Lifestyle habits are intertwined with how our genes are expressed, meaning we have a degree of control over how they work. Photo / Getty Images
Lifestyle habits are intertwined with how our genes are expressed, meaning we have a degree of control over how they work. Photo / Getty Images
You’ve probably referred to them negatively – blaming them for your weight, bad habits or thinning hair. But while you can’t change the genetic hand you’ve been dealt, you actually have more control over how your genes work than you think.
We are born with around 20,000 genes, stretches of DNA that contain instructions for cells. There are two copies of each – one inherited from each of our parents.
However, lifestyle habits are intertwined with how our genes are expressed and can effectively turn certain ones “on” or “off” – similar to light switches in your home.
Ultimately, this means in many cases, you can dim down genes linked to disease and dial up those connected with long life.
“Studies have shown that longevity in humans is about 25 per cent heritable. What it means is that how long we live is mostly (75 per cent) determined by the environment and only 25 per cent by our genes,” says Professor Joao Pedro Magalhaes, head of the Genomics of Ageing and Rejuvenation Lab at the University of Birmingham.
Lifestyle habits are intertwined with how our genes are expressed and can effectively turn certain ones “on” or “off” – similar to light switches in your home.. Photo / Getty Images
“If you exercise, that induces changes in your body that in turn affect how your genes are expressed. The same goes for diet.”
It’s “very hard” to draw a line between lifestyle changes, a change to gene expression and the knock-on effect on longevity, Magalhaes notes. However, there is some promising research.
“There is a gene called mTOR which regulates how our cells sense nutrients and – depending on that – decide whether to grow or not,” explains Dr Nick Ktistakis, group leader at the Babraham Institute, where researchers are studying the ageing process.
“Reducing the activity of mTOR has been shown to extend lifespan in many organisms, and would likely do so in humans. So, reducing mTOR activity is good for longevity,” he says.
One way to effectively switch off mTOR is to cut back on calories, according to studies conducted on animals, which had their food supply cut by up to half.
However, scientists admit the “sheer willpower” people would need to follow suit makes this unachievable, and make the somewhat obvious warning that the approach could trigger dangerous side effects, such as too much weight loss.
Therefore, researchers are studying a pharmaceutical alternative – a drug called rapamycin. It was originally developed as an immunosuppressant for organ transplant patients but, like caloric restriction, switches off mTOR. “Lots of work is being done with these drugs to see if they can affect longevity,” says Ktistakis.
“Rapamycin is one of the most robust life-extending drugs as it extends lifespan in rodents (up to 15 per cent) and is currently being tested in dogs. [It] is one of the most active areas of research in longevity pharmacology,” says Magalhaes.
However, separate studies have supported the evidence for calorie cutting to live longer. One by a team at Columbia University found people who cut their food intake by 25 per cent for two years slowed their biological ageing by 2 to 3 per cent. That conclusion was reached after they took blood samples from the volunteers to monitor chemical tags that regulate the expression of longevity-related genes.
The researchers noted that, while dramatic calorie cutting “is probably not for everyone”, simply following intermittent fasting (eating very little or nothing at all for a set period of time, such as one or two days a week) or time-restricted eating (consuming food within a fixed window each day, such as 10am and 6pm) could trigger similar results.
Exercise
Scientists are also excited about a gene called FOXO3. Studies dating back more than a decade show it activates autophagy – the process of cells getting rid of old and damaged parts, which is vital for increasing one’s healthy lifespan.
While, as with all genes, everyone has two copies of it, three in 10 people in the UK have one “supercharged” version, while one in 10 have two – meaning they have a “jet-engine” FOXO3 gene, according to Dr Craig Willcox, a professor of public health and gerontology at Okinawa International University in Japan. Only a genetic test can reveal which version a person has.
Exercise can activate the FOXO3 gene, protecting against cardiovascular and cardiometabolic disease. Photo / 123RF
“Our studies have shown that FOXO3 is at the centre of an ageing hub. It integrates signals from dozens of other genes that affect the ageing process. Think of it as a superintendent gene that is directing the ageing process, as well as protecting against age-related disease,” he says.
Research has shown FOXO3 protects against cardiovascular disease – one of the leading causes of death in the UK – and cardiometabolic disease, which includes heart attacks, diabetes and non-alcoholic fatty liver disease.
Exercise can switch on FOXO3 by alerting it “that it needs to get to work” and counterbalance the stress physical activity puts the body under, Willcox explains. In response, FOXO3 triggers the release of antioxidants that reduces inflammation.
How quickly the gene is activated depends on a person’s genes and lifestyle. But it will likely occur slowly over time, “just as working out will change your body shape over time”, he says. “The key point about lifestyle change is persistence and continuity,” Willcox adds.
Sleep
Other studies show sleep is vital.
When scientists at the University of Rochester compared how genes were regulated across dozens of animals, they found among the species that live the longest, genes linked to inflammation and the process of converting food into energy were dimmed down.
The team concluded this meant an unhealthy sleep schedule or exposure to light at night could increase the expression of genes that drive down people’s lifespans, despite their study focusing on animals.
Drink green tea and eat broccoli, oranges and berries
“AMPK is often seen as the ‘master switch’ of our metabolism and also viewed as a central junction for many nutrient responsive pathways associated with longevity,” says Dr Harpal Bains, medical director of the longevity-focused Harpal Clinic in London.
Both green tea and the antioxidant quercetin – found in onions, broccoli, citrus fruits and berries – can activate AMPK, she says.
Drinking good-quality green tea can make an important difference regarding how your genes are expressed. Photo / 123RF
“Finding a good-quality green tea is a fundamentally good way to support longevity, as green tea can support many areas of genetic expression,” Bains adds.
Caloric restriction and exercise also turn the dial up on this gene, she says.
“Caloric restriction is definitely not about eating as little as possible,” Bains notes. “This would be unhealthy, causing nutrient deficiencies and leading us to have inadequate fuel – not very good for our longevity at all. Instead, it is more about not overeating: we should be aiming to feel about 80 per cent full at each meal.”
