Binging Babies

It is hard to deny that United States culture is heavily influenced by consumption of controlled substances, especially alcohol. This influence becomes particularly concerning when it involves youth. But I am not going to get into the obvious effects of media on alcohol consumption and the negative effects alcohol consumption has on society at large. While these are important topics to be discussed, I would like to highlight some neurobiological studies showing the dysregulation of hormones and increase of neuroimmune danger signals caused by high levels of alcohol consumption. Understanding the extent of drinking, especially binge drinking (characterized by a blood-alcohol concentration of 0.08 or higher), is vital to developing effective alcohol related policies regarding youth.

This semester I had the opportunity to hear Dr. Magdalena Szymanska share her research about binge drinking effects on the brains hypothalamo-pituitary-adrenocortical (HPA) axis, which is important in the response to stress. In preliminary studies Dr. Szymanska showed that rat corticotrophin-releasing hormone (CRH), arginine vasopressin (AVP), and corticosterone (CORT) levels were altered in rats exposed to binge levels of ethanol (the chemical in alcohol that causes intoxication). Her subsequent research showed that dysregulation of theses hormones persists into adulthood (Szymanska 2011). In some of her even more recent research she has produced evidence that binge levels of alcohol consumption during adolescence can cause genetic changes that are passed down to rats children. Since the HPA axis has been shown to be important in the regulation of stress, research like Dr. Szymanska’s is important to help understand how alcohol induced dysregulation of hormones and modification of gene expression effect psychological disorders.

In 2012 Dr. Ryan Vetreno and Dr. Fulton Crews published a study that examined the effects of adolescent alcohol consumption (again in rats) on increased neuroinflammation and cognitive performance. Vetreno and Crews randomly assigned rats to either a test group that received intragastric ethanol or a control group that received intragastric injections of water. Then the effects of alcohol consumption were evaluated using immunohistochemistry and Barnes maze spatial and reverse learning assessment. Immunohistochemistry along with polymerase chain reaction is a biological lab technique used to quantify the amount of expression of a gene. In this study it was used to look at HMGB1, a molecular signal of neuroinflammation. Vetreno and Crews found that alcohol consumption caused increased levels of HMGB1 (aka the “danger signal”) in adult rat prefrontal cortex (the part of the brain that is important for cognitive functions). The Barnes maze was used to assess the correlation between cognitive deficits and increased gene expression of prefrontal cortex “danger signals”. Ventro and Crews found that while the ability of rats to form spatial memories was not impaired, their ability to unlearn and replace the formed spatial memories was impaired (they had impaired reverse learning abilities). This group of experiments helps us to understand how prefrontal cortex biological changes due to alcohol consumption relates to deficits cognitive abilities.

These are just two studies of many that help us understand how molecular and genetic changes in the brain due to adolescent alcohol consumption correlate to different psychological deficits. There is a lot more work that needs to be done to really understand how the adolescent brain is affected by alcohol and how those effects can be reversed. Personally, I hope that research findings like these can be adapted to serve as effective deterrents to keep youth from consuming large amounts of alcohol.

Articles:

Przybycien-Szymanska MM, Mott NN, Paul CR, Gillespie RA, Pak TR (2011) Binge-Pattern Alcohol Exposure during Puberty Induces Long-Term Changesin HPA Axis Reactivity. PLoS ONE 6(4): e18350. doi:10.1371/journal.pone.0018350

Ventro RP, Crews FT (2012) Adolescent Binge Drinking Increases Expression of the Danger Singnal Agonist HMGB1 and Toll-Like Receptors in the Adult Prefrontal Cortex. Neuroscience 226: 475-488.