Aging (Albany NY). 2016 Jan;8(1):12-5.

Nutrition and lifestyle in healthy aging: the telomerase challenge.

Boccardi V1, Paolisso G2, Mecocci P1.
  • 1Institute of Gerontology and Geriatrics, Department of Medicine, University of Perugia, Perugia, Italy.
  • 2Department of Medical, Surgical, Neurological, Aging and Metabolic Sciences, Second University of Naples, Naples, Italy.



Nutrition and lifestyle, known to modulate aging process and age-related diseases, might also affect telomerase activity. Short and dysfunctional telomeres rather than average telomere length are associated with longevity in animal models, and their rescue by telomerase maybe sufficient to restore cell and organismal viability. Improving telomerase activation in stem cells and potentially in other cells by diet and lifestyle interventions may represent an intriguing way to promote health-span in humans.

KEYWORDS: elderly; longevity; nutrition; telomerase; telomere

PMID: 26826704



Aging is a natural process characterized by a gradual decline in the function of organs and systems which progressively leads to an increased risk of diseases and, ultimately death. The old age population is increasing worldwide as well as the prevalence of age related diseases, such as neurodegenerative diseases, including Alzheimer’s disease, with a significant negative impact on health and care systems.  Reaching old age in good health is the aspiration of most of us, but our individual life expectancy is the intriguing result of a complex interweaving between genetic and environmental factors. In fact if we are lucky and we have inherited good genes, the probability to reach 100 years is very high. However, in this context, nutrition, diet and lifestyle represent the most important contributors to longevity and healthy aging affecting approximately 70-80% of an individual’s lifespan.

Many and complex mechanisms have been proposed to contribute to the aging process. A sustained DNA response  known as “cellular senescence”,  has been hypothesized as one of the most important  contributing factor to age-associated tissue dysfunction, reduced regenerative capacity and diseases evolution. This process is finely tuned by a powerful “biologic clock” regulated by telomere shortening. Telomeres are long sequences of nucleotides at the end of chromosomes, forming with specific proteins, an “end caps” which preserve genome stability and lead a cell to correctly divide. Telomeres, as the plastic tips on shoelaces, are able to keep chromosome ends from fraying and fused to each other, which would destroy or interfere genetic information. At each cell division, telomeres lose some of their length and when they get too short and dysfunctional, the cell is no longer able to divide becoming “senescent”. The accumulation of senescent cells in the body and the organism as a whole, make us older and often sick.



Figure 1

Figure 1. This figure shows as our “biological clock” can be delayed by telomerase activation, which working as a “super hero” is able to lengthen telomeres with each cell division leading to telomere erosion rate reduction which may allow us to live longer. Edited by Giuseppe Guida. All rights reserved.


Actually, new evidences are coming out suggesting that the biological clock, that until now was thought “untouchable”, can be regulated and/or slowed. In fact, published data suggested that extremely short or dysfunctional telomeres can be repaired by an enzyme, called “telomerase”, which can add nucleotides at the end of each chromosome sustaining telomere stability. Thanks to great scientists, Blackburn, Greider and Szostak to whom we owe the discovery of “how chromosomes are protected by telomeres and the enzyme telomerase”. These discoveries had a great impact within the scientific community, supporting that aging can be potentially delayed by telomerase activation which can lead to telomere erosion rate reduction (Figure 1). In contrast to adult stem cells, telomerase is “turned off” in  normal somatic human cells immediately after birth. However,  more recent studies, conducted in animal models,  have demonstrated that short telomeres rather than average telomere length are associated with age-related diseases and, their rescue by telomerase is sufficient to restore cell and organismal viability. Multi-generational study of populations with exceptional longevity found that they exhibit abnormal circulating high telomerase activity. Longer telomeres and higher telomerase activity in peripheral blood mononuclear cells, have been found in subjects following the Mediterranean diet- the better  proved elixir of long and healthy life. These data  further suggested the link between longevity, health span and telomerase activity. It is reasonable to hypothesize  that activating telomerase in adult stem cells and potentially in other cells in our body may extend their functions and help promote organ repair and regeneration.

Several pharmaceutical companies, worldwide,  are struggling to find a potential compound able to  slow the loss of telomere along with aging. But, how we can really interfere with this implacable shortening? There are three main mechanisms known so far: 1) interfering with factors that accelerated telomere shortening (i.e. inflammation and oxidative stress; 2) interfering with factors that slow telomere shortening; 3) interfering with telomerase activators. So, what a better way to keep telomeres long trough diet and lifestyle interventions which are able to modulate all the above described mechanisms? (Figure 2). Numerous evidences are showing that specific nutrients, as well as following a healthy life avoiding obesity, smoking and stress with the promotion of moderate physical exercise, provide all the necessary building blocks to support telomere stability and potentially extend lifespan.



Figure 2

Figure 2.  Telomere is influenced by a number of intrinsic and environmental factors that either accelerate or slow down natural telomere attrition, which causes aging and age-related diseases. Diet, nutrition and lifestyle are potential modulator of telomere shortening by many mechanisms (i.e. by reduction of inflammation and oxidative stress) including telomerase activation.


Essential References:

1)      Bär C, Blasco MA. Telomeres and telomerase as therapeutic targets to prevent and treat age-related diseases. F1000Res. 2016;5. pii: F1000 Faculty Rev-89.

2)       Boccardi V, Paolisso G, Mecocci P. Nutrition and lifestyle in healthy aging: the telomerase challenge. Aging (Albany NY). 2016 Jan;8(1):12-5.

3)      Boccardi V, Pelini L, Ercolani S, Ruggiero C, Mecocci P. From cellular senescence to Alzheimer’s disease: The role of telomere shortening. Ageing Res Rev. 2015 Jul;22:1-8.

4)      Boccardi V, Paolisso G. Telomerase activation: a potential key modulator for human healthspan and longevity. Ageing Res Rev. 2014 May;15:1-5.

5)       Boccardi V, Esposito A, Rizzo MR, Marfella R, Barbieri M, Paolisso G. Mediterranean diet, telomere maintenance and health status among elderly. PLoS One. 2013 Apr 30;8(4):e62781.

6)      Boccardi V, Paolisso G. Malleability of Short Telomeres by Telomerase Activators: A Mini-review.  Journal of Aging Science. 2013 Sept; doi:10.4172/2329-8847.1000108


Boccardi pictureContact Information:

Virginia Boccardi, MD, PhD.

Institute of Gerontology and Geriatrics, Department of Medicine, University of Perugia, S. Andrea delle Fratte, 06156 Perugia, Italy.

Phone number:  0755783524  Email address:



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