Missed opportunities for extending youth
It causes cancer, heart disease, dementia, and arthritis, but most undergraduate biology majors at U of G will never learn much about the process of aging. Worse yet, many will enter the workforce as pharmacists, physicians, and researchers with major misunderstandings concerning what aging is, what causes it, and how to potentially slow it down.
Based on outdated information taught in grade school, it is common for biology students to believe that aging is inevitable. Many people believe that the maximum length of the lifespan is predetermined by our DNA (deoxyribonucleic acid) — more specifically, by a component of our DNA called telomeres.
Telomeres are protective components of DNA that are often likened to the aglets found on the ends of shoelaces. Aglets protect the ends of our shoelaces from dirt and water that may otherwise cause them to fray. The American Physiological Association indicates that, similar to aglets, telomeres cap and protect both ends of our DNA from damage.
The source of this damage is a long story in itself, but to keep this discussion short the following will have to suffice: the DNA within a cell is placed in danger each time that cell begins to divide. This process occurs regularly because old and worn out cells need to be replaced by fresh new cells. According to a 2013 report by IP Tzanetakou and colleagues, if it weren’t for telomeres, your DNA would be truncated on both ends each time your cells divided. Fortunately, telomeres take the hits instead. Unfortunately, our telomeres can only take so much abuse before they are degraded to nothing.
Without telomeres, our DNA is shredded each time our cells divide, and with each subsequent division, more of our DNA becomes unintelligible to our cells. With our biological blueprints and instructions in disarray, our cells begin to dysfunction. JW Shay warns in his 2016 Cancer Discovery article that, eventually, our DNA will become so disordered that our cells won’t (or won’t know how) to divide anymore. These cells then accumulate damage, and die without a successor. With enough cell deaths in vital areas, the whole organism will perish. Therefore, a widely held belief amongst biology students is that the length of one’s life is determined by how long an individual’s telomeres can resist complete degradation.
While we’ve known that this conclusion is wrong for at least a decade now, this relationship between aging and telomeres has stayed afloat since it first generated widespread excitement in 1997, when Matthew Meyerson and colleagues published a breakthrough article in Cell Press. At the time, telomeres provided an explanation to the question of why cancer cells are biologically immortal. It turned out that cancer cells have a mechanism for regenerating their telomeres.
Last year, an article published in Royal Society Open Science revealed that telomeres play no role in how long an average person will live. You could live to be 140, and your telomeres would still be in good shape. Note that the oldest lived person, as of 2019, was Jeanne Calment who died at the age of 122. Furthermore, that same article notes that some animals could never use up their telomeres, even if they lived through the span of tens of human lives.
Despite this current research, we have a whole generation of biology students graduating this year who think telomeres are responsible for aging. With that framework in mind, you must conclude that nothing can be done to prolong youth and delay age-related diseases such as cancer, autoimmune disorders, and dementia. The reality is that there are hot leads in the field of aging — paths that scientists believe could possibly even lead to humans prolonging their youth by hundreds of years. What’s lacking right now is a generation of passionate youth to unravel these leads.
Feature photo edited by Alora Griffiths.