Telomeres, Diet & Longevity

[Dean Pomerleau]

It's not clear whether telomere shortening is a cause or a side-effect of aging, and Aubrey de Grey is concerned that direct manipulation of telomeres to make them longer (i.e. via increased expression of the telomerase enzyme)  is likely to be a bad idea due to concern about allowing cancer cells to replicate more readily.

 

But longer leukocyte telomeres do seem to be associated with longevity: study [2] found that centenarians have leukocyte telomeres as long as people who are much younger than themselves (and therefore unlikely from a statistical perspective to make it to 100), and the offspring of centenarians have longer telomeres than age and gender matched offspring of parents who died at a "normal" age. So having longer telomeres might be a sign of healthy aging (I can hear Michael Rae revving up his engines now :)).

 

With this in mind this new study [1] (provided to me by Al Pater - thanks Al !), found that components of a person's diet was predictive of their telomere length 10 years later. 

 

From the abstract:

 

The first factor labeled 'prudent dietary pattern' was characterized by

high intake of whole grains, seafood, legumes, vegetables and seaweed, whereas

the second factor labeled 'Western dietary pattern' was characterized by high

intake of refined grain, red meat or processed meat and sweetened carbonated

beverages.

 

In a multiple linear regression model adjusted for age, sex, body mass

index and other potential confounding variables [including from the full text - 

income status, smoking status, alcohol consumption status, physical activity

and calorie intake, and presence of hypertension, diabetes mellitus or

hypercholesterolemia], the prudent dietary pattern was positively associated with

[leukocyte telomere length - LTL].

 

In the analysis of particular food items, higher consumption of legumes, nuts, seaweed,

fruits and dairy products and lower consumption of red meat or processed meat and

sweetened carbonated beverages were associated with longer LTL.

 

So for what is may be worth (he says, expecting to be corrected and chastised by Michael :) for oversimplifying and ignoring important evidence...), eating what is considered by most to be a healthy diet may help to preserve your telomeres, and improve your chances of healthy aging.

 

--Dean

 

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[1] Eur J Clin Nutr. 2015 Sep;69(9):1048-52. doi: 10.1038/ejcn.2015.58. Epub 2015 Apr

15.

Association between dietary patterns in the remote past and telomere length.

Lee JY(1), Jun NR(1), Yoon D(2), Shin C(2,)(3), Baik I(1).

BACKGROUND/OBJECTIVES: There are limited data on the association between dietary
information and leukocyte telomere length (LTL), which is considered an indicator
of biological aging. In this study, we aimed at determining the association
between dietary patterns or consumption of specific foods and LTL in Korean
adults.
SUBJECT/METHODS: A total of 1958 middle-aged and older Korean adults from a
population-based cohort were included in the study. Dietary data were collected
from a semi-quantitative food frequency questionnaire at baseline (June 2001 to
January 2003). LTL was assessed using real-time PCR during the 10-year follow-up
period (February 2011 to November 2012).
RESULTS: We identified two major factors and generated factor scores using factor
analysis. The first factor labeled 'prudent dietary pattern' was characterized by
high intake of whole grains, seafood, legumes, vegetables and seaweed, whereas
the second factor labeled 'Western dietary pattern' was characterized by high
intake of refined grain, red meat or processed meat and sweetened carbonated
beverages. In a multiple linear regression model adjusted for age, sex, body mass
index and other potential confounding variables, the prudent dietary pattern was
positively associated with LTL. In the analysis of particular food items, higher
consumption of legumes, nuts, seaweed, fruits and dairy products and lower
consumption of red meat or processed meat and sweetened carbonated beverages were
associated with longer LTL.
CONCLUSIONS: Our findings suggest that diet in the remote past, that is, 10 years
earlier, may affect the degree of biological aging in middle-aged and older
adults.

PMID: 25872911

--------------------------

[2] Exp Gerontol. 2014 Oct;58:90-5. doi: 10.1016/j.exger.2014.06.018. Epub 2014 Jun
27.

Leukocyte telomere length and prevalence of age-related diseases in
semisupercentenarians, centenarians and centenarians' offspring.

Tedone E(1), Arosio B(2), Gussago C(3), Casati M(4), Ferri E(3), Ogliari G(3),
Ronchetti F(3), Porta A(3), Massariello F(3), Nicolini P(4), Mari D(2).

Centenarians and their offspring are increasingly considered a useful model to
study and characterize the mechanisms underlying healthy aging and longevity. The
aim of this project is to compare the prevalence of age-related diseases and
telomere length (TL), a marker of biological age and mortality, across five
groups of subjects: semisupercentenarians (SSCENT) (105-109years old),
centenarians (CENT) (100-104years old), centenarians' offspring (CO), age- and
gender-matched offspring of parents who both died at an age in line with life
expectancy (CT) and age- and gender-matched offspring of both non-long-lived
parents (NLO). Information was collected on lifestyle, past and current diseases,
medical history and medication use. SSCENT displayed a lower prevalence of acute
myocardial infarction (p=0.027), angina (p=0.016) and depression (p=0.021)
relative to CENT. CO appeared to be healthier compared to CT who, in turn,
displayed a lower prevalence of both arrhythmia (p=0.034) and hypertension
(p=0.046) than NLO, characterized by the lowest parental longevity.
Interestingly, CO and SSCENT exhibited the longest (p<0.001) and the shortest
(p<0.001) telomeres respectively while CENT showed no difference in TL compared
to the younger CT and NLO. Our results strengthen the hypothesis that the
longevity of parents may influence the health status of their offspring.
Moreover, our data also suggest that both CENT and their offspring may be
characterized by a better TL maintenance which, in turn, may contribute to their
longevity and healthy aging. The observation that SSCENT showed considerable
shorter telomeres compared to CENT may suggest a progressive impairment of TL
maintenance mechanisms over the transition from centenarian to
semisupercentenarian age.

PMID: 24975295

[keithsct]

I've always agreed with the argument that short lived species don't die because of telomere shortening to be compelling.  Rather they die because of garbage accumulation and damage from ROS cascade if I understand the theories on membrane fatty acid composition properly.  Studies on old human tissues have shown that when exposed to a young niche, the old stem cells will divide and differentiate.  So the limiting factor is something other than telomere shortening.  Perhaps in the future when other aging mechanism problems have been addressed, telomere enhancement may become the limiting factor.

[nicholson]

"So for what it may be worth    ...........   eating what is considered by most to be a healthy diet may help to preserve your telomeres, and improve your chances of healthy aging."

 

Might very well be true, about HEALTHY DIET, as mentioned in the quote above.

 

However, to add another angle to the story:  I recall that the lengths of the leukocyte telomeres of the Wisconsin CR monkeys are not significantly different from those of the ad-lib controls   ........  which one would think might be of some significance, but I am not exactly sure what.

 

Rodney.

[Dean Pomerleau]

I recall that the lengths of the leukocyte telomeres of the Wisconsin CR monkeys are not significantly different from those of the ad-lib controls   ........  which one would think might be of some significance, but I am not exactly sure what.

 

You are correct Rodney, at least by one metric of telomere length, CR didn't preserve telomeres [1], although it was the NIA rhesus monkeys, not Wisconsin monkeys.

 

Specifically, in both the CR and control monkeys, telomeres in frequently dividing white blood cells and skin cells got shorter as a function of age relative to the length of telomeres in infequently dividing muscle cells. This decrease in relative telomere length with age was not attenuated in the CR monkeys relative to controls. Nor was there a difference in absolute telomere length in any of the tissues tested between the CR and control animals.

 

But then again, for various reasons discussed elsewhere (most notably Michael Rae's comprehensive blog post on the topic), the NIA control monkeys may have been on partial CR, and/or the CR monkeys may not have been CRed enough for telomere (or lifespan) differences to show up... 

 

Or maybe it was just the good diet and obesity avoidance shared by both groups of NIA monkeys that made them live equivalently long, and have equivalently long telomeres...

 

--Dean

 

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[1] J Gerontol A Biol Sci Med Sci. 2011 Nov;66(11):1163-8. doi:

10.1093/gerona/glr136. Epub 2011 Aug 22.

 

Telomere dynamics in rhesus monkeys: no apparent effect of caloric restriction.

 

Smith DL Jr(1), Mattison JA, Desmond RA, Gardner JP, Kimura M, Roth GS, Ingram

DK, Allison DB, Aviv A.

 

Author information:

(1)University of Alabama at Birmingham, Main Campus, Birmingham, AL 35294-3360,

USA. dsmithjr@uab.edu

 

The role of telomere attrition in limiting the replicative capacity of cells in

culture is well established. In humans, epidemiologic evidence suggests telomere

length (TL) in leukocytes is highly variable at birth and inversely related to

age. Although calorie restriction (CR) significantly increases life span in most

rodent models, its association with TL is unknown. Using linear regression

analysis, TLs (as measured by Southern blot analysis) of skeletal muscle (a

postmitotic tissue that largely represents early development TL), fat,

leukocytes, and skin were tested for effects of age, sex, and diet in 48 control

and 23 calorie restriction rhesus monkeys. After controlling for the individual's

muscle mean TL, differences between leukocytes muscle and skin muscle were

significantly associated with age (p = .002; p = .002) and sex (p = .003; p =

.042), but not calorie restriction (p = .884; p = .766). Despite an age-dependent

shortening of TL in leukocytes and skin, calorie restriction did not

significantly affect TL dynamics in these samples.

 

PMCID: PMC3193524

PMID: 21860014

[Dean Pomerleau]

It appears that it is not just a good diet that helps preserve telomeres.

 

According to this new study [1], engaging in various forms of exercise was associated with longer leukocyte telomeres. People who engaged in the most leisure time physical activities were over 50% less likely than those who were least active to be in the lowest tertile of telomere length.

 

Again, it is not entirely clear how well telomere length predicts (let alone causes) improved health or longevity, but it is pretty clear from studies like [2] that increased exercise reduces mortality, providing some reason to suspect longer telomeres might be a good thing.

 

--Dean

 

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[1] Med Sci Sports Exerc. 2015 Nov;47(11):2347-52. doi: 10.1249/MSS.0000000000000695.

Movement-Based Behaviors and Leukocyte Telomere Length among US Adults.

Loprinzi PD(1), Loenneke JP, Blackburn EH.

INTRODUCTION: Short leukocyte telomere length (LTL) has become a hallmark
characteristic of aging. Some, but not all, evidence suggests that physical
activity (PA) may play an important role in attenuating age-related diseases and
may provide a protective effect for telomeres. The purpose of this study was to
examine the association between PA and LTL in a national sample of US adults from
the National Health and Nutrition Examination Survey.
METHODS: National Health and Nutrition Examination Survey data from 1999 to 2002
(n = 6503; 20-84 yr) were used. Four self-report questions related to
movement-based behaviors (MBB) were assessed. The four MBB included whether
individuals participated in moderate-intensity PA, vigorous-intensity PA,
walking/cycling for transportation, and muscle-strengthening activities. An MBB
index variable was created by summing the number of MBB an individual engaged in
(range, 0-4).
RESULTS: A clear dose-response relation was observed between MBB and LTL; across
the LTL tertiles, respectively, the mean numbers of MBB were 1.18, 1.44, and 1.54
(Ptrend < 0.001). After adjustments (including age) and compared with those
engaging in 0 MBB, those engaging in 1, 2, 3, and 4 MBB, respectively, had a 3%
(P = 0.84), 24% (P = 0.02), 29% (P = 0.04), and 52% (P = 0.004) reduced odds of
being in the lowest (vs highest) tertile of LTL; MBB was not associated with
being in the middle (vs highest) tertile of LTL.
CONCLUSIONS: Greater engagement in MBB was associated with reduced odds of being
in the lowest LTL tertile.

PMID: 25970659

 

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[2] JAMA Intern Med. 2015 Jun;175(6):959-67. doi: 10.1001/jamainternmed.2015.0533.

Leisure time physical activity and mortality: a detailed pooled analysis of the
dose-response relationship.

Arem H(1), Moore SC(1), Patel A(2), Hartge P(1), Berrington de Gonzalez A(1),
Visvanathan K(3), Campbell PT(2), Freedman M(1), Weiderpass E(4), Adami HO(5),
Linet MS(1), Lee IM(6), Matthews CE(1).

Comment in
JAMA Intern Med. 2015 Jun;175(6):968-9.

IMPORTANCE: The 2008 Physical Activity Guidelines for Americans recommended a
minimum of 75 vigorous-intensity or 150 moderate-intensity minutes per week (7.5
metabolic-equivalent hours per week) of aerobic activity for substantial health
benefit and suggested additional benefits by doing more than double this amount.
However, the upper limit of longevity benefit or possible harm with more physical
activity is unclear.
OBJECTIVE: To quantify the dose-response association between leisure time
physical activity and mortality and define the upper limit of benefit or harm
associated with increased levels of physical activity.
DESIGN, SETTING, AND PARTICIPANTS: We pooled data from 6 studies in the National
Cancer Institute Cohort Consortium (baseline 1992-2003). Population-based
prospective cohorts in the United States and Europe with self-reported physical
activity were analyzed in 2014. A total of 661,137 men and women (median age, 62
years; range, 21-98 years) and 116,686 deaths were included. We used Cox
proportional hazards regression with cohort stratification to generate
multivariable-adjusted hazard ratios (HRs) and 95% CIs. Median follow-up time was
14.2 years.
EXPOSURES: Leisure time moderate- to vigorous-intensity physical activity.
MAIN OUTCOMES AND MEASURES: The upper limit of mortality benefit from high levels
of leisure time physical activity.
RESULTS: Compared with individuals reporting no leisure time physical activity,
we observed a 20% lower mortality risk among those performing less than the
recommended minimum of 7.5 metabolic-equivalent hours per week (HR, 0.80 [95% CI,
0.78-0.82]), a 31% lower risk at 1 to 2 times the recommended minimum (HR, 0.69
[95% CI, 0.67-0.70]), and a 37% lower risk at 2 to 3 times the minimum (HR, 0.63
[95% CI, 0.62-0.65]). An upper threshold for mortality benefit occurred at 3 to 5
times the physical activity recommendation (HR, 0.61 [95% CI, 0.59-0.62]);
however, compared with the recommended minimum, the additional benefit was modest
(31% vs 39%). There was no evidence of harm at 10 or more times the recommended
minimum (HR, 0.69 [95% CI, 0.59-0.78]). A similar dose-response relationship was
observed for mortality due to cardiovascular disease and to cancer.
CONCLUSIONS AND RELEVANCE: Meeting the 2008 Physical Activity Guidelines for
Americans minimum by either moderate- or vigorous-intensity activities was
associated with nearly the maximum longevity benefit. We observed a benefit
threshold at approximately 3 to 5 times the recommended leisure time physical
activity minimum and no excess risk at 10 or more times the minimum. In regard to
mortality, health care professionals should encourage inactive adults to perform
leisure time physical activity and do not need to discourage adults who already
participate in high-activity levels.

PMCID: PMC4451435 [Available on 2016-06-01]
PMID: 25844730