A recent study has suggested that binge drinking in adolescence is associated with increased risk for psychological problems and alcohol use disorder later in life.
According to researchers some of these lasting changes are the result of epigenetic changes that alter the expression of a protein crucial for the formation and maintenance of neural connections in the amygdala — the part of the brain involved in emotion, fear and anxiety. Their results, which are based on the analysis of postmortem human brain tissue, are published in the journal Translational Psychiatry.
Epigenetics refers to chemical changes to DNA, RNA or specific proteins associated with chromosomes that change the activity of genes without changing the genes themselves. Epigenetic modifications are involved in the normal development of the brain, but they can be influenced by environmental or even social factors, such as alcohol and stress. These kinds of epigenetic alterations have been linked to changes in behavior and disease.
The researchers looked at postmortem human amygdala tissue. The amygdala is the part of the brain involved in emotional regulation. The specimens were from the brains of 11 individuals who started drinking heavily before the age of 21 or early-onset drinkers; 11 individuals who started drinking seriously after the age of 21, known as late-onset drinkers; and 22 individuals with no history of alcohol use disorder. The average age of death of the individuals from whom the samples were taken was 58 years old for those without alcohol use disorder; 55 years old for early-onset drinkers; and 59 for late-onset drinkers.
Amygdalae of individuals who were early-onset drinkers had about 30 per cent more of a molecule called BDNF-AS, a large non-coding RNA. Usually, RNA is involved in the production of proteins from DNA, but this one is not. BDNF-AS regulates a gene that produces a protein called BDNF. This protein is a growth factor and is crucial for the normal formation and maintenance of synapses throughout the brain. When there is more BDNF-AS, there is less BDNF.
The brain tissue of early-onset drinkers had 30 per cent to 40 per cent less BDNF compared with brain tissue from people with no history of alcohol use disorder. This reduction in BDNF was not seen in brain samples from late-onset drinkers or from people with no alcohol use disorder.
Lead author of the study, Subhash Pandey and his colleagues found that the increase in BDNF-AS in the early-onset drinkers is caused by decreased methylation of BDNF-AS. Methylation is a type of epigenetic change where a molecule containing a methyl group is added to another molecule and results in a change in genetic expression. The decreased methylation of BDNF-AS is believed to be caused by early-onset drinking and appears to be a long-lasting change.
“The epigenetic changes we saw in the amygdala of early-onset drinkers can alter the normal function of the amygdala, which helps regulate our emotions, and may cause individuals to be more susceptible for things like anxiety, which we have shown in other studies, or the development and maintenance of alcohol use disorder later in life,” said Pandey. (ANI)