In affluent, relatively secure nations, the lifespan of individuals is thought to be equally influenced by both the genetic variations inherited from parents and by environmental and lifestyle factors. This conclusion was reached by the authors of a study that re-analyzed data from twin research conducted in Denmark and Sweden.
For residents of these countries, it might not be surprising that their longevity is likely half determined by genes and half by their surroundings. However, earlier twin studies performed decades ago concluded that genes account for only a quarter of the variation in human lifespan.
“This slightly shifts the balance, suggesting that genetics plays a larger role, while the environmental contribution becomes a bit smaller,” states Joris Deelen, a member of the research team from Leiden University Medical Center in the Netherlands. “But at least 50 percent stems from environmental factors, so the environment continues to play a significant part.”
Heritability is a metric indicating the extent to which variability in a specific trait is attributable to genetics, compared to the extent it is due to the environment. As the researchers note, the heritability of any trait is not a fixed number valid for everyone, everywhere, at all times. Rather, it is applicable only to a specific population within a specific setting.
A classic illustration is the height of wheat. If seeds are sown in a flat, uniform field, almost all height variations will be due to genetics. But if those same seeds are planted across a more diverse landscape, almost all height variations will be caused by differences in soil, sunlight, water, and so on. The heritability of height in these two scenarios would differ significantly.
To estimate the heritability of human traits, geneticists often compare twins raised together with those raised apart. In this specific study, Deelen and his colleagues primarily utilized twin research involving individuals born in Sweden or Denmark between 1870 and 1935.
When they excluded deaths resulting from accidents or infections, as opposed to age-related diseases like heart attacks, the heritability of lifespan increased to approximately 50 percent.
This aligns more closely with what we understand about aging in animals, according to Deelen. “I believe it is more realistic that it is closer to 50 percent than to 25 percent.”
“Their paper estimates the heritability of maximum lifespan under ideal conditions, implying that only aging processes contribute, which is a much narrower question than overall lifespan,” comments Peter Ellis from the University of Kent in the UK. It is unsurprising that heritability is higher for this more restricted question, he adds.
Such findings suggest that numerous gene variants dictate variations in human longevity, and identifying them could potentially aid in developing life-extending medicines. Yet, very few such variants have been discovered thus far.
“It remains a major puzzle why so few genes associated with human longevity have been identified,” remarks De Magalhães.
One difficulty is that the majority of individuals participating in studies like the UK Biobank are still alive, meaning there is insufficient data to provide the necessary statistical power. Deelen posits that this is also linked to the high complexity of genetics.
For instance, Ellis points out the existence of trade-offs; for example, variants that temper the immune system reduce the risk of autoimmune diseases but simultaneously decrease defense against infections. This implies that the team’s assumption that mortality from infections is unrelated to lifespan may not necessarily be accurate, he suggests.
De Magalhães also observes that the role of genetics appears completely different when comparing species rather than individuals within the same species. “If you have a mouse genome, you cannot reasonably expect to live beyond three or four years,” he states. “On the other hand, if you possess the genome of a bowhead whale, you might live for over two centuries.”
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