An interesting new study from UCLA suggests that Latinos age at a slower biological rate than other ethnicities. This difference in aging is suggested as a possible explanation for an effect known as the “Hispanic Paradox”, the trend where Hispanic/Latino individuals in the U.S. have a longer life expectancy than Caucasians, yet have higher rates of risk factors for cardiac disease.
In Brief: Age Tracking
One of the tricky things about trying to determine how “aged” a person’s body is stems from how there is no single metric that can be used. While it is easy to point out how old someone is, the level of aging shown by their tissues will vary depending on what is measured and where the samples come from, as well as how much they correlate to actual life expectancy. For this study, the researchers decided to use the “epigenetic clock”, a relatively unexplored method for assessing biological aging.
In Brief: Epigenetics
The term “epigenetics” refers to changes to a DNA molecule that affect which genes are expressed, but do not alter the structure of the DNA sequence itself. To simplify, the epigenetic clock is the process of using the accumulation of these changes as a way to serve as a biomarker for how much aging a given part of the body has undergone.
The UCLA Study
The study looked at roughly 6,000 samples taken from the blood, saliva, and brains of seven different ethnicities. The groups were two separate African populations, African-Americans, Caucasians, East Asians, Latinos, and the Tsimane, an indigenous people from Bolivia that is genetically related to Latinos. The Tsimane were chosen because it was theorized that if Latinos had a slower intrinsic aging rate, they might as well.
The study focused on two elements of the epigenetic clock: expressions of “intrinsic epigenetic age acceleration” (IEAA) and “extrinsic epigenetic age acceleration” (EEAA). Again, to simplify, IEAA is the measure of epigenetic aging effects within a cell and EEAA refers to epigenetic aging in the immune system. More IEAA means more aging in normal cells, more EEAA means more aging in the immune system.
The main findings offered a possible suggestion for the “Hispanic Paradox” since it was found that the Latino and Tsimane had higher IEAA rates than the other groups, yet they also had more EEAA rates than others as well. The extra immune aging indicated by higher EEAA is thought to be why Latinos and the Tsimane have higher rates of inflammation and other risk factors for coronary heart disease.
The lower IEAA is theorized to be an explanation for why this increased inflammation doesn’t translate into a higher prevalence of disease. In other words, Latinos and Tsimane may be more prone to risk factors due to a more aged immune system, but reduced aging elsewhere may mean those risk factors don’t have as large an impact.
There some caveats to keep in mind when looking at these results, however. EEAA rates were highest among Latinos and the Tsimane, which makes sense since these groups have higher inflammation risks, but EEAA showed weak correlations to more well-known inflammation risk factors. IEAA also had insignificant associations to more well-studied risks for coronary heart disease.
This means that while the EEAA and IEAA rates may have some involvement or connection with the Hispanic Paradox, it is unclear how specifically that role relates to coronary heart disease.
It is also possible that there is a strong environmental involvement as well. The Tsimane are an indigenous, tribal people that live under very different conditions than the other groups. They are also the ones that have the lowest signs of diabetes, hypertension, obesity, clogged arteries, and other risk factors for coronary heart disease.
Nothing in the findings suggests how to slow the aging process, but it also wasn’t trying to do so. The researchers sought to compare how Latinos age on a molecular level compared with other ethnicities and found results that may explain why they live longer despite having more coronary risk factors. The use of epigenetic measurements for this kind of purpose is still fairly new, so more work will be needed to both verify and develop potential clinical implications for the findings.
Horvath, S., “An epigenetic clock analysis of race/ethnicity, sex, and coronary heart disease,” Genome Biology, 2016; 10.1186/s13059-016-1030-0.