Research in the field of addiction has brought to light new discoveries regarding the use of oxytocin in reducing alcohol consumption. While most current pharmacological treatments for alcohol addiction are little better than a placebo at limiting intake, researchers continue to look for a pill that would effectively help people quit their alcohol abuse.
Studies involving the interaction between oxytocin and alcohol are providing hope for one day creating a pharmaceutical that could make alcoholics less likely to drink and less intoxicated if they do drink. The pill could also potentially reduce the symptoms of alcohol withdrawal syndrome when alcoholics go "cold turkey".
New research could possibly lead to such a medication and revolutionize the field of addiction treatment.
The Effects of Oxytocin
Oxytocin is sometimes called the "love hormone" because it promotes sociability and long-term bonding. Studies where humans took nasal puffs of oxytocin showed that the hormone had pro-social effects.
Further research in the 1980s showed that oxytocin can also interact with alcohol to prevent the development of tolerance to alcohol's sedative and blood temperature reducing effects. The hormone also was shown to reduce the severity of alcohol withdrawal in a study with rodents. More recent studies have discovered that oxytocin causes both immediate and long-lasting inhibition of alcohol consumption in rodents and also promotes addiction-resistant behavior.
The hormone prevents addiction by reducing anxiety, creating higher sociability and promoting greater activity of the natural oxytocin system. Studies with rats showed that oxytocin can completely prevent the problems with coordination caused by alcohol. Rats given the hormone and an intoxicating dose of alcohol were able to behave as though they were completely sober.
Further Research and Creating a Medication
Researchers in recent studies determined that oxytocin can reduce drunken behavior because it prevents alcohol from acting at specific sites in the brain that are connected with intoxication.
These sites in the brain are known as delta subunit-containing GABA-A receptors and they also play a role in alcohol addiction and tolerance with receptors affecting the appetite a person has for alcohol.The discovery that oxytocin prevents alcohol from acting at these receptors is significant because it suggests a previously unknown mechanism involved in the interactions between the hormone and alcohol.
In studies with rodents, the hormone has proven to reduce alcohol consumption both in the short term and long term as well as preventing intoxication, reducing withdrawal symptoms and promoting resistance to addiction and relapse. These findings need to be translated for human beings in order to create a successful medication that would take advantage of the interactions between oxytocin and alcohol.
In order to create a pill that would utilize the effects of oxytocin, scientists must find a way to deliver the large oxytocin molecule to the brain effectively. Rodents can be administered the hormone directly into the brain but humans are normally provided with nasal sprays which work as a "back door" to the brain.
This method may or may not be effective in raising oxytocin levels in the brain. Some trial studies provided alcoholics going through detoxification with intranasal oxytocin which successfully reduced their alcohol cravings and they required less standard pharmacological treatment for their withdrawal symptoms. However, human studies have yet to show the "sobering" effect of oxytocin and more tests are required to determine whether it can prevent intoxicated behavior in humans.
The assumption based on existing research is that oxytocin will help reduce the coordination problems associated with alcohol consumption as well as reducing slurred speech and aggressive behavior. Researchers will continue to study the effects of oxytocin on human subjects and try to find a way to create an effective medication that will help alcoholics reduce or eliminate their addictive behavior.