Chronic drinking and smoking cause both separate and interactive brain injury

interactions are also influenced by genetic factors. Therefore, co-morbidity of drinking and smoking can be considered to be a final outcome of genetics, environment, and pharmacological interactions between alcohol and nicotine."

- Smoking may attenuate gamma-aminobutyric acid (GABA)A receptor adaptations associated with alcohol dependence and may contribute to the co-occurrence of alcoholism and smoking. In light of this, benzodiazepines used to treat alcohol withdrawal may have different effects on alcohol-dependent individuals who smoke versus those who do not.

"GABA is an inhibitory amino acid in the human brain and is critical in counterbalancing the biological action of the excitatory amino acid glutamate," explained Meyerhoff. "In a healthy human brain, both amino acids are present in equilibrium. In disease stages such as addiction, to either alcohol or nicotine, this equilibrium is out of balance. During alcohol withdrawal, GABA concentrations may increase, but the densities of receptors are still relatively low. Benzodiazepines may strengthen the responses of (GABA)A receptors to GABA binding, thereby having a soothing effect on the user."

- In-vivo magnetic resonance studies suggest that chronic smoking in recently detoxified alcohol-dependent individuals compounds alcohol-induced brain tissue loss and neuronal injury. Chronic smoking may also hinder neurobiological and cognitive recovery during short-term abstinence from alcohol.

"We studied recently detoxified alcoholics in treatment using in-vivo magnetic resonance," said Meyerhoff. "The specific methods we used were magnetic resonance imaging (MRI), which measures the size of many different brain structures, and magnetic resonance spectroscopic imaging (MRSI), which measures certain naturally occurring chemicals in the brain that tell us about injury to specific brain cells. Our analyses showed that chronically smoking alcoholics have greater


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