Humans are still evolving — and we’re using the changes to weed out Alzheimer’s

A large-scale study of the human genome has uncovered evidence that our bodies are still evolving.  

By analysing the genomes of 210,000 people in the US and UK, researchers at Columbia University found that genetic variants that make people more likely to contract Alzheimer’s disease, for example, are less common in people who live longer. The same was found with genetic variants linked to heavy smoking.

People who live longer are, typically, more likely to pass on their genes. This means that the traits they possess are more likely to be spread throughout the population, whereas traits they don’t possess are consigned to the evolutionary rubbish pile. This is a basic tenant of natural selection; the process where organisms better suited to an environment survive and pass useful genes to their offspring.

This new research claims to show natural selection in action over a short period of time. The findings insinuate that sets of genetic mutations predisposing people to negative traits such as heart disease, asthma, high cholesterol, heavy smoking and obesity are all less common in people with longer lifespans.

Thanks to the rise in genomic sequencing, the scientists were able to track the relative rise and fall of hundreds of thousands of people across a number of generations. What they saw was a drop in the frequency of certain genes; most notably, in women over 70, a fall of the ApoE4 gene linked to Alzheimer’s. They also noticed a sizeable drop, starting in middle age, in the frequency of a mutation in the CHRNA3 gene associated with heavy smoking in men.

“It may be that men who don’t carry these harmful mutations can have more children, or that men and women who live longer can help with their grandchildren, improving their chance of survival,” said study co-author Molly Przeworski, an evolutionary biologist at Columbia.

We asked the authors of the paper, published in PLOS Biology, whether this research indicates that diseases like Alzheimer’s could be eradicated altogether, given a long enough timeframe.

“In principle, yes,” said the study’s lead author, Hakhamanesh Mostafavi. “However, that relies on the assumption that these genetic variants remain deleterious for a long time, in face of environmental changes.

“The genetic variant associated with heavy smoking is a good example,” he added. “If people smoke, those who carry this variant tend to smoke more, and consequently are more exposed to the adverse effects of smoking. However, in environments where no-one smokes – at present or in the future – this variant does not have an effect.”

As Mostafavi suggests, the development of many traits very much depends on how advantageous or disadvantageous they are within given environmental conditions. He also told Alphr that survival is only one component of evolutionary fitness. “It could be that a genetic variant kills you, but makes you more fertile and thus its effects balance out, or is even favoured, because of that.”

Elsewhere in the study, the researchers concluded that those genetically predisposed to delayed puberty and childbearing tended to live longer – with a one-year puberty delay lowering death rate by 3-4% in men and women, and a one-year childbearing delay lowering death rate in women by 6%. It could be the case that these tendencies have a positive effect on the survival of a person’s children, and therefore means they’re more likely to be passed through the generations.

While the availability of large genetic datasets makes studies such as this possible, the sample size still restricts analysis to variants to those that are most common in the population. Mostafavi believes that, as genomic sequencing becomes even more widespread, figuring out which variants matter to survival or fertility could become easier:

“These datasets are growing every day, and soon approaches like ours could be applied to the genetic data for millions of samples to look at the effect of rarer genetic variants across the genome.”