Aging is inevitable, but some studies suggest the effects of aging can be reversed.
In simple terms, aging is defined as the process of becoming older, which involves a number of biological mechanisms that lead to deterioration of health – both cognitive and physical – over time.
Of course, aging is inevitable. While many of us would like to stop the clock and avoid blowing out those birthday candles – an unsubtle reminder that we are another year older – it is beyond the realms of medical science.
What may be within reach one day, however, are ways to reduce or reverse the effects of aging, and we’re not talking about anti-aging face creams or cosmetic surgery.
Increasingly, studies have focused on strategies that could combat aging at its core – the cellular processes that contribute to age-related diseases and changes in our physical appearance as we become older.
In this spotlight, we explore the biological causes of aging, investigate what strategies researchers are proposing to fight the effects of aging, and look at what you can do to boost your chances of healthy aging.
The genetic aging theory
Many researchers believe the effects of aging are a result of numerous genetic and environmental factors, and these effects vary from person to person.
The genetic aging theory suggests that, just like hair color and height, our lifespan is influenced by the genes we inherit from our parents.
Such a theory may ring true; studies have shown that children of parents who have a long lifespan are more likely to live a longer life themselves.
And research from Sweden’s Karolinska Institutet (resource no longer available at www.nature.com) – published in 2013 – suggested that the aging process is influenced by mitochondrial DNA that we inherit from our mothers.
The team found that female mouse models passed mutations in mitochondrial DNA – which they accumulated through environmental exposures during their lifetime – to offspring, which reduced their lifespan.
But while evidence for the genetic aging theory is strong, the fact remains that healthy aging and longevity is largely influenced by our environment – that is, what we eat, how much we exercise, where we live and the compounds and toxins we are exposed to throughout our lifetime.
Oxidative stress and telomere length
Our DNA accumulates damage from environmental exposures as we age. While cells are capable of repairing most of this damage, sometimes it is beyond repair.
This most often occurs as a result of oxidative stress, where the body does not possess enough antioxidants to fix the damage caused by free radicals – uncharged molecules that cause DNA damage. Oxidative stress has been identified as a key player in the aging process.
Another major cause of DNA damage is the shortening of telomeres. These are the caps at the end of each DNA strand that protect our chromosomes – the thread-like structures that contain all our genetic data.
Telomeres are the caps at the end of each DNA strand that protect our chromosomes; their shortening speeds up the aging process.
Telomeres naturally shorten as we age, reducing in length each time a cell divides. But when telomeres become too short, they are no longer able to protect the chromosomes, leaving them susceptible to damage that can lead to premature aging and disease development.
A recent study from the UK’s University of Cambridge suggests that telomere shortening as a result of environmental exposures may even be passed to offspring.
The team found that rats that had lower oxygen in the womb during pregnancy – often caused by smoking during pregnancy in humans – gave birth to offspring with shorter telomeres than rats that had higher oxygen exposure.
What is more, the oxygen-deprived offspring were found to have abnormalities in their blood vessels – a sign of faster aging and a predisposition to heart disease.
“We already know that our genes interact with environmental risk factors, such as smoking, obesityand lack of exercise to increase our risk of heart disease,” notes senior author Prof. Dino Giussani, from the Department of Physiology Development & Neuroscience at Cambridge, “but here we’ve shown that the environment we’re exposed to in the womb may be just as, if not more, important in programming a risk of adult-onset cardiovascular disease.”
The evidence for telomere length as a major player in the aging process has become so strong that researchers are looking to use telomeres as a biomarker for age-related diseases.
Last year, for example, Medical News Today reported on a study in which researchers revealed how a distinct telomere pattern in the blood could be used to predict cancer development.
But what if researchers found a way to extend telomere length to protect against age-related diseases and the other effects of aging? Or what if they identified a strategy that could protect against oxidative stress?
Such approaches may not be too far from reality.
Extending telomere length to slow aging
Last year, MNT reported on a study published in The FASEB Journal, in which researchers from Stanford University School of Medicine in California revealed they have discovered a way to increase the length of human telomeres.
Researchers have uncovered ways to increase telomere length, which could slow aging.
The team – including study coauthor Helen Blau – used a modified form of ribonucleic acid (RNA) that consisted of the coding sequence for TERT – the active component of telomerase, an enzyme that maintains telomere health – to extend the length of telomeres.
By applying three applications of the modified RNA to human cells in a lab, they found they could increase the length of telomeres by around 1,000 nucleotides – around 10% – in a matter of days.
Blau and colleagues said their findings bring us a step closer to combatting both age-related and genetic diseases.
“One day it may be possible to target muscle stem cells in a patient with Duchenne muscular dystrophy, for example, to extend their telomeres. There are also implications for treating conditions of aging, such as diabetes and heart disease. This has really opened the doors to consider all types of potential uses of this therapy,” says Blau.
But according to other research, there may be ways in which we can extend telomere length ourselves in order to slow the aging process.
In December 2014, a study reported by MNT suggested following a Mediterranean diet – typically high in vegetables, fruits, nuts and olive oil, but low in saturated fats, dairy, meat and poultry – may lengthen telomeres.
From studying more than 4,600 healthy, middle-aged women, the team found that those who had greater adherence to a Mediterranean diet had longer telomeres than those with lower adherence to the diet.
Another study, published in September 2014 in the British Journal of Sports Medicine, suggested that reducing the amount of time sitting may protect against telomere shortening and extend lifespan.
Eradicating mitochondria to rejuvenate aging cells
Last month, Dr. João Passos, of the Institute for Aging at Newcastle University in the UK, and colleagues revealed a new strategy that they say could reverse the aging process: removing mitochondria from cells.
Mitochondria are described as the “powerhouses” of cells, giving them the energy to function, but previous research has also associated mitochondria with oxidative stress.
In their study, published in The Embo Journal, Dr. Passos and colleagues increased mitophagy – a process cells normally use to get rid of faulty mitochondria – in aging human cells, enabling them to eradicate all mitochondria.
They found that eliminating mitochondria from the aging cells triggered a rejuvenation process, reducing markers of cellular aging to levels that are normally seen in younger cells.
“This is the first time that a study demonstrates that mitochondria are necessary for cellular aging. Now we are a step closer to devising therapies which target mitochondria to counteract the aging of cells,” says study coauthor Dr. Clara Correia-Melo.
Reversing brain aging
When it comes to aging, one of the biggest concerns is how it will affect our cognitive function.
The majority of people will see a decline in cognitive skills as they age. This is because certain areas of the brain – particularly those linked to learning and memory – shrink as we get older, interfering with connections between nerve cells.
Others may experience a more severe form of cognitive decline, such as Alzheimer’s disease, which affects around 5.1 million adults aged 65 and older in the US, though this condition is thought to be triggered by the build-up of plaques and tangles in the brain, rather than brain shrinkage.
But increasingly, researchers are uncovering medical strategies that show promise for reversing brain aging. Last month, MNT reported on a study published in The Journal of Neuroscience, in which researchers successfully reversed aging in the brains of rats.
The team – from the University of California-Irvine – gave 11 rats a drug called ampakine every day for 3 months, while a further 12 rats received a placebo.
From brain scans conducted during treatment, the researchers found “middle-aged” rats in the placebo group had shorter dendrites – branch-like fibers that aid brain cell communication – and fewer dendritic branches than the “adolescent” rats that received the placebo.
The middle-aged rats that received ampakine, however, were found to have dendrites and dendritic branching that was comparable to those of the adolescent rats, suggesting that ampakine may be a promising compound for reversing brain aging.
Commenting on the results, study coauthor Gary Lynch says:
“There is a tendency to think that aging is an inexorable process, that it is something in the genes, and there is nothing you can do about it. This paper is saying that may not be true.”