Some individuals who fill their lives with fitness and healthy habits die younger than peers who live a much less healthy life. New research into the epigenetics of aging sheds some fresh light on the perplexing phenomenon of premature aging.
Epigenetics, a relatively new sphere of research, is proving to be a fascinating and far-reaching topic.
In short, epigenetics charts changes in chromosomes that take place without modifying the DNA sequence itself.
By altering the ways in which DNA is packaged and replicated, changes can be made to the whole organism without a single base pair of DNA being moved out of place.
Researchers from the University of California-Los Angeles (UCLA) set out to examine how epigenetics might influence human aging.
The team wanted to investigate whether epigenetics could offer insight into the question of premature aging, specifically. As Dr. Douglas Kiel, professor at Harvard Medical School and senior scientist at the Institute of Aging Research at Hebrew SeniorLife, says:
“In geriatric medicine, we are always struck by the difference between our patients’ chronological age and how old they appear physiologically.”
To open up this question, the UCLA scientists led a team of 65 researchers in seven countries. They used data from 13 separate studies, including the Women’s Health Initiative and Framingham Heart Study. In all, 13,000 people’s DNA was analyzed from blood samples.
By recording age-related changes to human DNA and calculating an individual’s biological age, the team found that they could accurately estimate someone’s lifespan.
The paper, published this week in the journal Aging, explains how a higher biological age – regardless of chronological age – predicts an earlier death.
“Our research reveals valuable clues into what causes human aging, marking a first step toward developing targeted methods to slow the process.”
Steve Horvath, project lead, professor of human genetics and biostatistics
Using a series of molecular methods, the scientists measured each individual’s rates of aging. One of the techniques used was an epigenetic clock, designed by Prof. Horvath in 2013.
Prof. Horvath’s epigenetic clock works by tracking methylation. Methylation is a process where methyl groups are added to DNA; this generally leads to a reduction in gene transcription, altering a person’s phenotype without altering their genotype.
Methylation is natural and steadily occurs over time; the team found that by comparing an individual’s chronological age with their blood’s biological age, they could predict life expectancy.
“We were stunned to see that the epigenetic clock was able to predict the lifespans of Caucasians, Hispanics, and African-Americans.
This rang true even after adjusting for traditional risk factors like age, gender, smoking, body mass index, disease history, and blood cell counts.”
First author Brian Chen, the National Institute on Aging
The team found that around 5 percent of the population age at a faster rate and have a decreased life expectancy. Prof. Horvath says: “Accelerated aging increases these adults’ risk of death by 50 percent at any age.”
As an example, if we compared two 60-year-old men who have stressful jobs and smoke; the first man has a top aging rate, the other is average. The likelihood of the first man dying in the next 10 years is 75 percent, whereas the latter of the two has just a 60 percent chance of dying in the next 10 years.
These findings might help explain why certain people who live otherwise healthy lives seem to die young. However, this is not free rein to take up smoking and heavy drinking. As Prof. Horvath mentions, traditional risk factors like high blood pressure and diabetes “still predict mortality more strongly than one’s epigenetic aging rate.”
The large and thorough nature of this study gives it a great deal of weight. The next step is to see whether these findings can be utilized in real-world situations. As Dr. Kiel explains: “If we can prove that DNA methylation accelerates aging, we can devise strategies to slow the rate and maximize a person’s years of good health.”
The importance of epigenetic changes and how they impact premature aging are yet to be fully explained. It may be that they influence other factors already present in an individual. For instance, perhaps they enhance the effects of certain diseases or remove our ability to fight them off.
Because epigenetics is receiving a great deal of attention currently, answers to these questions are likely to gradually trickle in. Medical News Today asked Chen about other research he is currently involved in.
“Our current focus is on understanding what biological mechanisms control the ‘ticking’ of the epigenetic clock and investigating the implications of having a discrepancy between one’s epigenetic age and their chronological age,” he replied.
Asked what type of study he would like to carry out given unlimited time and funds, Chen told MNT:
“We and a number of other groups are now trying to develop a similar clock in animal models. This will allow the greater scientific community to understand the role of the epigenetic clock in relation to other markers of aging. Animal models will allow us to examine differences in the clock across tissues and across the lifespan in the same individuals.”