We all know that genetics play a role in how long we live. But we do not know exactly how.
Alexander Graham Bell, the inventor of the telephone, was interested in ageing and in the 1900s he found that people who lived long had long-lived children.
Whether this is due to genetics or is a result of providing support to children remains unknown. Sometimes bad luck just strikes, despite having the best genes.
Jeanne Louise Calment, who died in 1976 at the age of 122, provides a sad example of how bad luck negates good genes. Her daughter Yvonne, died at the age of 36 of pneumonia. Luckily, she left a son Frederic, who become a physician. He lived with Jean Louise in her apartment. However, he died in a motorbike accident at the same age as his mum. Sometimes bad luck negates any genetic advantages.
There are three classic experiments that define genetic advantages to living longer. The first approach is a classic experiment by Michael Rose who, by allowing eggs of old flies to hatch, found that the next generation lived longer. The new generation seemed to know that similar to their parents, they need to live longer to reproduce. We also find this among humans. The older your mother was when she conceived you, the longer you will likely live.
The second type of experiment uses a naturally occurring disorder in a flatworm that produces less growth hormone which makes them live much longer. Through a series of trial and errors Cynthia Kenyon from the University of California, San Francisco managed to chemically knock out one of the genes in normal flatworms and nearly doubling their lifespan.
The third type of genetic observation was with mice, in particular the work done by Richard Miller and his infamous dwarf mouse called Yoda. Again, nature leads the way in showing us about the longevity advantage of having less growth hormones. There are three types of dwarf mice that share this longevity characteristic: Snell, Ames and Laron dwarf mice. These mice live about three times longer than average.
By knocking out a gene to stop growing we could live longer. Somehow, the body knows that we need to live longer in order to be able to pass on its genes. We have examples among humans as well. In a southern Ecuador community of 250 individuals who have Laron syndrome – causing a deficiency in primary growth hormone – although protected against disease, especially cancer, this apparent protection does not translate to living longer. They engage in risk behaviours, in particular alcoholism, that negate this genetic advantage.
We all know that genetics play a role in how long we live. But we do not know exactly how
No one wants to have a stunted growth to live longer. But what about having older parents to increase longevity? In biology, there is always a dark side. We know that women having children at much older ages increases the risk of certain genetic problems.
It has also been reported in 2014 by Boris Rebolledo-Jaramillo with Pennsylvania State University and his colleagues that children of older mothers face greater risk of developing diabetes, dementia and heart disease. As for older fathers, their children are more likely to have dwarfism or Apert syndrome.
Newer research in 2012 by Augustine Kong at Reykjavik University, Iceland also suggests that there is an increased risk for autism and schizophrenia. There is a “goldilocks effect”, not too old and not too young, just right.
The surprising result in genetic research is the finding that as we age we are also changing our genes. It was always assumed that our genes are unchanging and that they are given to us exclusively by our parents. But we are learning that we also add and modify our genes as we age.
We acquire one per cent of our genes from bacteria, viruses and archae – single cell micro-organisms. These ‘plasmids’ help us fight infection and if we are constantly being infected, then they insert themselves into our DNA so we can develop this protection ourselves. Sometimes our own genes change position in our chromosomes so they gain higher priority. These genes are known as ‘jumping genes’ or as ‘transposons’.
Such strange genetic behaviour was first discovered by Barbara McClintock in the 1940s who was awarded the Nobel Prize for medicine in 1983. How plasmid and jumping genes do this remains an absolute mystery. Her work provided evidence that the composition of our genes – our genome – changes while we are living. The longer we live, the more likely that these new genetic improvements are transmitted to our children. So now we have figured out the method of how Michael Rose’s flies create a time stamp on their genes. Plasmids are at work throughout the ageing process.
We develop immunity from the day we are born and some of these biological adaptations end up in our genes through the transfer of external genetic material. Our genes are more permeable than we once thought. We get genes not just from our parents but also from the environment.
In addition, we also get genetic material from our twins in the womb and mothers get genes from their children. We find male chromosomes in mothers who had baby boys. We are a magnet for adaptive genetic material from our environment.
Barbara McClintock was also the first scientist to correctly speculate on the basic concept of how some genes can be switched on and off – known as epigenetics, above genes. Sometimes a defective gene (e.g. for diabetes or Alzheimer’s disease) can be switched off – through diet, exercise and mild trauma.
As we age we pick up new genetic material and modify existing genes (epigenetics) before we pass these genes on to our children. Our lives are devoted to just this aim, making sure that our children are best prepared to the new world they face.
Mario Garrett was born in Malta and is currently a professor of gerontology at San Diego State University in California, US.