The Science Behind Growing Old
Riddhi Datta
What if time stood still? What if the relentless march of ageing could be stopped, freezing us in eternal youth? This captivating premise has fuelled countless works of fiction.
Remember Adaline Bowman – Blake Lively's character in The Age of Adaline? Adaline was driving at night when her car plunged into icy water and was struck by lightning. As a result, Adaline froze in time, forever appearing 29 years old.
In reality, however, we still do not have a magic formula to stop ageing. But this intriguing field has motivated scientists around the globe to delve deeper into the secrets of growing old. Significant strides have been made in understanding this complex process and how it is influenced by biological and environmental factors.
So what happens when we grow old?
Ageing is a complex biological process involving a plethora of changes at molecular and cellular levels. These changes result from the wear and tear of our everyday life. It involves a gradual decline in cellular functions which enhances susceptibility to age-related disorders.
One of the major culprits for this degenerative process is DNA damage, which comes from exposure to mutagenic agents in the environment or as a part of inherent errors in the biological processes. Think about the polluted air we breathe in or the traces of pesticides in our food.
Our exposure to environmental mutagens is increasing everyday. To counter this, our body has an elaborate system for DNA repair that detects and efficiently corrects the damage. If, however, the machinery fails to repair DNA damage correctly, harmful mutations accumulate gradually leading to genomic instability.
DNA damage is also the root for inflammation. Both genomic instability and inflammation are the hallmarks of ageing. In fact, a strong correlation has been found between DNA damage and age-related diseases like Alzheimer’s disease, cardiovascular issues, osteoporosis, atherosclerosis, and even cancer.
Telomere attrition
Another factor responsible for the ageing process is telomere attrition. Remember Amitabh Bachchan’s character, Auro, in Paa? That eight year old kid was suffering from accelerated ageing and looked like an old man. That is a rare medical condition called progeria resulting from a defective telomere length.
Telomeres are repetitive sequences that span the ends of our chromosomes. They are responsible for maintaining chromosomal integrity and determine the number of times a cell can divide.
As the cell continues to divide, the telomere shortens and this process significantly contributes to ageing. For example, telomere length decreases 20 bases per year in our cardiac tissue. And the risk for coronary heart disease is associated with telomere length shorter than 200 bases. In addition to cardiac issues, telomere dysfunction has been linked to a range of age-linked degenerative diseases.
The mitochondria, stem cells and environmental factors
Growing old is also related to the mitochondria – the powerhouse of the cell. These cellular organelles are the sites for energy production and are crucial for stress resilience. As we age, there is a gradual decline in the mitochondria’s ability to perform its cellular functions. Scientists have shown that mitochondrial dysfunction can result in premature ageing, shortened life-span, anaemia, osteoporosis and hearing loss in mice.
Ageing in almost all living beings is characterised by impairment in tissue maintenance and regeneration. This is largely due to a decline in the stem cell population. Stem cells are special cells that can switch-on and off their cell division cycle according to the body’s needs.
Throughout our life, these stem cells take care of the repair and regeneration of tissues. With time, cellular damage accumulates in the stem cells which impair their regenerative ability. This makes repair of the regular wear and tear in the body difficult.
Another intriguing factor that modulates ageing is epigenetic changes. Epigenetic changes are reversible chemical modifications in DNA that results from environmental factors, lifestyle, stress and pathologies.
Interestingly, scientists have devised epigenetic clocks which are mathematically derived age estimators based on DNA methylation in individuals. This ‘EpiAge’ is a measure of the biological age and typically differs from the chronological age. It reflects the impact of lifestyle and environmental factors that can either delay or accelerate ageing.
So can we stop ageing?
Growing old is a biological process that is linked to numerous physiological, psychological and social repercussions. Since ageing is associated with chronic disorders and declining cognitive abilities, older adults are often marginalised in society. Subtle age-related humour that perpetuates negative stereotypes about the elderly can lead to decreased self-esteem, loneliness, anxiety and depression.
But can we really stop ageing? Nobel laureate Venki Ramakrishnan addresses this issue in his book Why We Die: The New Science of ageing and the Quest for Immortality.
He emphasises that the real challenge is addressing ageing in a way that preserves our identity, and doing so safely and effectively. The key is not to halt ageing but to delay age-linked degeneration for a healthier later life.
The most crucial factor in this line is a healthy lifestyle and mental well-being. Similar to science fiction, recent scientific advancements offer intriguing possibilities for delaying age-related degeneration.
Research has shown that precise caloric restrictions can trigger cellular reprogramming and anti-ageing effects in mice. More excitingly, a drug called rapamycin, which has the potential to reverse ageing, is being studied. Anti-ageing therapy employing pluripotent stem cells is also being explored.
However, let’s not forget the challenges Adeline endured in the film. Perhaps it would be better to abandon the fantasy of eternal youth and embrace ageing gracefully.
Riddhi Datta is a Molecular Biologist and Assistant Professor in the Post Graduate Department of Botany, Barasat Government College.
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