Brookhaven Lab finds alcoholism-genetics link
Related mediaExperiments at Brookhaven and Cold Spring Harbor labs
Scientists at Brookhaven National Laboratory have provided the first experimental evidence demonstrating how chronic alcoholism is influenced by a pre-existing genetic makeup that drives the urge to drink.
The research, conducted in specially bred mice by neuroscientist Dr. Peter Thanos and colleagues, found that brains lacking a particular receptor were more likely to become vulnerable to alcohol. Humans also have the receptor, but when it's presence is low, Thanos said, alcoholism generally occurs.
"Some people can go to a party and have a drink and nothing happens, but others can go to a party and one drink can lead to catastrophic consequences," said Thanos, who found alcohol exposure trips a biochemical switch in those who are genetically vulnerable, causing a seemingly unquenchable desire for more inebriating stimulation.
BLOG: The Daily Apple | PHOTOS: Dropping LBs
DATA: Explore hospital rankings | Compare hospital charges | Uninsured people in NY | Docs paid by Novartis | Compare hospital infection data | How LI reps voted on health bills
WEIGH IN: Ask your fitness questions
Thanos said his studies not only help demystify how alcohol affects the brain, but support earlier investigations suggesting alcoholism runs in families.
He and his team compared the brain's response to long-term alcohol drinking in two strains of mice. One strain lacked the gene for a specific brain receptor known as dopamine D2, the brain's "pleasure and reward" chemical. The other strain had the brain receptor.
When exposed to alcohol over a six-month period, the dopamine D2-deficient mice developed critical biochemical changes in parts of the brain long associated with alcoholism and addiction.
Thanos said he focused on the dopamine system because many studies have strongly suggested dopamine D2-deficiency may make people less likely to experience ordinary pleasures and therefore more vulnerable to alcoholism, drug abuse and obesity.
Alcohol exposure in D2-deficient mice also caused a surprising increase in another brain chemical, known as the cannabinoid type-1 receptor. The cannabinoid receptors are located near dopamine receptors and are also known to play a role in alcohol overconsumption and addiction.
The Brookhaven research is published in the latest edition of the journal Alcoholism Clinical Experimental Research.
Jeffrey Reynolds, executive director of the Long Island Council on Alcoholism and Drug Dependence in Williston Park, said the study is welcome news because it supports what many believe - alcoholism is a genetic disease.
"This is the kind of research that is important in terms of real life," Reynolds said. "The identification of genes associated with alcoholism supports the disease-model of addiction," he said, highlighting how alcoholism and drug abuse are not problems with "bad behavior or poor self control."
But Jeffrey Parsons, an addiction expert and chairman of psychology at Hunter College in Manhattan, said while "the majority of addiction experts would agree that alcoholism runs in families, I think there is still a lot of uncertainty as to whether it is genetic or environmental.
"What's still missing is a full understanding of the Brookhaven [mice] study," Parsons said. "We need to know if it is exactly the same for humans."