patients with chronic heart failure. Journal of the American College of Cardiology, 49(13), 1459–1464. https://doi.org/10.1016/j.jacc.2007.01.027
[15] Wu, X., Amos, C. I., Zhu, Y., Zhao, H., Grossman, B. H., Shay, J. W., Luo, S., Hong, W. K., & Spitz, M. R. (2003). Telomere dysfunction: a potential cancer predisposition factor. Journal of the National Cancer Institute, 95(16), 1211–1218. https://doi.org/10.1093/jnci/djg011
[16] McGrath, M., Wong, J. Y., Michaud, D., Hunter, D. J., & De Vivo, I. (2007). Telomere length, cigarette smoking, and bladder cancer risk in men and women. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 16(4), 815–819. https://doi.org/10.1158/1055-9965.EPI-06-0961
[17] Chin, L., Artandi, S. E., Shen, Q., Tam, A., Lee, S. L., Gottlieb, G. J., Greider, C. W., & DePinho, R. A. (1999). p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis. Cell, 97(4), 527–538. https://doi.org/10.1016/s0092-8674(00)80762-x
[18] Meeker A. K. (2006). Telomeres and telomerase in prostatic intraepithelial neoplasia and prostate cancer biology. Urologic oncology, 24(2), 122–130. https://doi.org/10.1016/j.urolonc.2005.11.002
[19] Sampson, M. J., Winterbone, M. S., Hughes, J. C., Dozio, N., & Hughes, D. A. (2006). Monocyte telomere shortening and oxidative DNA damage in type 2 diabetes. Diabetes care, 29(2), 283–289. https://doi.org/10.2337/diacare.29.02.06.dc05-1715
[20] Valdes, A. M., Richards, J. B., Gardner, J. P., Swaminathan, R., Kimura, M., Xiaobin, L., Aviv, A., & Spector, T. D. (2007). Telomere length in leukocytes correlates with bone mineral density and is shorter in women with osteoporosis. Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA, 18(9), 1203–1210. https://doi.org/10.1007/s00198-007-0357-5
[21] Shen Z. (2011). Genomic instability and cancer: an introduction. Journal of molecular cell biology, 3(1), 1–3. https://doi.org/10.1093/jmcb/mjq057
[22] De Lange T. (2005). Telomere-related genome instability in cancer. Cold Spring Harbor symposia on quantitative biology, 70, 197–204. https://doi.org/10.1101/sqb.2005.70.032
[23] Valdes, A. M., Andrew, T., Gardner, J. P., Kimura, M., Oelsner, E., Cherkas, L. F., Aviv, A., & Spector, T. D. (2005). Obesity, cigarette smoking, and telomere length in women. Lancet (London, England), 366(9486), 662–664. https://doi.org/10.1016/S0140-6736(05)66630-5
[24] Astuti, Y., Wardhana, A., Watkins, J., Wulaningsih, W., & PILAR Research Network (2017). Cigarette smoking and telomere length: A systematic review of 84 studies and meta-analysis. Environmental research, 158, 480–489. https://doi.org/10.1016/j.envres.2017.06.038
[25] Nordfjäll, K., Eliasson, M., Stegmayr, B., Melander, O., Nilsson, P., & Roos, G. (2008). Telomere length is associated with obesity parameters but with a gender difference. Obesity (Silver Spring, Md.), 16(12), 2682–2689. https://doi.org/10.1038/oby.2008.413
[26] Cherkas, L. F., Hunkin, J. L., Kato, B. S., Richards, J. B., Gardner, J. P., Surdulescu, G. L., Kimura, M., Lu, X., Spector, T. D., & Aviv, A. (2008). The association between physical activity in leisure time and leukocyte telomere length. Archives of internal medicine, 168(2), 154–158. https://doi.org/10.1001/archinternmed.2007.39
[27] Alexeeff, S. E., Schaefer, C. A., Kvale, M. N., Shan, J., Blackburn, E. H., Risch, N., Ranatunga, D. K., Jorgenson, E., Hoffmann, T. J., Sakoda, L. C., Quesenberry, C. P., & Van Den Eeden, S. K. (2019). Telomere length and socioeconomic status at neighborhood and individual levels among 80,000 adults in the Genetic Epidemiology Research on Adult Health and Aging cohort. Environmental Epidemiology, 3(3), e049. https://doi.org/10.1097/ee9.0000000000000049
[28] Steinert, S., Shay, J. W., & Wright, W. E. (2004). Modification of subtelomeric DNA. Molecular and cellular biology, 24(10), 4571–4580. https://doi.org/10.1128/mcb.24.10.4571-4580.2004
[29] Benetti, R., García-Cao, M., & Blasco, M. A. (2007). Telomere length regulates the epigenetic status of mammalian telomeres and subtelomeres. Nature genetics, 39(2), 243–250. https://doi.org/10.1038/ng1952
[30] Epel, E. S., Blackburn, E. H., Lin, J., Dhabhar, F. S., Adler, N. E., Morrow, J. D., & Cawthon, R. M. (2004). Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America, 101(49), 17312–17315. https://doi.org/10.1073/pnas.0407162101
[31] Arsenis, N. C., You, T., Ogawa, E. F., Tinsley, G. M., & Zuo, L. (2017). Physical activity and telomere length: Impact of aging and potential mechanisms of action. Oncotarget, 8(27), 45008–45019. https://doi.org/10.18632/oncotarget.16726
[32] Tucker, L. A. (2017). Physical activity and telomere length in U.S. men and women: An NHANES investigation. Preventive Medicine, 100, 145–151. https://doi.org/10.1016/j.ypmed.2017.04.027
[33] Cherkas, L. F., Hunkin, J. L., Kato, B. S., Richards, J. B., Gardner, J. P., Surdulescu, G. L., Kimura, M., Lu, X., Spector, T. D., & Aviv, A. (2008). The association between physical activity in leisure time and leukocyte telomere length. Archives of internal medicine, 168(2), 154–158. https://doi.org/10.1001/archinternmed.2007.39
[34] Denham, J., Nelson, C. P., O’Brien, B. J., Nankervis, S. A., Denniff, M., Harvey, J. T., Marques, F. Z., Codd, V., Zukowska-Szczechowska, E., Samani, N. J., Tomaszewski, M., & Charchar, F. J. (2013). Longer leukocyte telomeres are associated with ultra-endurance exercise independent of cardiovascular risk factors. PloS one, 8(7), e69377. https://doi.org/10.1371/journal.pone.0069377
[35] Du, M., Prescott, J., Kraft, P., Han, J., Giovannucci, E., Hankinson, S. E., & De Vivo, I. (2012). Physical activity, sedentary behavior, and leukocyte telomere length in women. American journal of epidemiology, 175(5), 414–422. https://doi.org/10.1093/aje/kwr330
[36] Atrooz, F., & Salim, S. (2020). Sleep deprivation, oxidative stress and inflammation. Advances in protein chemistry and structural biology, 119, 309–336. https://doi.org/10.1016/bs.apcsb.2019.03.001
[37] Liang, G., Schernhammer, E., Qi, L., Gao, X., De Vivo, I., & Han, J. (2011). Associations between rotating night shifts, sleep duration, and telomere length in women. PloS one, 6(8), e23462. https://doi.org/10.1371/journal.pone.0023462
[38] Jackowska, M., Hamer, M., Carvalho, L. A., Erusalimsky, J. D., Butcher, L., & Steptoe, A. (2012). Short sleep duration is associated with shorter telomere length in healthy men: findings from the Whitehall II cohort study. PloS one, 7(10), e47292. https://doi.org/10.1371/journal.pone.0047292
[39] Saxton, R. A., & Sabatini, D. M. (2017). mTOR Signaling in Growth, Metabolism, and Disease. Cell, 168(6), 960–976. https://doi.org/10.1016/j.cell.2017.02.004
[40] Iglesias, M., Felix, D. A., Gutiérrez-Gutiérrez, Ó., De Miguel-Bonet, M., Sahu, S., Fernández-Varas, B., Perona, R., Aboobaker, A. A., Flores, I., & González-Estévez, C. (2019). Downregulation of mTOR Signaling Increases Stem Cell Population Telomere Length during Starvation of Immortal Planarians. Stem cell reports, 13(2), 405–418. https://doi.org/10.1016/j.stemcr.2019.06.005
[41] González-Estévez, C., & Flores, I. (2020). Fasting for stem cell rejuvenation. Aging, 12(5), 4048–4049. https://doi.org/10.18632/aging.102912
[42] Epel, E. (2012). How “Reversible” Is Telomeric Aging? Cancer Prevention Research, 5(10), 1163–1168. https://doi.org/10.1158/1940-6207.capr-12-0370
[43] Farzaneh-Far, R., Lin, J., Epel, E. S., Harris, W. S., Blackburn, E. H., & Whooley, M. A. (2010). Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease. JAMA, 303(3), 250–257. https://doi.org/10.1001/jama.2009.2008
[44] Vannice, G., & Rasmussen, H. (2014). Position of the academy of nutrition and dietetics: dietary fatty acids for healthy adults. Journal of the Academy of Nutrition and Dietetics, 114(1), 136–153. https://doi.org/10.1016/j.jand.2013.11.001
[45] Papanikolaou, Y., Brooks, J., Reider, C., & Fulgoni, V. L., 3rd (2014). U.S. adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003-2008. Nutrition journal, 13, 31. https://doi.org/10.1186/1475-2891-13-31
[46] Hefner, H. (n.d.). Hugh Hefner Quotes. Quotefancy. Retrieved from https://quotefancy.com/quote/1232088/Hugh-Hefner-I-truly-believe-that-age-if-you-re-healthy-age-is-just-a-number#:~:text=Hugh%20Hefner%20Quote%3A%20%E2%80%9CI%20truly,age%20is%20just%20a%20number.%E2%80%9D
