Alcoholism: A Neurological Perspective

After an intensive course regarding alcoholism with Dana Most and Dr. Adron Harris in the Waggoner Center for Alcohol and Addiction Research at the University of Texas at Austin, alcoholism, its causes, diagnosis, prognosis, and FDA-approved treatments were investigated. Here is the report written under their guidance.

Alcoholism is one of the foremost problems in society today. The DSM-5 manual helps doctors tell what disease you may have and better allows them to treat you for that specific disease. To be considered an alcoholic, according to the DSM-5, one must meet a certain number of the common criteria for alcoholism such as consuming larger amounts of alcohol than was intended and unsuccessful efforts to stop alcohol consumption. With more than 17.6 million affected with alcoholism, the separation of the facts and fictions of alcohol becomes of utmost importance. Many people believe that alcoholism only pertains to heavy and continuous drinkers, and while the majority of people affected with alcoholism are heavy and continuous drinkers, there still remains a population that acquires alcoholism through just a “couple of drinks”¹ . The increasing desire to consume alcohol as well as the increasing desire to attain alcohol can be critical symptoms. The motivation to do normal daily activities and work is reduced and replaced by drinking alcohol. It is not just the amount or chronicity of alcohol and alcohol consumption that causes alcoholism. A combination of factors such as age, genetics, gender, emotional status, and alcohol availability, to name a few, can lead to the development of alcoholism.

Alcoholism can essentially be described as a positive feedback loop, or in more common terms, an infinite loop. This description is so apt because of key mechanisms inside the brain, at the molecular level. Neurotransmitters, chemical signals that serve as messengers between nerve cells and carriers of the nerve impulse, and the receptors for them such as dopamine and glutamate play a primary molecular role in alcoholism. The consumption of alcohol increases the release rate of dopamine, which induces feelings of happiness and euphoria, giving alcohol its euphemistic name:  “liquid-courage”² . The consumption of alcohol inhibits the glutamate receptor activity, which results in calmness and anxiolysis (reduced anxiety)³ . The combination of the feelings of euphoria and reduced anxiety lull the drinker into a false sense of security, or even a perceived escape from depression⁴ .

When alcohol is consumed regularly and in mass quantities, the body begins to build tolerance. Tolerance is developed a number of different ways, and due to a number of different reasons, but the primary two relate to the protective actions of the liver and the brain. The liver normally produces an enzyme called alcohol dehydrogenase, which breaks down the alcohol in the liver. As larger quantities of alcohol are consumed, the liver produces larger quantities of alcohol dehydrogenase, and becomes accustomed to doing so. Thus, the drinker requires more alcohol to achieve the same feelings of contentment⁵ .

The brain plays a role in tolerance due to the actions of neurotransmitter systems such as glutamate and dopamine signaling. The brain adapts to the increase in dopamine by increasing the amount of dopamine receptors. As these systems become accustomed, larger quantities of alcohol are required to achieve the increases in dopamine levels and the euphoria associated with them. As the amount of alcohol a drinker consumes increases, so does the amount of deceptive serenity, creating a desire within the drinker to keep consuming alcohol and increasing serenity⁶ .

Understanding the fundamental impact of alcohol inside the human body requires an in-depth analysis of specific neuron functions. A neuron is an electrically excitable cell that has the capability of transferring information through electrical and chemical signals. The chemical signals that a neuron processes are called neurotransmitters. Neurotransmitters can be expressed in two ways: excitatory and inhibitory. Excitatory neurotransmitters stimulate the electrical activity in the brain and inhibitory neurotransmitters decrease the electrical activity in the brain. Neurotransmitters work as a lock and key. When the neurotransmitters are released from the chemical vesicles encompassing them after reaching the pre-synaptic barrier, the neurotransmitters must bind to a certain specific receptor on the post-synaptic site to allow the electrical impulse to go through the post-synaptic barrier. Alcohol has numerous effects in exciting and inhibiting certain neurotransmitters because it affects the production of these neurotransmitters inside the vesicles and the availability of receptor sites.

Conversely, the neurotransmitter dopamine is excited by alcohol consumption.  As an increasing amount of alcohol is consumed, an increasing amount of dopamine neurotransmitters are produced, and an increasing number of receptors are needed to acquire the same effect of pleasure. Once alcohol is taken away from the system, the large numbers of receptors remain, causing anhedonia, or unhappiness, because these large numbers of receptors cannot be filled⁷ .

There are three major FDA-approved drugs that are used to treat alcoholism. No one treatment can treat alcoholism because of the many different biological mechanisms involved. Disulfiram targets the liver enzymes that metabolize alcohol, resulting in nausea, headaches, and even vomiting when drinking alcohol by keeping the alcohol in the acetyl aldehyde state, which is the state that normally induces such effects. Its purpose is to associate these uncomfortable symptoms with alcohol consumption, thus, decreasing the desire to consume alcohol. The second drug, Naltrexone, targets the brain and is an opiate antagonist, which essentially means that Naltrexone blocks the feelings of pleasure and happiness associated with taking opiates, and has the same effect on alcohol consumption. Its purpose is to decrease the desire to consume alcohol, known as craving. The last drug, Acamprosate, deals with the neurotransmitter and receptor imbalance in the brain. By fixing this imbalance, Acamprosate regulates symptoms of alcohol withdrawal, and reduces the desire to consume alcohol to maintain the same high state of pleasure. Acamprosate is primarily used in those who have already decided to quit alcohol use but are going through various stages of alcohol withdrawal and dependence. One of the major goals of Acamprosate is to reduce craving and the chance of relapse occurring. While these drugs may help alleviate some symptoms of alcoholism, they are not effective alone. Abstinence programs, social changes, and other lifestyle modifications must be used in accordance with these drugs to reap the full benefits and increase the chance of effectively treating alcoholism. These programs and changes help reduce the risk of relapse, and it is important to note that every time an alcoholic relapses, the alcoholism worsens because the body cannot handle the sudden increase in alcohol intake after a clean period; it is detrimental to both mental and physical health and the body deteriorates further⁸ .

While these three FDA-approved drugs are most commonly used to treat alcoholism, there are additional FDA-approved drugs for other disorders and diseases that can aid in the treatment of alcoholism. For example, Topamax, also known as topiramate, is used to treat seizures and migraines⁹ . But when used as a treatment for alcoholism, Topamax displays characteristics of all three of the FDA-approved drugs for alcoholism. Topamax corrects some of the chemical imbalances in the brain with the neurotransmitters and the receptors, decreasing the overall desire to consume alcohol, causing less pleasure from the consumption of alcohol, and inducing feelings of nausea and sickness when alcohol is consumed. Another example would be fluoxetine. Fluoxetine is FDA-approved to treat depression, anxiety, and obsessive-compulsive disorder. Sometimes, alcoholism is caused by depression, as the person feels the need to temporarily relieve their emotional pain by drinking it away. By taking depression drugs such as fluoxetine, the person can route alcoholism before it takes root in the body. Because addiction disorders and mood disorders are related through physical, chemical, and mental symptoms, the regulation of the neurotransmitter serotonin plays an important role in the success of fluoxetine. Many mood-related disorders and diseases coexist with alcoholism, such as depression and anxiety. These disorders are caused by the depletion of serotonin in the brain, as decreasing levels of serotonin correlate with increasing levels of unhappiness¹⁰ . Fluoxetine optimizes the usage of the small levels of serotonin remaining after continued alcohol consumption, which ultimately leads to the body gradually producing increasing amounts of serotonin and decreasing the desire for alcohol consumption.

It is important to note that it is not just adults that are affected by alcohol; young people are too. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) states that approximately 14.2% or 5.4 million people ages 12-20 have participated in binge drinking¹¹ . Furthermore, according to the NIAAA, about 90% of all alcoholics, including underage alcoholics, do not seek treatment partly because alcoholism is stigmatized into seeming like a self-imposed disease¹² . In reality, alcoholics do not deserve to be put down or even feel like they are going to be put down, because alcoholism is uncontrollable, and alcoholics should have full support from their peers in treatment.

 Overall, there are many factors to alcoholism that must be considered throughout all times of the process. A person must understand the consequences of alcohol consumption before the actual consumption itself. A person must limit himself or herself when consuming the alcohol. And finally, a person must use the proper and most effective means to rid himself or herself of any remnants of alcoholism or an alcohol-related disorder. If you or someone you know has alcoholism or an alcohol-related disorder, these are some steps, although not foolproof, to get you through the process of alcoholism:

1. Immediately see your doctor when you begin to express symptoms of alcoholism and have consumed large amounts of alcohol in the past. Ask them to consider FDA-approved drugs for alcoholism.
2. If these drugs do not work, consider FDA-approved drugs that are not approved for alcoholism but are approved for diseases and disorders related to alcoholism.
3. Always believe in yourself and never lose hope.

1. “Almost Alcoholic.” : You Don’t Have to Be Alcoholic to Have a Drinking Problem. HelpGuide. Web. 10 Aug. 2015. <http://www.helpguide.org/harvard/almost-alcoholic.htm>. [↩]
2. “Liquid Courage: Is Your Relationship Dependent on Alcohol? – …” EmpowHER. Web. 10 Aug. 2015. <http://www.empowher.com/relationships-amp-family/content/liquid-courage-your-relationship-dependent-alcohol>. [↩]
3. Valenzuela, C. Fernando. “Alcohol and Neurotransmitter Interactions.” National Institute on Alcohol Abuse and Alcoholism. Web. 10 Aug. 2015. <http://pubs.niaaa.nih.gov/publications/arh21-2/144.pdf>. [↩]
4. Kennedy, Murphy. “Self-Medicating with Alcohol?” HereToHelp. Web. 10 Aug. 2015. <http://www.heretohelp.bc.ca/visions/alcohol-vol2/self-medicating-with-alcohol>. [↩]
5. “Tolerance and Beyond.” Rochester.edu. University Health Service. Web. 10 Aug. 2015. <https://www.rochester.edu/uhs/healthtopics/Alcohol/tolerance.html>. [↩]
6. “Short-Term Effects of Alcohol.” Drugscom RSS. Web. 10 Aug. 2015. <http://www.drugs.com/forum/general/short-term-effects-alcohol-63769.html>. [↩]
7. Kandel, Eric R. Principles of Neural Science. 4th ed. New York: McGraw-Hill, Health Professions Division, 2000. Print. [↩]
8. “Relapse after Many Years – Alcohol Rehab.” Alcohol Rehab. Web. 10 Aug. 2015. <http://alcoholrehab.com/addiction-recovery/relapse-after-many-years/>. [↩]
9. Paparrigopoulos, Thomas, Elias Tzavellas, Dimitris Karaiskos, Georgia Kourlaba, and Ioannis Liappas. “Treatment of Alcohol Dependence with Low-dose Topiramate.” Medscape. Web. 10 Aug. 2015. <http://www.medscape.com/viewarticle/739790>. [↩]
10. “What Is Serotonin? What Does Serotonin Do?” Medical News Today. MediLexicon International. Web. 25 Aug. 2015. <http://www.medicalnewstoday.com/articles/232248.php>. [↩]
11. “Underage Drinking.” National Institute on Alcohol Abuse and Alcoholism. Web. 26 Aug. 2015. <http://www.niaaa.nih.gov/alcohol-health/special-populations-co-occurring-disorders/underage-drinking>. [↩]
12. “Alcohol Use Disorder.” National Institute on Alcohol Abuse and Alcoholism. Web. 10 Aug. 2015. <http://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/alcohol-use-disorders>. [↩]