Why we can’t live forever: understanding the mechanisms of ageing

MERLIN THOMAS, BAKER IDI HEART & DIABETES INSTITUTE

Share on print There are a number of processes involved in ageing and unfortunately there's no way to stop them. However, we can slow them down slightly with diet and lifestyle, according to Merlin Thomas.  Image: nocameraz/iStockphoto Ageing is the sum of many processes acting in concert to produce the signs and symptoms we know as “getting old”. Of course, there’s no way to stop the ageing process, but a better understanding of the different mechanisms of ageing can help us slow it and enjoy better health as the years advance. Perhaps one of the most easily recognisable features of ageing is that of loss – whether loss of memory or a full head of hair. When we look in the mirror, many of the features we identify as “old” are simply a threshold. Although the time it takes to reach any arbitrary threshold can be considered “ageing”, many other factors can shorten or extend this time. Greying hair Ageing hair greys when the cells that pigment the hair become damaged. By the age of 50, half of all hair follicles in half of all men have lost their pigment. But ageing is not the only factor involved; smoking, sunlight exposure, inflammation, stress and other factors all act on the hair to shorten the time it takes for the grey to take over. This is how we can appear to get older faster, because it takes less ageing time to reach a point when all the dark hairs have gone. More importantly, by preventing or reducing these modifiable lifestyle factors, we can appear to age more slowly, even if we never change our ageing speed. Consequently, slowing ageing does not mean stopping time, but stepping away from the edge so that time is no longer the enemy. Injury and mileage With ageing comes an accrual of injury. As Indiana Jones once quipped about his lack of stamina, “It’s not the years, honey, it’s the mileage.” The human body accumulates a lot of “natural shocks” over a lifetime, which ultimately threatens its integrity and underlies many of the phenomena we recognise as ageing. A good example is damage to the genetic code, which is known as “mutations”. These errors become more common and more significant the more times a sequence has been copied and recopied, and eventually they can change the way cells function. But while overuse may be an important factor, atrophy from lack of use is another contributor to ageing. All cells require stimulation for healthy growth and activity. Hearing or visual loss, for instance, seems to speed up when people are deprived of stimulation. By contrast, those who continue to be active physically, mentally, socially and spiritually not only retain the greatest quality of life, but find the impacts of ageing seem to slow. Reparing the body Some parts of the body may be more susceptible to ageing because they have limited abilities for repair. Other parts defend stoutly, at least initially. But as we age, these repair mechanisms can become less effective, so that any stress potentially becomes more injurious. As we get older there are a number of ways to compensate, to keep things ticking over normally. The appearance of ageing can be the physical manifestation of these compensations, like a walking stick or hearing aid. These compensations may also be evident in the ageing body. The ageing heart, for instance, adapts – getting bigger and contracting longer to maintain function despite the extra demands of stiff vessels. The atria also work harder and faster to fill the heart. This augmented atrial contraction can sometimes be heard as a fourth heart sound (called a “gallop” rhythm) if you listen with a stethoscope in an elderly patient. Can we live forever? Our design is incompatible with indefinite survival. As is the case with a toaster, lifespan is limited. Given reliability of components, some toasters will survive longer than others, although they do roughly the same job. But eventually, one morning your toast will not pop. Similarly in humans, some parts simply can’t be replaced. We have a complement of specialised (post-mitotic) cells that have very limited or no capacity to divide. These include the neurons of the brain, the beating muscle of the heart and the insulin-producing cells of the pancreas. They cannot be replaced, which is why the effects of ageing may be more important and more obvious in these cells and the functions that they serve. Is ageing a disease? In most people’s minds, ageing is synonymous with having more disease. But it’s not the same thing. Take, for example, our bones. From about 20 years of age, our bones get progressively thinner. At some point, bone loss becomes so significant that its integrity is compromised, leading to an increased risk of fractures. This point (or disease) is called osteoporosis. While bone loss is not separate from ageing, it is not the same thing. A number of other factors (such as smoking and inactivity) can also contribute to bone loss and therefore osteoporosis (disease). Ageing just moves you closer to the edge in a way that makes it easier for other factors to push you over and initiate disease. Equally, preventing disease can slow the impacts of ageing. Ageing is the sum of life Ultimately, ageing is not one factor but the sum of many: some damaging, some protective. In youth, these forces are kept in balance. But with the passage of time there is an accrual of injury and the memories of its effects. Although our design is incompatible with indefinite survival, it does not mean that we can’t shift the odds in our favour with smarter choices in our diet and lifestyle. Plan to take the long way home. This is an edited version of an article that appears in the latest issue of Perspectives, an opinion-led journal published by Baker IDI Heart and Diabetes Institute. Editor's Note: This article was originally published by The Conversation, here, and is licenced as Public Domain under Creative Commons. See Creative Commons - Attribution Licence.