Demystifying Longevity - What it is and Why it Matters

Demystifying Longevity - What it is and Why it Matters


1. Introduction to Longevity

Health - ours and those of other people - even by preventive reduction of mortality risks - has that 'price' of activities that could affect our present vitality and those of our future. For example, 'smoking makes you tired' does not cause a generalized slowdown of all physical activities but only affects those who are important for adoption choices. Recent studies restart the debate over health and private savings although, from theory, it would be expected that the relationship between health and wealth was much stronger. Indeed, among the many results that spring from the theory of optimal inter-temporal choices, it is possible or probable that taxonomy changes strictly positive or negative income in life. If we were totally rational agents, the absence of assets or the number of assets would depend on the income that we are more or less certain to collect, perhaps for the rest of our days. The presence of periods alive with zero income and non-negative consumption will generate the need to keep funds that will eventually be spent in survival activities. On the off chance that mortality were deterministic and genetically programmed, every agent would try to exchange as much consumption as much as possible from future periods of life - not alive - in periods of life still spent with non-zero utility.

Longevity - the ever-increasing number of days we go about our daily activities - plays a primary role in economic behavior because it reverses the short-term problem of food and nutrition into a long-term collective flourishing. People invest in health in order to enrich their lives, while governments provide collective health care to prolong their useful life. Mortality is also crucial to determine the rational decision with regard to savings and the allocation of resources across time. But we also have some irrational health care behaviors and this is where we will begin.

Aging is a universal experience, an intrinsic part of the human condition that has fascinated scientists, philosophers, and laypeople for centuries. At its core, aging is the gradual decline of biological functions and the ability to adapt to metabolic stress, leading to an increased risk of disease and death. But what exactly causes aging, and can we extend our lifespan through scientific advancements? This blog delves into the biology of aging, the factors influencing longevity, and the latest techniques aimed at prolonging life.

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What is Aging and How Does It Occur?

Aging is a complex, multifaceted process influenced by genetic, environmental, and lifestyle factors. Biologically, it involves the progressive accumulation of damage to cells, tissues, and organs over time. This damage results from various mechanisms, including oxidative stress, DNA damage, telomere shortening, and the accumulation of senescent cells.

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Figure 1. A conceptual model of how our understanding of aging biology will need to integrate perspectives from diverse disciplines. The precise definition of disciplines is somewhat arbitrary. (Cohen et al., 2020)

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  • Oxidative Stress: Cells produce energy through metabolism, a process that generates reactive oxygen species (ROS) as byproducts. These ROS can damage cellular components, such as DNA, proteins, and lipids, leading to oxidative stress. Over time, the accumulation of this damage contributes to the aging process.?
  • DNA Damage: Our DNA is constantly exposed to environmental factors like UV radiation, chemicals, and even normal metabolic processes that can cause mutations. While our cells have repair mechanisms, their efficiency declines with age, leading to the accumulation of genetic damage.
  • Telomere Shortening: Telomeres are protective caps at the ends of chromosomes that shorten with each cell division. When telomeres become too short, cells can no longer divide and become senescent or die. This process is a crucial factor in cellular aging.
  • Senescent Cells: Senescent cells are aged cells that have lost the ability to divide but remain metabolically active. They secrete inflammatory factors and other molecules that can damage surrounding tissues and contribute to age-related diseases.


Figure 2. Systemic consequences of aging (Colloca et al., 2020)

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Longevity: Beyond the Natural Lifespan

Longevity refers to the length of time an individual lives, particularly the length of time they remain healthy and free from serious disease. While the average human lifespan has increased dramatically over the past century due to advancements in medicine, sanitation, and nutrition, scientists are now focusing on extending the "healthspan" – the period of life spent in good health.


Techniques to Extend Longevity

  • ?Lifestyle Interventions: While scientific advancements are promising, lifestyle choices remain crucial for longevity. Regular physical activity, a balanced diet rich in fruits and vegetables, stress management, and avoiding harmful habits like smoking and excessive alcohol consumption are all vital for promoting a long and healthy life.
  • Regenerative Medicine: Stem cell therapy and tissue engineering aim to replace or rejuvenate damaged tissues and organs. By replenishing aged cells with new, healthy ones, regenerative medicine holds the potential to significantly extend the healthspan and potentially the lifespan of individuals.
  • Genetic and Epigenetic Modifications: Advances in genetic engineering have opened up new possibilities for extending lifespan. Techniques such as CRISPR-Cas9 allow for precise modifications of genes associated with aging and longevity. Additionally, epigenetic modifications – changes in gene expression without altering the underlying DNA sequence – are being explored as a way to promote healthy aging.
  • Pharmacological Interventions: Several drugs have been identified that can mimic the effects of caloric restriction and promote longevity. One of the most well-known is rapamycin, which inhibits the mTOR pathway, a key regulator of cell growth and metabolism. Other promising compounds include metformin, a diabetes drug that has been shown to extend lifespan in animal models, and senolytics, which selectively eliminate senescent cells.
  • Caloric Restriction and Fasting: Studies have shown that reducing caloric intake without malnutrition can extend lifespan in various organisms, from yeast to mammals. Caloric restriction is believed to reduce metabolic stress and enhance cellular repair mechanisms. Intermittent fasting, which involves cycles of eating and fasting, has also been shown to promote longevity by improving metabolic health and reducing inflammation.


The quest for longevity is deeply rooted in our desire to live healthier, more fulfilling lives. Understanding the biology of aging provides a foundation for developing interventions that can extend not just our lifespan but also our health span. From dietary strategies and pharmacological agents to cutting-edge genetic and regenerative therapies, the future of longevity research holds exciting possibilities. As science continues to unravel the mysteries of aging, the dream of a longer, healthier life becomes ever more attainable.

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Author

?evval Y?ld?z



References

1- Colloca, G., Di Capua, B., Bellieni, A., Fusco, D., Ciciarello, F., Tagliaferri, L., Valentini, V., & Balducci, L. (2020). Biological and Functional biomarkers of aging: definition, characteristics, and how they can impact everyday cancer treatment. Current Oncology Reports, 22(11). https://doi.org/10.1007/s11912-020-00977-w

2- Cohen, A. A., Kennedy, B. K., Anglas, U., Bronikowski, A. M., Deelen, J., Dufour, F., Ferbeyre, G., Ferrucci, L., Franceschi, C., Frasca, D., Friguet, B., Gaudreau, P., Gladyshev, V. N., Gonos, E. S., Gorbunova, V., Gut, P., Ivanchenko, M., Legault, V., Lema?tre, J. F., . . . Fül?p, T. (2020). Lack of consensus on an aging biology paradigm? A global survey reveals an agreement to disagree, and the need for an interdisciplinary framework. Mechanisms of Ageing and Development, 191, 111316. https://doi.org/10.1016/j.mad.2020.111316

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