Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Dec 18:10:1508.
doi: 10.3389/fphys.2019.01508. eCollection 2019.

Are We Ill Because We Age?

Affiliations
Review

Are We Ill Because We Age?

Tamas Fulop et al. Front Physiol. .

Abstract

Growing elderly populations, sometimes referred to as gray (or silver) tsunami, are an increasingly serious health and socioeconomic concern for modern societies. Science has made tremendous progress in the understanding of aging itself, which has helped medicine to extend life expectancies. With the increase of the life expectancy, the incidence of chronic age-related diseases (ARDs) has also increased. A new approach trying to solve this problem is the concept of geroscience. This concept implies that the aging process itself is the common cause of all ARDs. The corollary and consequence of such thinking is that we can and should treat aging itself as a disease. How to translate this into the medical practice is a big challenge, but if we consider aging as a disease the problem is solved. However, as there is no common definition of what aging is, what its causes are, why it occurs, and what should be the target(s) for interventions, it is impossible to conclude that aging is a disease. On the contrary, aging should be strongly considered not to be a disease and as such should not be treated; nonetheless, aging is likely amenable to optimization of changes/adaptations at an individual level to achieve a better functional healthspan.

Keywords: adaptation; age related diseases; aging; aging as a disease; anti-aging medicine; functional healthspan; geroscience; optimization of aging.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Conceptualization of the contribution of aging as a physiological process. Biological aging is a normal process that results from intrinsic (hallmarks of aging) and extrinsic factors (stress). In the absence of major insult during lifespan, individuals will experience very few symptoms (paucisymptomatic) related to change in health status despite the loss of physiological functions. However, upon certain triggering, uncontrolled inflammation may occur resulting in a persistent activation and disbalance of physiological functions leading to age-related diseases. Intervention strategies to modulate aging and reduce the susceptibility to diseases are represented. Aging can only be successfully modulated as long as it is considered a multifaceted process and not a disease in need of a specific cure. Ultimately, aging represents a time-dependent lifelong process, where under constant pressure the organism adapts or dysregulates which excludes the concept that aging is a disease.

References

    1. Anisimov V. N. (2009). Carcinogenesis and aging 20 years after: escaping horizon. Mech. Ageing Dev. 130, 105–121. 10.1016/j.mad.2008.02.004, PMID: - DOI - PubMed
    1. Anisimov V. N. (2015). Metformin for cancer and aging prevention: is it a time to make the long story short? Oncotarget 6, 39398–39407. 10.18632/oncotarget.6347, PMID: - DOI - PMC - PubMed
    1. Anstey K., Stankov L., Lord S. (1993). Primary aging, secondary aging, and intelligence. Psychol. Aging 8, 562–570. 10.1037/0882-7974.8.4.562, PMID: - DOI - PubMed
    1. Arai Y., Martin-Ruiz C. M., Takayama M., Abe Y., Takebayashi T., Koyasu S., et al. (2015). Inflammation, but not telomere length, predicts successful ageing at extreme old age: a longitudinal study of semi-supercentenarians. EBioMedicine 2, 1549–1558. 10.1016/j.ebiom.2015.07.029 - DOI - PMC - PubMed
    1. Attaallah A., Lenzi M., Marchionni S., Bincoletto G., Cocchi V., Croco E., et al. (2019). A pro longevity role for cellular senescence. Geroscience. 10.1007/s11357-019-00066-2 - DOI - PMC - PubMed

LinkOut - more resources