U.S. Hispanics Age More Slowly Than Caucasians and African-Americans

MedicalResearch.com Interview with:

Michael Gurven, Professor Department of Anthropology University of California Santa Barbara, CA 93106

Dr. Michael Gurven

Michael Gurven, Professor
Department of Anthropology
University of California
Santa Barbara, CA 93106

MedicalResearch.com: What is the background for this study?

Response: Understanding the sources of ethnic and sex disparities in health and longevity is critical in order to insure the health and well-being of everyone. We often hear about disparities due to differences in health care access, education, income, and sometimes genetic differences. But what we’ve done here is to employ a new biomarker developed by Steve Horvath, called the “epigenetic clock”, which measures the cumulative changes to the epigenome, i.e. alterations to DNA that affects gene activity and
expression but do not alter the DNA itself. This new measure is arguably
one of the best biomarkers of aging out there today – so it’s indeed a
biological measure, but tells a different story than conventional genetic
differences. Instead epigenetic age is influenced by the lived experience,
physical and social environment, and genetic make-up of individuals.

MedicalResearch.com: What are the main findings?

Response: What we found was that ethnicities vary in their rate of overall aging,
even when you account for socioeconomic differences. U.S. Hispanics age
more slowly than Caucasians and African-Americans, which is consistent with
a well-known paradox in epidemiology called the “Hispanic paradox”. This is
where Hispanics are known to live longer than Caucasians, despite
experiencing higher rates of diabetes and other diseases. The epigenetic
clock supports this finding, suggesting that the Hispanic paradox is not a
demographic artifact due to say, out-migration when sick, or only a
healthier subset having migrated to the U.S.

Tsimane Native Americans of South America show even slower aging rates than
Hispanics, a curious observation given their lower life expectancy and high
rates of infectious disease. One possibility is that survivors to middle
age may be more robust than U.S. populations that suffer very little
pre-adult mortality. But if the epigenetic aging measure is instead tapping
into something else – we could potentially learn a lot from further study
of this and similar populations.

Another important finding is that men show higher aging rates than women –
regardless of whether the samples came from blood, saliva or even brain
tissue. This result could shed light on another epidemiological paradox –
the sex morbidity/mortality paradox wherein men experience higher mortality
but women higher morbidity.

MedicalResearch.com: What should readers take away from your report?

Response: All experiences and exposures can imprint their signature in our biology.
The epigenetic aging measures are biological – but this is not separate
from the environmental factors we know matter in life. For example, one
hypothesis to explain the Hispanic paradox emphasize the strong family ties
and social support of many Hispanic families. Such a notion is not an
alternative to what we show here, but instead such a social support network
may leave its biological signature in the epigenome. In fact, how the
social environment and psychosocial stress affect disease risk and aging is
getting a lot of attention right now. Our study supports this body of work,
but raises more questions. How or why do particular social environments
leave an epigenetic signature affecting aging, and why does this not always
predict the likelihood of having heart disease or diabetes, top sources of
morbidity and mortality in the U.S.?

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: The epigenetic clock measure has been wildly successful as a predictor of
important outcomes – ethnic differences in aging as reported in our paper,
but also all-cause mortality, frailty, cognitive/physical fitness in the
elderly, as well as specific diseases like Alzheimer’s and lung cancer. So
it’s definitely tapping into important underlying aspects of health and
aging – but what exactly is the epigenetic clock capturing, and how exactly
do different experiences affect its ticking? To what extent does it merely
reflect the sum of many independent processes, versus a more global aging
process? How does the epigenetic clock vary in different tissues of the
body, and why might it vary? These and other questions need to be studied
before we can responsibly think about using this knowledge to improve

MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.


Genome Biol. 2016 Aug 11;17(1):171. doi: 10.1186/s13059-016-1030-0.
An epigenetic clock analysis of race/ethnicity, sex, and coronary heart disease.
Horvath S1,2, Gurven M3, Levine ME4, Trumble BC3, Kaplan H5, Allayee H6, Ritz BR7, Chen B8, Lu AT4, Rickabaugh TM9, Jamieson BD9, Sun D10, Li S10,Chen W10, Quintana-Murci L11, Fagny M12, Kobor MS13, Tsao PS14,15, Reiner AP16, Edlefsen KL17, Absher D18, Assimes TL14.

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