The process of ageing occurs in practically all living things and the questions “how” and “why” we age have been people’s lips for centuries! Yet exactly how and why we age remains shrouded in uncertainty, and the precise answers to these fundamental questions have (so far!) eluded even the brightest and most brilliant of boffins. Nowadays, there are a whole load of theories on how we age, and realistically it’s more than likely that the true answer isn’t as simple as any single one of these – a combination of one, some, many or indeed all of the current theories (and future theories) will likely be the closest to the truth we’re going to get!

Programmed vs. Damage Theories

The theories of ageing come under two main headings: ‘programmed theories’ and ‘damage theories’. Programmed theories dictate that ageing is a controlled process, and largely indicate that a program of age-inducing gene expression is activated. This would be like how growth and development happens, but would instead act to down-regulate our maintenance and repair functions, leading to a gradual loss of function in our bodies which manifests as ageing and end in death.

‘Damage theories’ do not involve a programmed ageing process, but instead say that ageing is due to an accumulation of damage from factors such as environmental stresses. These insults lead to gradual loss of function of molecules in the body: these damaged molecules cause dysfunction at the tissue level, which manifests as ageing and eventually leads to failure of the body’s systems.

Programmed theories

A number of theories come under the banner of ‘programmed ageing’ theories. These include the ‘endocrine theory’ and the ‘immunological theory’. The endocrine theory suggests that levels of certain hormones (signalling molecules that have widespread effects throughout the body) act like a biological clock which eventually ticks down to a time that signals for ageing to begin and progress. Insulin signalling via the IGF-1 receptor is one pathway under investigation in relation to this theory, and there is a lot of emerging research into these pathways and their effects on longevity (exciting stuff!).

The immunological theory of ageing relates to the gradual decline in immune function as we get older. The theory is that as our immune systems get weaker, we become more vulnerable to infections which induce stresses at both the cellular level and at the level of the whole body. These stresses cause a decline in the body’s functions and eventually lead to death. Altered immune function has also been linked to many age-related diseases, including cardiovascular disease, Alzheimer’s and cancer, and so may well be a key player in the bigger picture of ageing.

Damage theories

There are a whole load of different theories that come under the banner of ‘damage and error’ ageing theories, including the ‘wear and tear theory’, ‘rate of living theory’, as well as the ‘free radical’ and ‘somatic DNA damage’ theories.

The ‘wear and tear theory’ is a simple concept: just like everything in life, our bodies, its cells and its tissues, wear out with use. Like a phone that’s a few models out of date, we gradually slow down and bits of us start crashing, eventually packing in all together!

The ‘rate of living theory’ is almost like a ‘live fast, die young’ way of thinking: its basis is in the observation that organism with high cellular metabolic rates tend to have a shorter lifespan. Notably the rate of living theory doesn’t hold true in all organisms, and so certainly doesn’t explain the ageing process on its own!

The ‘free radical theory of ageing’ is one that regular Beauty by the Geeks followers will recognise! Highly reactive species of molecules known as free radicals (including reaction oxygen species) damage molecules in our cells by stealing electrons and generating more radicals. Damage can be done by reactive species originating from the environment (exogenous damage) or from radicals generating within the cells themselves during processes like respiration (endogenous damage). DNA, proteins, lipids and many other molecules can all be damaged by these reactive species, and the theory is that as this damage accumulates it manifests as ageing. Antioxidants produced by the body neutralise these pesky free radicals to help protect against damage, and some studies have shown that increasing antioxidant levels (whether by consumption in the diet or by other methods) can increase lifespan. Don’t be sold too quickly though – there is a lot of conflicting data regarding antioxidants and lifespan!

“Antioxidants” themselves have certainly become an anti-ageing buzzword, and nearly all of the skincare products we see on the high street contain some form of antioxidant with the hope of protected our beloved skin from free radical damage from the environment. There is now a growing body of evidence that topical antioxidants can help protect molecules like collagen and elastin in the skin from free radical damage, helping fend off visible signs of ageing such as wrinkles and reduced skin elasticity, which is largely the scientific basis for these antioxidant-containing anti-ageing formulations. Many scientists now believe that the free radical theory of ageing represents only one means of causing the damage that accumulates over time, and so is not paint the entire ageing picture by itself.

Lastly, the ‘somatic DNA damage theory’: this theory identifies that DNA (the instructions for building life) is constantly damaged throughout life. The vast majority of DNA damage is repaired by very efficient mechanism in our cells (well done those cells!), but it cannot all be repaired perfectly. Gradually, this damage accumulates and the instructions become more difficult for the cell to read and understand properly. Part of this theory covers the role of specialized structures on the ends of our chromosomes called telomeres (chromosomes are discrete portions of our genetic information made of huge amounts of DNA).

Quite simply, the telomeres protect the chromosomes from damage, but are gradually eroded over time as the cells divide, and so telomeres become shorter and shorter with age. Eventually the telomeres become so small that it signals for the cell to permanently give up trying to divide, a state called ‘senescence’, or alternatively are signalled to die. This is to avoid chromosomes becoming damaged in the absence of adequate telomeres to protect their precious DNA. One part of this theory is that eventually our ability to renew our body’s cells becomes diminished because many of them are unable to divide (perhaps because of those eroded telomeres), which manifests as ageing and loss of tissue function.

These theories interlink, overlap and are by no means the only ageing theories out there! And even these ones aren’t anywhere near fully explained here – it’s a very complicated business this ageing malarkey! Enough to give anyone wrinkles! Whilst what we’ve discussed is a simplified version of what could be going on in our bodies, it’s certainly very interesting and hugely relevant in terms of finding ways to slow down the ageing process and protect against age-related diseases (and in some cases potentially keeping visible signs of ageing at bay).

Please do get in touch with any questions on ageing if this article has tickled your fancy!