NOV 12, 2015

The Difference between Your Real Age and Your Epigenetic Age

WRITTEN BY: Sarah Hertrich
Our DNA encodes genes which express specific patterns that lead to the production of a specific protein which has a specific function. When one gene is turned on, it may cause neighboring genes to also be turned on. In some cases, these genes may remain turned on for many generations even if it was only exposed to a certain signal for an instance. When gene expression patterns are inherited in the absence of gene mutations and the initiating signal, it is known as epigenetic regulation. One way that expression patterns are inherited is through DNA methylation which typically switches the expression of a certain gene off. Researchers have linked abnormal DNA methylation to several human diseases.



Scientists have been using DNA methylation as a marker to estimate their “epigenetic age” which is a concept that can be considered a form of biological age. Epigenetic age is estimated to be within about 3 years of actual age on average. The difference between epigenetic age and actual age is known as age acceleration (AA). If a person has a positive AA, it means that their biological age is greater than their actual age and if a person has a negative AA it means their biological age is less than their actual age. AA has been found to be associated with health conditions such as obesity, Down’s syndrome, HIV, physical and cognitive fitness and mortality in older individuals. Until recently there has been no research on the prenatal factors that affect AA in children.
 


Researchers from the University of Bristol in Bristol, UK used the Horvath age estimation method to determine the epigenetic age of 1018 mother-child pairs from the Avon Longitudinal Study of Parents and Children. Associations were discovered between AA and sex, birth weight and whether or not birth was performed by caesarean section. AA was also affected by behaviors and characteristics of the mother prior to birth including smoking, weight, BMI and her selenium and cholesterol levels. Children from non-drinkers had a higher AA on average which appeared to resolve when the infant progressed into childhood. In addition, they found that early life exposures to clinically relevant variables are associated with AA in adolescence. Further studies should be completed to understand the factors that affect epigenetic aging as well as AA in order to develop treatments and prevention for health conditions associated with abnormal DNA methylation mediated by epigenetic regulation.

Source: Human Molecular Genetics; Molecular Biology of the Gene (Sixth Edition)