Can We Stop Ageing?

Gerontology, the science of ageing and age-related physiological and pathological changes, has become a field of ongoing research as humanity furthers its quest towards immortality.

Yes, we want to live forever !

We don’t want to turn frail and die eventually. Our creative race is looking for remedies to prevent the age-related loss of functionality, diseases and develop a permanent cure.

As humans who occupy the top of the food chain and are the most developed intellectually, we reign supreme. But with more power comes more greed and sinister thoughts.

At the onset of 20th century, our life expectancy rose to about 50 years as compared to our prehistoric relatives. Industrial revolution and developments in public health infrastructure led to improved hygiene, better control of infections and epidemics, and reduced infant mortality. Clean water was available readily, we had developed advanced techniques to repair and heal our bodies, and were successful in eradicating previously incurable conditions.

By the turn of 21st century, our longevity increased by fifty percent, and life expectancy soared to 75 years. Mortality reduced for all age groups and life expectancy increased, resulting in a disproportionate rise in the elderly population. With it came its share of age-related morbidity.

Let us look at the definition of ageing and its causes.

It is defined as a process of intrinsic, progressive and generalised physical deterioration that occurs over time, beginning at about the age of reproductive maturity ("Handbook of the Biology of Ageing. (eBook, 2005) [WorldCat.org]").

From years of research, we have come to a consensus that ageing is a result of one or more of the following factors–

• accumulation of DNA damage,

• exposure to reactive oxygen species,

• loss of telomeres from our chromosomes,

• generalised wear and tear at cellular, molecular, tissue and systemic levels, and/or

• reduction in stem cell function (regenerative capacity).

Major killer diseases, like cancer, cardio-vascular disease, and dementia, are strongly related to ageing.

Ageing is characterised by a generalised decline in function and increased reproductive capacity. It is apparent in organisms whose growth completes before reproductive maturity, and that includes humans.

At the cellular level, ageing starts with the damage to macro molecules and organelles, that leads to loss of cell function. It is followed by tissue compromise which leads to systemic stress. It further damages nearby tissues, causing loss of function due to wear and tear.

Genetic research has provided an insight into the elements of ageing.

Gene-based research either targets a group of genes that mimic accelerated ageing or activates a single genetic mutation that slows ageing and extends lifespan. For this, researchers study vertebrates, invertebrates and fungi, including budding yeast (Saccharomyces cerevisiae), nematode worm (Caenorhabditis elegans), fruit fly (Drosophila melanogaster) and mouse (Mus musculus).

Research has identified genes that extend the life spans of these organisms. Moreover, studies with calorie restriction, exposure to lower temperatures and other environmental modifications have shown some success.

The outcomes of these research models were usually recorded in terms of their effect on the initial mortality rates or on the slope of mortality trajectory.

For instance, exposure to lower temperatures slowed the rate of ageing in fruit fly by lowering the slope of mortality trajectory, with no effect on the initial mortality rate. It is because lower temperatures reduce the rate of most molecular processes, while higher temperatures accumulate irreversible damage.

In industrialised human societies, initial mortality rates have fallen due to better sanitation, disease control and interventions, while the slope of mortality trajectory has remained constant. This suggests that the overall health has improved but the damage accumulation has not been reversed.

Similarly, calorie restriction was shown to extend the life span in rodents and decrease the appearance of neoplasms in primates.

In humans, genetic mutations causing Progeria or Werner Syndrome have shown that while subjects display overt signs of ageing, like wrinkles, alopecia or cardiovascular diseases, they do not necessarily show signs of wear and tear, like arthritis.

Although a single gene mutation has been shown to affect lifespan in invertebrates, it is yet to be applied in humans. There are some ethical dilemmas that need answering before venturing into immortality.

Medical specialists currently investigate and manage age-related issues basing the prognosis on a single disease. However, ageing is a complex polygenic process. We don’t know much about the temporal changes and their dynamics during the ageing process.

In contrast, we know that interventions at different stages of ageing may help if there is some reversibility present. Once the stage of irreversibility is reached, it leads to a downward spiral. Research, therefore, should be directed towards improving health during ageing, rather than increasing the life span of the population.

Gerontologists aim for compressed morbidity i.e. treatments targeting physiological changes during ageing to increase life expectancy and not the overall life span of the population. This may create a society with more elderly people who are functional and can contribute to the socioeconomic progress of humanity.

More radical research intends to decelerate or arrest ageing where treatments are targeted either to slow the process or to continually replace wear and tear to maintain vitality and function.

It is imperative to consider the ethics of such research and the overall effects of an ever-increasing life expectancy on the limited resources available to us on our planet.

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