The secret to how we age lies not in our DNA but in ageing itself – as well as environmental factors.
This is according to the newest study looking at how these factors affect the expression profiles of many of our genes (made up of DNA) as we get older. The level at which genes are expressed – that is, ratcheted up or down in activity – determines everything from our hormone levels and metabolism to the mobilisation of enzymes that repair the body, explains a news release on the study.
“How do your genetics – what you got from your sperm donor and your egg donor and your evolutionary history – influence who you are, your phenotype, such as your height, your weight, whether or not you have heart disease?” said co-author, Peter Sudmant, UC Berkeley assistant professor of integrative biology.
There’s been a huge chunk of work done in human genetics to understand how genes are turned on and off by human genetic variation, said Sudmant, adding that their project came about by asking how that is influenced by an individual’s age. Commented Sudmant:
Simply put, our individual genetic makeup can help predict gene expression when we are younger. Unfortunately, it becomes less useful in predicting which genes are ramped up or down when we’re older than 55 years, based on the dataset in this study.
For example, identical twins have the same set of genes, but as they age, their gene expression profiles diverge. So, this means twins can age much differently from each other.
What’s the point of these findings?
Researchers who are trying to better understand how humans age and to learn how to slow down this process have to study the genes expressed later in life and improve them.
So, these results can help researchers study the link between diseases of ageing and genetic variation in humans. “Almost all human common diseases are diseases of ageing: Alzheimer’s, cancers, heart disease, diabetes. All of these diseases increase their prevalence with age,” he said.
Massive amounts of public resources globally have been poured into identifying genetic variants that predispose you to these diseases. Said Sudmant:
Results support previous theory
The current study supports a theory by Nobel-prize winner Dr Peter Medawar who in 1952 proposed that genes that are turned on when we are young are more constrained by evolution (since they are critical to ensuring we survive to reproduce). However, after we reach reproductive age, genes expressed are under less evolutionary pressure. This means we would expect a lot more variation in how genes are expressed later in life.
Sudmant explained:
Sudmant also told Medical News Today: “When we do studies to identify the genetics underlying disease, we often end up with many genes that we could potentially target. Our study now quantifies how age impacts the expression of genes in the population. We argue that age-associated genes might be better therapeutic targets than the ones that vary in their expression as a function of human genetics.”
What about the environment?
Our environment impacts ageing, too, the study indicates. This includes the air we breathe, the water we drink, the food we eat, as well as our levels of physical exercise. According to Sudmant, the environment amounts to up to a third of gene expression changes with age.
Commenting on the findings, Dr Giuseppe Passarino, professor of genetics at the University of Calabria in Italy, who was not involved in the study, told MNT:
“This [study] does not imply that genetics is not important for ageing. There are many studies showing that the similarities between relatives regarding the quality of ageing (presence of diseases or inabilities) are very high.
“In fact, although the genes expressed later in life are not selected, still they are important for our life.” In other words, humans are equipped with highly selected “alleles” (a specific copy of a gene) for the first part of their life, he said, and with alleles that are less selected for the second part.
