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Lifestyle effects on telomeric shortening as a factor associated with biological aging: A systematic review



BACKGROUND: Telomeres are structures located at the chromosome ends, whose function is protecting DNA from attrition caused during cell division. Telomeric length serves as a mitotic clock, activating senescence and cellular cycle arrest when it reaches a shortening limit, which causes aging. Lifestyle is a factor that can affect telomeric shortening. Unhealthy habits have been linked to accelerated telomeric shortening, while healthy lifestyles are known to reduce this process and slow down aging. Current community has expressed an interest in improving lifestyle choices; however, an increase in unhealthy habits and chronic stressors have been seen. OBJECTIVE: This review aims to show the influence that different lifestyles have on telomeric length. METHODS: The review was carried out following the PRISMA statement in three databases. Twenty-eight research articles and nine review articles were reviewed, identifying six main lifestyles habits. RESULTS: Regular moderate-vigorous physical activity, dietary patterns rich in vegetables and antioxidants, and the stress control techniques were related to greater telomeric lengths and improvements in the oxidative response by reducing the levels of oxidative stress markers. On the contrary, stress, obesity, smoking, and alcoholism showed a negative effect of shorter telomeres, which can be a factor of early aging. CONCLUSION: The previous demonstrates the influences of lifestyles on telomere shortening rates and aging, therefore they should be considered as areas of interest for future research, and personal and community health improvement.
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Nutrition and Healthy Aging 1 (2020) 1–9
DOI 10.3233/NHA-200096
IOS Press
Lifestyle effects on telomeric shortening as
a factor associated with biological aging:
A systematic review
Raul Enrique Espinosa-Otaloraa, Jairo Fl´
orez-Villamizarc, Clara In´
es Esteban-P´
Maribel Forero-Castroband Johana Mar´
aEscuela de Ciencias Biol´ogicas. Grupo de investigaci´on en Ciencias Biom´edicas (GICBUPTC). Universidad
Pedag´ogica y Tecnol´ogica de Colombia, Tunja – Colombia
bMaestr´ıa en Ciencias Biol´ogicas. Universidad Pedag´ogica y Tecnol´ogica de Colombia, Tunja - Colombia9
cEscuela de Ciencias de la Educaci´on. Grupo de investigaci´on en Tendencias Pedag´ogicas. Universidad
Pedag´ogica y Tecnol´ogica de Colombia, Tunja – Colombia
dDepartamento Biogenetica reproductiva. invitro, Bogota - Colombia
BACKGROUND: Telomeres are structures located at the chromosome ends, whose function is protecting DNA from attrition
caused during cell division. Telomeric length serves as a mitotic clock, activating senescence and cellular cycle arrest when
it reaches a shortening limit, which causes aging. Lifestyle is a factor that can affect telomeric shortening. Unhealthy habits
have been linked to accelerated telomeric shortening, while healthy lifestyles are known to reduce this process and slow down
aging. Current community has expressed an interest in improving lifestyle choices; however, an increase in unhealthy habits
and chronic stressors have been seen.
OBJECTIVE: This review aims to show the influence that different lifestyles have on telomeric length.20
METHODS: The review was carried out following the PRISMA statement in three databases. Twenty-eight research articles
and nine review articles were reviewed, identifying six main lifestyles habits.
RESULTS: Regular moderate-vigorous physical activity, dietary patterns rich in vegetables and antioxidants, and the stress
control techniques were related to greater telomeric lengths and improvements in the oxidative response by reducing the
levels of oxidative stress markers. On the contrary, stress, obesity, smoking, and alcoholism showed a negative effect of
shorter telomeres, which can be a factor of early aging.
CONCLUSION: The previous demonstrates the influences of lifestyles on telomere shortening rates and aging, therefore
they should be considered as areas of interest for future research, and personal and community health improvement.
Keywords: Telomere, telomeric shortening, aging, lifestyle
ACEs Adverse childhood experiences31
AGEs Advanced Glycation End-products32
DNA Deoxyribonucleic Acid
Corresponding author: Johana Marin Suarez - Maestr´
ıa en
Ciencias Biol´
ogicas, Tunja – Colombia, Colombia. Tel.: +57
3168268376; E-mail:
ESTHER Epidemiological Study on the 33
Chances of Prevention, Early 34
Recognition, and Optimized 35
Treatment of Chronic Diseases 36
in the Older Population 37
HPA Hypothalamic-Pituitary 38
-Adrenal Axis 39
HPFS Health Professionals 40
Follow-up Study
ISSN 2451-9480/20/$35.00 © 2020 – IOS Press and the authors. All rights reserved
This article is published online with Open Access and distributed under the terms of the Creative Commons Attribution Non-Commercial License (CC BY-NC 4.0).
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2R.E. Espinosa-Otalora et al. / A systematic review
LTL Leukocyte Telomere Length41
MDD Major Depressive Disorder42
NHANES National Health and Nutrition43
Examination Survey44
NO Nitrogen Oxides45
PBMC Peripheral Blood Mononuclear Cells46
pb Pares de Bases47
PCR Polymerase Chain Reaction Technique48
PRISMA Preferred Reporting Items for49
Systematic reviews and50
rLTL relative Leukocyte Telomere Length52
SAM Sympathetic-Adrenal-Medullary53
SOD Superoxide Dismutase55
1. Introduction
Telomeres are nucleoprotein structures located at57
the ends of every chromosome. They are made of non-
coding DNA, which are responsible for the recogni-59
tion and protection of this part of the chromosome
[1, 2]. They consist of a sequence of DNA tandem61
repeats (TTAGGG) and are associated with Shelterin62
complex proteins. These proteins form a loop-shaped63
structure known as the Telomeric Loop at the end64
of the chromosome, which helps prevent erroneous
DNA damage pathway activation [3, 4]. Telomeres66
also act as a mitotic clock that determines the replica-
tive capacity of the cell. With each division, cell life
erosion can occur [5, 6]. This erosion is caused by
the inability of DNA-polymerase to fully replicate70
linear DNA, which is called end replication problem71
[7]. Once the telomere reaches a critical shortening72
point, the Hayflick limit, the senescence and cell73
cycle arrest pathways are activated. The proliferative
cell capacity and tissue recovery are limited, which75
causes aging [3, 8, 9]. Likewise, telomeres have mec-
hanisms to lengthen themselves and reduce erosion77
effects caused by cell division; the main one is the
Telomerase enzyme [1]. This reverse transcriptase79
enzyme is responsible for adding de-novo telomeric80
repeats using a homologous RNA template, which81
compensates for erosion caused by terminal replica-82
tion problems [1, 2]. However, this enzyme is exp-83
ressed primarily during embryonic development and84
after birth. It is active in the male germ line, stem cell,
and certain types of cancer [4, 10].
In addition to erosion caused by cell division,
both genetic and environmental factors can affect
the length of the telomere. Telomere shortening is 89
evident in different degrees, and they are indicative 90
of biological aging [6, 10]. Oxidative stress, for exam- 91
ple, accelerates telomere shortening due to telomeric 92
DNA guanine oxidation, which activates DNA dam- 93
age response by cleavage. Consequently, telomere 94
segments are lost in a greater amount than in cell 95
division [3, 4]. Another main factor to telomere sho- 96
rtening has been lifestyle choices [11]. Unhealthy 97
habits and chronic stressors have been linked to an 98
accelerated shortening of telomeres [6]. On the other 99
hand, healthy lifestyles have been shown to delay 100
shortening and even lengthen the telomere, which is 101
reflected in slower biological aging [12, 13]. 102
PBMC (peripheral blood mononuclear cells) are a 103
type of proliferating cells in which replication leads to 104
constant telomere wear, which allows good correla- 105
tions between telomere length and aging, in addition 106
PBMC present a high correlation with the telom- 107
ere length in other tissues, for this reason they are 108
a useful cell type for the analysis of the rate of 109
aging in humans [14, 15]. However, the effect of spe- 110
cific diseases, a specific tissue aging, or cell-specific 111
adaptations can be better reflected by the telomeric 112
lengths of different cell types. Regarding the analy- 113
sis of the aging rate in humans, PBMC (peripheral 114
blood mononuclear cells) allow obtaining good cor- 115
relations between telomere length and aging, Because 116
it is an easily accessible sample (peripheral venipunc- 117
ture), Furthermore, blood is a tissue that is in contact 118
with all the other tissues of the body, essential for the 119
transport of oxygen, nutrients and metabolic waste, 120
and it has been described that there is a correlation 121
between the telomeric length of peripheral lympho- 122
cytes and the telomeric length of various types of 123
tissues.. PBMC are a type of proliferating cells in 124
which replication leads to a constant shortening of 125
telomeres; however, the telomeric lengths of differ- 126
ent cell types may better reflect the effect of specific 127
diseases, the aging of a specific tissue, or specific 128
adaptations of the cell. [14]. 129
Currently, there has been a growing interest in 130
improving the quality of life and slowing down aging. 131
Telomere shortening and its role in aging has gained 132
recognition since the 1990s [15]. Nonetheless, the 133
increase in unhealthy lifestyles and other chronic 134
stressors, such as living in big cities, have raised the 135
need to improve the overall health of the commu- 136
nity. Because of this, the objective of this review is 137
to demonstrate the influence that current healthy and 138
unhealthy lifestyles have on telomeric length since it 139
is a biological aging factor.
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R.E. Espinosa-Otalora et al. / A systematic review 3
2. Methodology140
The review was carried out following the PRISMA141
(Preferred Reporting Items for Systematic reviews
and Meta-Analyzes) statement, taking into account143
five inclusion criteria: (1) research or review articles144
in Spanish or English; (2) studies carried out among145
healthy patients or those suffering from pathologies146
related to lifestyle or aging; (3) works related to147
the effect of lifestyles or lifestyle intervention tests
on telomeric length; (4) articles with information
on telomeric length as an effector of cell aging; (5)
publications between the years 2008-2018. Based on
the criteria, articles were searched for on PubMed152
(NCBI), ScienceDirect, and Scielo databases, using153
key descriptors: telomere length, aging, and lifestyle.154
Once the articles were selected, according to the
screening and selection process proposed in the156
PRISMA statement, the information relevant to cri-
teria 3 and 4 was extracted in order to develop this158
review. Additionally, we tabulated the information159
based in the year of publication, applicability to
everyday life, and the journal ranking.161
A total of 1,596 records were found in the three 162
databases (142 from PubMed, 1,432 from ScienceDi- 163
rect, and 22 from Scielo). Only 830 of the records 164
were published between 2008–2018. Furthermore, 165
125 articles (51 from PubMed, 71 from ScienceDi- 166
rect, and 3 from Scielo) that met criteria (1) and (2) 167
indicated the information we were looking for in the 168
title. Of the previous 125 articles, 67 were chosen 169
after reading the abstract (37 from PubMed, 28 from 170
ScienceDirect, and 2 from Scielo), which fulfilled cri- 171
teria (2), (3) and (4). Finally, 36 research articles were 172
chosen after reading the full text. We finally decided 173
on 28 articles that included all of the criteria (18 from 174
PubMed, 9 from ScienceDirect, and 1 from Scielo). 175
Additionally, 9 review articles (2 from PubMed, 6 176
from ScienceDirect, and 1 from Scielo) were taken 177
into account for theoretical support (Fig. 1). 178
3. Results and discussion 179
The research articles were grouped according to 180
lifestyle. In all of the articles that took into account 181
Fig. 1. Flowchart of the article selection process.
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4R.E. Espinosa-Otalora et al. / A systematic review
age and/or a follow-up, a negative relationship be-182
tween age and telomere length was reported with
varying effects according to lifestyle. Nineteen of184
the articles focused on the effect of healthy lifestyles185
on telomere length, which included physical activity186
(7 articles), diet and nutrient consumption (5 arti-
cles), and psychological stress control (7 articles).188
The previous habits had a positive correlation with189
telomere length and, in some cases, lengthened the190
telomeres over time (Supplementary Tables 1, 2 and
3). Likewise, one of these articles demonstrated a192
significant effect on telomere length through a com-193
prehensive lifestyle intervention based on physical
activity, diet, stress control, and social support. In195
comparison to the control group, the lifestyle changes
yielded increased telomerase activity and lengthening197
over time [13]. On the other hand, 6 of the articles198
focused on unhealthy lifestyle habits, such as smok-
ing, alcohol consumption, and sedentarism. Only 3 of200
the articles focused on psychological stress regarding201
adverse events and/or psychological syndromes, and202
they showed a negative effect on telomeres (telomere203
shortening) in comparison to healthy controls (Sup-204
plementary Table 4).205
4. Healthy lifestyles and their effect on the
4.1. Physical activity
Regular physical activity has been shown to have a
positive effect on telomere length. Moderate levels of
physical activity have been studied extensively and211
are most closely related to longer telomere lengths212
independent of other possible confounding factors213
such as: Body Mass Index, diseases, and demographic
characteristics, among others [16, 17]. In a study con-
ducted by Du et al. [5], older women (average age
of 59 years old) who had moderate or high physi-
cal activity showed a significantly longer leukocyte218
telomere length (LTL) than less active women. For219
this study, this difference in telomere length is cal-220
culated as an average of 4.4 years of aging among
participating women. In another study, Tucker [18]222
found that participants in NHANES (National Health223
and Nutrition Examination Survey) with high phys-
ical activity had significantly longer telomeres. On225
average, the participants’ telomeres were 140 bp (Ba-226
se Pairs) longer than sedentary people, which is equ-227
ivalent to being an average of 9 years younger [18].
In addition to moderate or vigorous physical activ- 228
ity, higher intensity exercise levels also showed a 229
positive correlation to telomere length. This may 230
include resistance training, triathlon training at a 231
competitive level, or almost any sport at a profes- 232
sional or elite level. The positive impact of this level 233
of exercise is mainly due to the physiological pro- 234
cesses activated by these levels of physical activity. 235
Colon, et al. [19] found greater telomere lengths in 236
competitive level triathletes in comparison to recre- 237
ationally active people. This demonstrates a positive 238
relationship between telomere length and athlete 239
development parameters, such as VO2max or greater 240
aerobic capacity in triathletes. The previous allows 241
for greater performance, as well as reliance on oxida- 242
tive metabolism pathways. These characteristics are 243
part of the same phenotype as longer telomere lengths 244
[19]. The relationship between telomere length and 245
high intensity exercises is mainly due to the capacity 246
of redox balance (oxidation-reduction) caused by the 247
effects of this level of exercise on the body [20]. For 248
example, resistance training has been shown to gen- 249
erate a higher availability of nitric oxide (NO) and 250
an increase in the activity of SOD (superoxide dis- 251
mutase enzyme), indicating a greater regulation of 252
the levels of nitrogen free radicals (produced by the 253
reaction NO with O2) and ROS, which is associated 254
with an improvement in the oxidative response and a 255
reduction in oxidative stress markers [20]. Likewise, 256
an adaptation of specific antioxidants/oxidative stress 257
markers, an improvement in the maintenance of LTL 258
and a reduction in DNA methylation levels has been 259
observed in resistance training practitioners, indicat- 260
ing a greater antioxidant capacity in the cell. which 261
can provide better telomere maintenance and pre- 262
vent DNA damage from oxidative stress [14]. Taking 263
into account these effects on redox homeostasis and 264
telomere length, maintaining regular physical activ- 265
ity at a moderate to intense level can be considered 266
as a factor that helps reduce telomeric shortening, 267
improving the oxidative response, thus contributing 268
to prevent accelerated aging. 269
4.2. Diet 270
Diet has shown to have different effects on telom- 271
ere length depending primarily on the type of food 272
consumed. Foods with unhealthy characteristics have 273
been linked to shorter telomeres. In a study con- 274
ducted by Fretts, et al. [9], American Indians of the 275
Strong Heart Family tested the relationship between 276
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R.E. Espinosa-Otalora et al. / A systematic review 5
the consumption of processed and unprocessed red277
meat with LTL. They found that the consumption
of processed red meat is related to shorter LTL.279
For each serving of meat consumed, telomere length280
shortened by approximately 4 years; however, no281
relationship was found regarding the consumption
of unprocessed red meat [9]. Telomere shortening283
due to the consumption of processed red meat may284
be linked to high protein, fat, and AGE (Advanced285
Glycation End-products) contained within the meat.
These substances cause oxidative stress and trigger287
an inflammatory response, which promotes the oxi-288
dation of DNA and the accelerated shortening of
telomeres [9, 21].290
Healthy foods and supplements have been shown to
have a positive effect on telomere length. Tucker [22],292
for example, investigated the relationship between293
dietary fiber consumption (self-reported) and leuko-
cyte telomere length (LTL) in participants of the295
NHANES study (National Health and Nutrition296
Examination Survey, USA). They found that a higher297
consumption of dietary fiber results in longer telom-298
eres. For every 10g of fiber (per 1000 kcal) consumed,299
telomeres were 67 base pairs longer equivalent to300
4.3 years less of aging [22]. Another study by Non-
ino, et al. [23] found a positive relationship between
telomere length and drinking green tea in obese303
women. After an 8-week period of drinking green
tea, obese women showed a significant increase in305
telomere length compared to telomere length before306
the intervention; effect that can be explained due to
the antioxidant components present in green tea, such308
as flavonoids and mainly epigallocatechin-3-gallate
(EGCG) [23].
Some nutrients have also been shown to increase311
telomere length, notably omega-3 fatty acids, vita-312
mins, and minerals. This is due to their antioxidant313
capability (Omega 3, Vitamins C and E), oxidative314
stress control, inflammatory and immune response315
(Vitamins D, A, and B12), or DNA damage response
action (Folate and Nicotinamide) which can control317
telomere length and aging [21, 24].
Diets rich in fruits and vegetables, such as the319
Mediterranean diet, have also been shown to have a320
positive effect on telomere length, thereby, decreas-321
ing the aging process [25, 26]. A study conducted by322
Gong et al. [27] A study by Gong et al. [27] found323
among 4 dietary patterns that only the ‘rich in vegeta-324
bles’ pattern that was characterized by a major intake
of fruits, whole grains, various groups of vegetables,
dairy products, nuts, eggs and tea, was positively
related to TL in women, while the other patterns did
not show a statistical relationship with TL [27]. This 329
positive effect of the dietary pattern on LT is largely 330
due to the antioxidant capacity of these foods, which 331
contributes to the reduction of oxidative stress, which 332
has been related to the maintenance of telomeres [28]. 333
In this way,it is advisable to increase the consumption 334
of fruits and vegetables and other foods with antiox- 335
idant potential, in order to help regulate the length of 336
telomeres, improve the response of cells to oxidative 337
stress, and reduce damage to DNA that causes aging. 338
4.3. Techniques for the control of psychological 339
stress 340
Controlling psychological stress has been shown 341
to have a positive effect on the maintenance of 342
telomeres. Different techniques to control stress have 343
shown an effect on reducing the length of telomeres 344
over time, as well as improving complications from 345
disease and age. Duan, et al. [29] found that Tai Chi 346
has been related to increased telomerase activity in 347
peripheral blood mononuclear cells after 6 months in 348
middle-aged adults (55–65 years). This increase in 349
telomerase activity may act as a contributing factor 350
to the maintenance of telomeres [29]. Krishna, et al. 351
[30] compared healthy and active yoga practitioners 352
(30–40 years) to healthy non-yoga practitioners and 353
found that regular practitioners of yoga had longer 354
telomere lengths, a reduction in systemic oxidative 355
stress markers (total antioxidant status), and lower 356
Malondialdehyde and homocysteine levels [30]. 357
Meditation and other techniques have been shown 358
to maintain the length of telomeres and control the 359
factors involved in their shortening. A follow-up 360
study conducted by Ornish, et al. [13] found that a 361
comprehensive 5-year lifestyle intervention, which 362
included meditation, was associated with longer telo- 363
meres, and an increase (at 3 months of intervention) 364
and subsequent reduction (at 5 years of intervention) 365
in telomerase activity among men diagnosed with 366
low-risk prostate cancer through an active surveil- 367
lance (biopsy). Dada, et al. [31] and Tolahunase, et 368
al. [32] found that meditation during yoga practice 369
resulted in longer telomeres, a reduction in oxida- 370
tive stress markers, and lower DNA damage in sperm 371
cells [13, 31, 32]. Meditation techniques alone have 372
also demonstrated an effect on telomere length. Hoge, 373
et al. [33] conducted a study on people (ages 18 or 374
older) practicing Metta Meditation or love-kindness 375
(which focuses on positive intention, kindness, and 376
human warmth) in comparison to non-practitioners 377
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6R.E. Espinosa-Otalora et al. / A systematic review
of yoga or meditation. They found a significantly378
higher leukocyte telomere length only in the women
practicing this meditation technique [33]. In another380
study conducted by Conklin, et al. [34], the partic-381
ipants engaged in a month of Insight Meditation (a382
vipassana practice, based on meditative withdrawal
and focus on deep and isolated concentration) showed384
an average increase in telomeric length of 104.2 bp385
in peripheral blood mononuclear cells (equivalent to386
a 4-year decrease in aging), in addition to present-
ing slightly higher patterns of telomerase activity and388
gene expression related to telomere biology, (mainly389
Atrip, Cct1, Cct6, Gar1 and Hnrnpa1) in meditat-
ing practitioners after 3-weeks of Insight meditative391
withdrawal [34].
The capability of these practices on telomere mai-393
ntenance is mainly linked to both physical and psy-394
chological qualities. Since these practices are mind-
body interventions, they have moderate to intense396
levels and utilize various breathing techniques that397
contribute to the improvement of conditions related398
to lifestyle (Body Mass Index and glucose levels),399
inflammatory response, and the reduction of oxida-400
tive stress levels in the body. Therefore, cell damage401
is decreased, and telomere maintenance mechanism
are activated. This contributes to the cell’s longevity
and improves the health of the cell at the somatic and404
reproductive level. The appearance of aging in rela-
tion to diseases like cancer is reduced both at and early406
and future age [29–34]. Different stress management407
techniques have an important role in both psycho-
logical and physical health, which also contribute to409
the regulation of oxidative stress levels and telomere
shortening. Thus, it is advisable to regularly prac-
tice these techniques and reduce the effects of psy-412
chological stress as a means to slow down one’s aging.413
5. Unhealthy lifestyles and their effect on414
5.1. Smoking and alcoholism
Although cigarette and alcohol consumption have417
been linked to other diseases (including cancer),418
their effect on telomere length is still unclear. While419
some studies generally report these factors as being420
negatively related to telomeric length, other stud-421
ies report an insignificant or null relationship. For422
example, Latifovic et al. [35] conducted a cross-423
sectional study among men and women (20–50
years) to determine the influence of alcohol, cigarette425
consumption, and physical activity (self-reported) on 426
the Relative Length of Leukocyte Telomere (rLTL) 427
measured by quantitative PCR. The findings showed 428
that daily cigarette consumption was related to shorter 429
rLTL (on average 0.096 relative units shorter than 430
in non-smokers). However, they found no relation- 431
ship between alcohol consumption (self-reported as 432
moderate by the participants) and telomere length 433
compared to other research studies [35]. Likewise, 434
Muezzinler, et al. [36] studied a subsample of men 435
and women (50–75 years) from the ESTHER study 436
(Epidemiological Study on the Chances of Preven- 437
tion, Early Recognition, and Optimized Treatment 438
of Chronic Diseases in the Older Population). They 439
found an inverse relationship between smoking and 440
LTL, where current smokers had shorter telomeres 441
than non-smokers. In addition, the intensity of the 442
habit was related to lower LTL, but they found that 443
smoking was associated with lower rates of telom- 444
ere shortening during the 8-year follow-up. As a 445
secondary result, shorter telomeres were found in 446
association to increased alcohol consumption [36]. 447
Although alcohol consumption is a major risk fac- 448
tor for morbidity and mortality, its link to telomere 449
length is still unknown. Some studies have shown 450
telomere shortening when alcohol consumption is 451
increased, while others have reported beneficial 452
health benefits with moderate consumption [24]. In 453
the case of smoking, the intensity of consumption 454
has been linked to telomere shortening [37]. Revesz 455
et al. [38] found that smoking was associated with 456
shorter telomeres, along with other factors. Huzen, et 457
al. [39] found smoking as a factor related to telomeric 458
length change, where active smokers had an annual 459
shortening rate of three times over non-smokers. 460
Moreover, people who quit smoking had an annual 461
telomere shortening rate comparable to people who 462
had never smoked. The negative effect of smoking 463
on telomere length may be due to the free radicals it 464
produces, which induce oxidative stress. This results 465
in an accelerated shortening of the telomeres [37]. 466
Even though the effect of these lifestyle factors on 467
telomeric length may not be entirely clear, they can 468
be considered as potential accelerators of telomeric 469
shortening. Because of this, a reduction in their con- 470
sumption is recommended in order to improve one’s 471
health and slow down biological aging. 472
5.2. Sedentary lifestyle and obesity 473
Sedentary behavior and obesity have also been 474
associated with a negative effect on telomere length 475
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R.E. Espinosa-Otalora et al. / A systematic review 7
and aging [23, 40]. Sedentary behavior has been476
related to reduced mitochondrial activity (an impor-
tant determinant of biological aging). It is also a478
predictor for conditions like obesity, which has been479
directly related to shorter telomeres [5, 40].480
Joshu, et al. [41] conducted a study on 596 men
(40–75 years) participating in the HPFS (Health Pro-482
fessionals Follow-up Study), who were surgically483
treated for prostate cancer. Prostatectomy tissue sam-484
ples were measured, taking into account cell type
and telomeric length. They found that the men with486
increased anthropometric measures (adiposity, hip487
circumference, and weight gain starting at 21 years
of age) and lower amounts of physical activity had489
shorter telomeres only in stromal prostate cells. Addi-
tionally, they found that overweight or obese men,491
who were less active, had telomeres 20.7% shorter492
in stromal cells than active and normal-weight men.
This ratio can be translated into a 29% increase of494
having fatal prostate cancer [41]. Likewise, another495
study conducted by Grun, et al. [42] in adults aged496
18–65 discovered shorter telomeres in patients with497
severe or morbid obesity, as well as an increase in498
macromolecule oxidative damage (lipid peroxidation499
and protein oxidation) and antioxidant response sys-
tems non-enzymatic levels (total reactive antioxidant
potential and total antioxidant reactivity). Also, they502
found increased levels of Shelterin complex (TRF1,
TRF2, POT1 and DKC1) expression, where TRF1504
levels were the main contributor to telomeric short-505
ening in people with obesity [42]. The increase in
Shelterin components expression indicated an adap-507
tive antioxidant response insufficiency. Together with
metabolic dysfunction and chronic inflammation,
Shelterin components expression contributes to an510
increase in oxidative stress levels, accelerated telom-511
eric shortening, and premature biological aging [23,512
42]. In this way, it is crucial to control Body Mass513
Index, prevent obesity, and reduce sedentary habits.514
Therefore, accelerated aging and pathologies could
be prevented early on.516
6. Conclusion
Biological aging is a complex process specifically
linked to telomeric shortening. This shortening, lim-519
its the proliferative capacity of cells, which over time520
reduces the capacity of tissue recovery and acceler-521
ates aging. Environmental factors can influence the522
rate at which this process occurs. Environmental fac-
tors can influence the speed at which this process524
occurs, of which lifestyles have been related as the 525
main factors involved in the acceleration or deceler- 526
ation of this process. The studies presented in this 527
review show that different lifestyles can have a cer- 528
tain influence on the length of telomeres, showing 529
an apparent reduction or increase in telomere length 530
depending on the nature of the lifestyle. 531
Unhealthy lifestyles (sedentary lifestyles, obe- 532
sity, smoking, and alcohol) have negative effects on 533
telomeric length, which is reflected in an acceler- 534
ated shortening of the telomere and development 535
of premature aging. On the other hand, healthy 536
lifestyles (physical activity, stress management, and 537
antioxidant-rich diets) show telomere maintenance 538
and even a lengthening effect. In this way, different 539
lifestyles have an apparent impact on the biological 540
aging rate, which is why it is advisable to control 541
habits that negatively impact telomere length and sup- 542
port those that contribute to maintenance and / or 543
lengthening of these. 544
Different lifestyles have an apparent impact on the 545
rate of biological aging, which is why it is advisable to 546
control habits that negatively impact telomere length 547
and support those habits that contribute to the main- 548
tenance and/or lengthening of telomere. Although 549
the different studies presented show the influence 550
of different lifestyle habits on telomere length and 551
implicitly on aging, they are mostly carried out on 552
a type of cell that, although it reflects globally the 553
telomeric shortening in the body (such as PBMC are), 554
do not allow to generate estimations towards a total 555
aging process of the organism, both chronological 556
and biological, this because the possible relationship 557
of the effects of lifestyle on specific tissues or the 558
adaptive response of some cells types to the lifestyles 559
changes can’t be reflected. For this reason, lifestyles 560
should be considered an area of interest for future 561
research, taking into account in turn different types 562
of cells, this in order to obtain better estimates of an 563
aging process and the effects of different styles of life 564
on telomere length in the body, with a view to improv- 565
ing physical and psychological health and general life 566
expectancy at the individual and community level. 567
Acknowledgments 568
We thank Alexander Ortiz Carvajal and Anne 569
nalosa from International Institute of Languages of 570
Universidad Pedag´
ogica y Tecnol´
ogica de Colombia 571
for their English language editing services.
Uncorrected Author Proof
8R.E. Espinosa-Otalora et al. / A systematic review
Author Contributions572
REEO and JMS wrote the paper and edited the573
manuscript; REEO, JMS, JFV, MFC, and CIEP stud-
ied the concepts; REEO, JMS, JFV, MFC, and CIEP575
prepared the manuscript; all authors participated in576
discussions and critically reviewed the manuscript;577
JMS and MFC approved the final version of the578
Conflict of interest580
The authors declare no conflict of interest.581
This work was supported by a research project583
funded by “Vicerrector´
ıa de Investigaci´
on y Ext-584
on” from Universidad Pedag´
ogica y Tecnol´
de Colombia, Tunja Colombia (SGI code 2429).
Supplementary material587
The supplementary tables are available from588
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Full-text available
Telomeres act as a mitotic clock and telomere-related senescence has been linked to age-related physiological decline. There is increasing evidence lifestyle factors can influence telomere length (TL). The purpose of this study was to determine the effect of competitive triathlon training on TL. Seven competitive male triathletes and seven recreationally active males participated in the study. Relative TL was measured using quantitative polymerase chain reaction. Physiological parameters key to athletic performance such as maximal oxygen intake, lactate threshold, and running economy were also measured. Triathletes had longer telomeres than the recreationally active (1.257 ± 0.028 vs. 1.002 ± 0.014; p < .0001). Positive association was found between TL and maximal oxygen intake, lactate threshold, and running economy (R2 = .677, .683, and .696, respectively). This study indicates that competitive triathlon training buffers against age-related telomere shortening, and there is a correlation between exercise behaviors, higher maximal oxygen intake, and TL.
Full-text available
Leukocyte telomere length (LTL), a biological marker of aging that is associated with age-related diseases, is longer in master endurance runners (ER) than age-matched controls, but the underlying mechanisms are poorly investigated. The LTL, nitric oxide (NO), and redox balance of ER master runners were analyzed and compared to untrained middle-aged and young adults. We hypothesized that NO and redox balance at baseline would be related to longer LTL in ER athletes. Participants (n=38) were long-term ER runners (n=10; 51.6±5.2yrs; 28.4±9.4yrs of experience) and untrained age-matched (n=17; 46.6±7.1yrs) and young controls (n=11; 21.8±4.0yrs). Volunteers were assessed for anamnesis, anthropometrics, and blood sampling. Pro-oxidants, antioxidants, and DNA extraction were measured using commercial kits. Relative LTL was determined with qPCR analyses (T/S). While the middle-aged controls had shorter LTL than the young group, no difference was observed between ER athletes and young participants. A large effect size between the LTL of ER athletes and middle-aged controls (d=0.85) was also observed. The ER athletes and untrained young group had better redox balance according to antioxidant/pro-oxidant ratios compared to middle-aged untrained participants, which also had lower values for redox parameters (TEAC/TBARS, SOD/TBARS, and CAT/TBARS; all p<0.05). Furthermore, the NO level of ER athletes (175.2±31.9μM) was higher (p<0.05) than middle-aged controls (67.2±23.3μM) and young participants (129.2±17.3μM), with a significant correlation with LTL (r=0.766; p=0.02). In conclusion, ER runners have longer LTL than age-matched controls, which in turn may be related to better NO bioavailability and redox balance status.
Full-text available
Introduction: inflammation and oxidative stress are factors that may play a substantial role in telomere attrition. In line of this, obesity is associated with telomere shortening. Green tea had anti-inflammatory and antioxidant effects and may alter telomere length (TL). Objectives: we evaluated the effect of decaffeinated green tea supplementation in obese women on TL. Methods: we conducted a cross-sectional interventional study with ten obese (body mass index [BMI] > 40 kg/m²) and eight normal weight (BMI > 18.5 and < 24.9 kg/m²) women (age between 27 and 48 years). The supplementation was carried out with capsules (each contained 450.7 mg of epigallocatechin-3-gallate) during eight weeks. Anthropometric and dietary intake assessment, and blood collection (for biochemical and TL analysis by quantitative PCR) were performed before and after supplementation. Normal weight patients were evaluated at a single moment. Results: we observed a significant increase on TL after supplementation (1.57 ± 1.1 to 3.2 ± 2.1 T/Sratio; p < 0.05). Moreover, we found shorter TL in obese patients (day 0) when compared to normal weight individuals (3.2 ± 1.9 T/Sratio; p < 0.05) and an inverse association between TL and BMI, even after age adjustment (beta = -0.527; r² = 0.286; IC = -0.129, -0.009). Conclusion: obesity is related to shorter telomeres. Green tea supplementation during eight weeks promotes telomere elongation in obese women.
Full-text available
The relationship between fiber intake and telomere length was evaluated using a cross-sectional design and an NHANES sample of 5674 U.S. adults. Another purpose was to test the impact of potential confounders on the association. Fiber consumption was measured using a 24 h recall and telomere length was indexed using the quantitative polymerase chain reaction method. Overall, the U.S. adults had low fiber intake (median: 6.6 g per 1000 kcal)-less than one-half the recommendation of the Dietary Guidelines for Americans. With age, gender, race, housing status, and misreported energy intake controlled, the relationship between fiber intake per 1000 kcal and telomere length was linear (F= 9.5,p= 0.0045). Specifically, for each 1 g increment in fiber intake per 1000 kcal, telomeres were 8.3 base pairs longer. Because each additional year of chronological age was associated with telomeres that were 15.5 base pairs shorter, results suggest that a 10 g increase in fiber intake per 1000 kcal would correspond with telomeres that are 83 base pairs longer. On average, this would equate to 5.4 fewer years of biologic aging (83 ÷ 15.5). With smoking, BMI, alcohol use, and physical activity controlled, as well as the other covariates, each 10 g increment in fiber accounted for telomeres that were 67 base pairs longer (F= 7.6,p= 0.0101), a biologic aging difference of about 4.3 years. In conclusion, significant fiber consumption accounts for longer telomeres and less biologic aging than lower levels of fiber intake.
Full-text available
A growing body of evidence suggests that meditation training may have a range of salubrious effects, including improved telomere regulation. Telomeres and the enzyme telomerase interact with a variety of molecular components to regulate cell-cycle signaling cascades, and are implicated in pathways linking psychological stress to disease. We investigated the effects of intensive meditation practice on these biomarkers by measuring changes in telomere length (TL), telomerase activity (TA), and telomere-related gene (TRG) expression during a 1-month residential Insight meditation retreat. Multilevel analyses revealed an apparent TL increase in the retreat group, compared to a group of experienced meditators, similarly comprised in age and gender, who were not on retreat. Moreover, personality traits predicted changes in TL, such that retreat participants highest in neuroticism and lowest in agreeableness demonstrated the greatest increases in TL. Changes observed in TRGs further suggest retreat-related improvements in telomere maintenance, including increases in Gar1 and HnRNPA1, which encode proteins that bind telomerase RNA and telomeric DNA. Although no group-level changes were observed in TA, retreat participants' TA levels at post-assessment were inversely related to several indices of retreat engagement and prior meditation experience. Neuroticism also predicted variation in TA across retreat. These findings suggest that meditation training in a retreat setting may have positive effects on telomere regulation, which are moderated by individual differences in personality and meditation experience. ( #NCT03056105).
Background: It has been hypothesized that cancer treatments cause accelerated aging through a mechanism involving the shortening of telomeres. However, the effect of cancer treatments on telomere length is unclear. Methods: We systematically reviewed the epidemiological evidence evaluating the associations between cancer treatment and changes in telomere length. Searches were performed in PubMed for the period of January 1966 through November 2016 using the following search strategy: telomere AND (cancer OR tumor OR carcinoma OR neoplasm) AND (survivor OR patient). Data were extracted and the quality of studies was assessed. Results: A total of 25 studies were included in this review. Ten were solid cancer studies, 11 were hematological malignancy studies, and 4 included a mixed sample of both solid and hematological cancers. Three of the 10 solid tumor studies reported a statistically significant association between cancer treatment and telomere length shortening, and one reported longer telomere length after treatment. Among the hematological cancer studies, three showed statistically significant decreases in telomere length with treatment, and two showed elongation. When these studies were rated using quality criteria, most of the studies were judged to be of moderate quality. Conclusions: The findings from this review indicate that the effect of cancer treatment on telomere length may differ by cancer type and treatment as well as other factors. Definitive conclusions cannot be made based on the published literature, because sample sizes tended to be small; treatments, cancer types, and biospecimens were heterogenous; and the length of follow-up times differed greatly.
Obesity is a prevalent multifactorial chronic disorder characterized by metabolic dysregulation. Sustained pro-oxidative mediators trigger harmful consequences that reflect at systemic level and contribute for the establishment of a premature senescent phenotype associated with macromolecular damage (DNA, protein, and lipids). Telomeres are structures that protect chromosome ends and are associated with a six-protein complex called the shelterin complex and subject to regulation. Under pro-oxidant conditions, telomere attrition and the altered expression of the shelterin proteins are central for the establishment of many pathophysiological conditions such as obesity. Thus, considering that individuals with obesity display a systemic oxidative stress profile that may compromise the telomeres length or its regulation, the aim of this study was to investigate telomere homeostasis in patients with obesity and explore broad/systemic associations with the expression of shelterin genes and the plasma redox state. We performed a cross-sectional study in 39 patients with obesity and 27 eutrophic subjects. Telomere length (T/S ratio) and gene expression of shelterin components were performed in peripheral blood mononuclear cells by qPCR. The oxidative damage (lipid peroxidation and protein carbonylation) and non-enzymatic antioxidant system (total radical-trapping antioxidant potential/reactivity, sulfhydryl and GSH content) were evaluated in plasma. Our results demonstrate that independently of comorbidities, individuals with obesity had significantly shorter telomeres, augmented expression of negative regulators of the shelterin complex, increased lipid peroxidation and higher oxidized protein levels associated with increased non-enzymatic antioxidant defenses. Principal component analysis revealed TRF1 as a major contributor for firstly telomeres shortening. In conclusion, our study is first showing a comprehensive analysis of telomeres in the context of obesity, associated with dysregulation of the shelterin components that was partially explained by TRF1 upregulation that could not be reversed by the observed adaptive non-enzymatic antioxidant response.
Background: Few studies have evaluated the relationship between diet quality and telomere integrity in humans. Telomeres are regions of non-coding DNA localized at the end of each chromosome whose length, in addition to indicating life expectancy, indicates an overall health status. The objective of this systematic review is to compile the existing evidence on the relationship between telomere length and diet quality to further explore the impact that some nutrients, foods and dietary patterns may have on telomere homeostasis and therefore, in precision nutrition strategies. Material and methods: A bibliographic review was performed in the PubMed database to identify published articles (in English or Spanish) until December 2016 that met the following criteria: included human subjects; cross-sectional studies; case-control studies; prospective cohort studies or intervention studies; evaluating the relationship of nutrients, foods or dietary patterns on telomere integrity. The search strategy included the following keywords: nutrients or food OR food groups OR diet OR dietary pattern OR eating pattern OR dietary habits OR diet type AND telomere attrition OR telomere length. In total, 19 cross-sectional studies, five case-control studies, five prospective cohort studies, and two intervention studies were included, including those articles that were found for being listed in other publications. Results: Positive associations were found between telomere length and adherence to the Mediterranean diet and consumption of vegetables and fruits. The results observed for other nutrients, foods or dietary patterns were incoherent although it seems that processed meats, cereals, alcohol and sweetened beverages could be associated with shorter telomeres. Conclusions: Dietary intervention, and in particular the promotion of a Mediterranean-style diet, may play a role in the protection of telomere integrity.
Telomeres are dynamic nucleoprotein-DNA structures that cap and protect linear chromosome ends. Because telomeres shorten progressively with each replication, they impose a functional limit on the number of times a cell can divide. Critically short telomeres trigger cellular senescence in normal cells, or genomic instability in pre-malignant cells, which contribute to numerous degenerative and aging-related diseases including cancer. Therefore, a detailed understanding of the mechanisms of telomere loss and preservation is important for human health. Numerous studies have shown that oxidative stress is associated with accelerated telomere shortening and dysfunction. Oxidative stress caused by inflammation, intrinsic cell factors or environmental exposures, contributes to the pathogenesis of many degenerative diseases and cancer. Here we review the studies demonstrating associations between oxidative stress and accelerated telomere attrition in human tissue, mice and cell culture, and discuss possible mechanisms and cellular pathways that protect telomeres from oxidative damage.
In multicellular organisms, regulation of telomere length in pluripotent stem cells is critical to ensure organism development and survival. Telomeres consist of repetitive DNA that are progressively lost with each cellular division. When telomeres become critically short, they activate a DNA damage response that results in cell cycle arrest. To counteract telomere attrition, pluripotent stem cells are equipped with telomere elongation mechanisms that ensure prolonged proliferation capacity and self-renewal capacity. Excessive telomere elongation can also be deleterious and is counteracted by a rapid telomere deletion mechanism termed telomere trimming. While the consequences of critically short telomeres are well established, we are only beginning to understand the mechanisms that counteract excessive telomere elongation. The balance between telomere elongation and shortening determine the telomere length set point in pluripotent stem cells and ensures sustained proliferative potential without causing chromosome instability.