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Why Is Alcohol So Addictive? It’s More Complex Than You Think

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Alcohol is a legal and readily available substance in the United States. The interaction between alcohol and dopamine, serotonin, and other neurochemicals produces feelings of euphoria and sedation. Alcohol is an accepted part of many types of celebrations, events, and rituals, including personal rituals like enjoying a relaxing evening at home.

While alcohol is legal for individuals over the age of 21, it is a mind-altering substance that has a high risk of misuse and addiction.

In this article:

Alcohol Addiction As a Medical Condition

Research has long attempted to understand individual differences in alcohol consumption, such as why some individuals can drink heavily for a short time and then stop using alcohol easily, while others seem to develop alcohol use disorder (AUD)—the clinical diagnosis of alcohol addiction—after using alcohol for a comparatively short period of time.

Our contemporary understanding of AUD is of a medical condition characterized by changes in mood, behavior, and even brain chemistry and structure. Research refutes the previous cultural stigmas that individuals who find it difficult to control how much or how often they use alcohol lack the willpower to stop, are making poor life choices, or do not have the motivation or emotional investment necessary for sobriety.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-5), which clinicians use to evaluate and diagnose mental health conditions, defines AUD as “a problematic pattern of alcohol use leading to clinically significant impairment or distress.”1

AUD can only be diagnosed by a licensed mental health professional, who evaluates your experience of alcohol use and misuse based on presence of 11 clinical criteria within the last year. The first two criteria are 1) using alcohol more or in higher amounts than you intend to and 2) persistently wanting to control or stop alcohol use or trying to stop unsuccessfully multiple times.1 These criteria alone illustrate the inaccuracy of considering willpower or strength of character to be the cure for AUD.

Clinicians recognize that AUD is a highly treatable, but not curable, condition that many individuals need external resources to address.

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Alcohol and Its Euphoric Effects

Several biological interactions make alcohol use feel pleasurable: 2,3,4

  • Dopamine and serotonin—Alcohol and dopamine and serotonin are connected by the neurochemical processes that occur when you use alcohol. Dopamine and serotonin production increase in the brain, which contributes to a sense of euphoria—or the “buzz” or “high” associated with intoxication.
  • Endorphins—Recent studies show that alcohol and endorphins are connected. Endorphins are closely associated with the reward center of the brain, creating a form of positive reinforcement linked to alcohol use.
  • GABA neurotransmitters—GABA is an inhibitory neurotransmitter. In other words, GABA’s job is to regulate the brain’s “excitability,” thereby keeping your mood, stress levels, and fear responses in check. Alcohol use prompts unnaturally high production of GABA, which can result in profound feelings of relaxation. This effect is sometimes referred to as an anxiolytic, or anxiety-reducing, neurochemical response.

The neurochemical effects of alcohol not only make alcohol use feel good, but can encourage repeated use of alcohol. The dopamine rush while drinking makes many people feel that alcohol can decrease anxiety symptoms, relieve tension, or increase their social ability.5 All of these desired effects come from the increased dopamine level and its depressant effects on the central nervous system, which can lower heart rate, body temperature, and respiration to physically trick the body into feeling calmer.3

The alcohol and endorphins connection can serve as an even stronger incentive for repeated alcohol use and chronic alcohol misuse. Studies show that when an individual resumes drinking after a period of abstinence, they may experience a “catch-up phenomenon,” where more endorphins are released, contributing to the individual’s euphoric state and strongly contributing to the initiation and maintenance of physical alcohol dependence.4

The combined “buzz” and anxiolytic effect of alcohol created by GABA neurotransmitters means drinking may lower inhibitions to promote a sense of comfort and calm in social gatherings and decrease anxiety symptoms when alcohol is used. These effects can encourage repeated alcohol use, patterns of alcohol use in specific situations (e.g., parties), and potentially increase the frequency or amount of drinking to achieve the same or greater effects.2

Alcohol and Social Influence

There is a demonstrated social component to an individual’s relative risk of developing an alcohol use disorder (AUD). Many of the family associations that were once thought to indicate an “alcoholism gene” are now recognized to reveal a connection between having substance use behaviors modeled in your home of origin and an increased risk of misusing substances later in life.6

Studies show that when alcohol is misused in your home of origin, you may develop a strong prefrontal cortex response to both the smell and presence of alcohol.7

Codependency with family members or friends who misuse alcohol is also closely linked with chronic use or misuse of alcohol.8 You may find yourself continuously in places and situations where alcohol is readily available and frequently being used, making it difficult to separate your own decisions about alcohol use from the alcohol use of those around you. The influence of your social circle can affect you at any age and studies show prefrontal reactions that affect executive functioning—including decision-making—when in the presence of a loved one who has a substance use disorder.8

Many individuals begin using alcohol due to social influence in their peer group. Alcohol may first be used when in a group of peers who are also drinking or in an effort to gain social acceptance. This behavioral pattern is particularly common among the adolescent and young adult groups, where drinking is seen as a pivotal part of social engagement.9

Because alcohol is an integral part of many social gatherings and alcohol use creates the anxiety-reducing effects discussed in the previous section, some individuals may be encourage to use alcohol repeatedly or misuse it progressively as part of social rituals.2

Many individuals have their first drink of alcohol at a social gathering, where a link between the idea of using alcohol and friendship begins, which can put these individuals at risk of developing a problem with alcohol.10 They may develop a positive association with alcohol, contributing to continued and increased drinking.

You may also have positive experiences or experience positive outcomes in your social life while using alcohol that feel linked to alcohol use. This may lead to chronic alcohol misuse, which can develop into AUD if the frequency and amount of alcohol used progressively increases over a long period of time in an effort to achieve the same “buzz” or calm and positive social effects.2

Alcohol Addiction and Age of Exposure

The risk of alcoholism may increase if an individual is exposed to alcohol at an earlier age. Studies show that adolescents who have been exposed to substances multiple times before age 15 are 2-3 times more likely than adolescents who have no early exposure to substances to be substance dependent by age 32.11

While the primary concerns of alcohol use during pregnancy related to pregnancy outcomes (e.g., miscarriage, low birth weight) and congenital conditions (e.g., fetal alcohol syndrome), exposure to alcohol in utero may influence future alcohol use and risk of addiction. Studies show that in utero exposure to alcohol during fetal development potentially contributes to the baby’s overall risk of developing a substance use disorder, including AUD, in adulthood.12

Alcohol Tolerance and Addiction

One of the consequences of chronic alcohol use is the development of alcohol tolerance. Tolerance develops when there is a less intense physiological response to the same amount of alcohol. Your body, in a sense, becomes used to a certain amount of alcohol and you no longer experience the same intensity of euphoria, sedation, or other desired effects with that amount.11

Developing a tolerance means your body will require a larger amount of alcohol to achieve the same effect as before. Tolerance leads many people to increase the amount of alcohol they consume to achieve the desired effect, such as euphoria, increased sociability, or decreased anxiety.11

While tolerance is not the same as addiction, tolerance is one of the clinical criteria for alcohol use disorder (AUD). The presence of a tolerance for alcohol combined with any other clinical criteria within the last year can be adequate for an AUD diagnosis.1 The increased use of alcohol can also increase the risk of future alcohol addiction due to the progressive nature of AUD.11

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Alcohol Withdrawal and Addiction

Physical dependence on alcohol, like tolerance, is not the same as alcohol use disorder (AUD). However, dependence—or the state where you begin to need alcohol to function normally—is often seen in individuals with AUD and is widely considered a warning sign of high addiction risk.

When you are physically dependent on alcohol, you will experience withdrawal symptoms when you do not use alcohol or you dramatically decrease how much you use it. These are more significant symptoms than a “hangover” and can include:12

  • Insomnia
  • Nausea or vomiting
  • Sweating
  • Increased heart rate
  • Agitation
  • Anxiety

In cases of severe withdrawal, you could potentially experience tremors, hallucinations, or seizures. 12 These symptoms can be part of a potentially life-threatening condition called delirium tremens (DTs).

The withdrawal symptoms from alcohol can be unpleasant and difficult to manage. For some people, the fear or experience of these symptoms leads to repeated alcohol use in order to avoid withdrawal symptoms.13  This use of alcohol—or another substance, including prescription, over-the-counter, and illegal substances—to alleviate or avoid withdrawal symptoms is one of the clinical criteria that can be used to evaluate if an AUD is present.1

Many individuals need withdrawal management services, sometimes called “detox,” to get through the withdrawal process without using substances. While some people can safely detox in an outpatient setting, seek medically supervised withdrawal management services if you experience any medically significant symptoms, such as seizure.12

Alcohol Addiction and Genetics

Studies indicate that there may be a genetic component that increases the likelihood that an individual who misuses alcohol—or any other substance—will develop a substance use disorder.16

There is not, as popular cultural sometimes claims, an “alcoholism gene” that would be detectable if you had your personal genome sequenced. Instead, certain traits—such as behavioral dysregulation, high impulsivity, and anxiety—that have been observed to be associated with a high occurrence of substance use disorders are thought to be able to be inherited genetically. 16

These genetic traits do not create, predict, or guarantee the development of alcohol use disorder (AUD) or any other addiction, however, certain genetic traits are thought to be associated with the development of behavioral patterns that increase the risk of substance use progressing to addiction.

This understanding may partially explain why some people seem to find alcohol “more addictive” than others.16 How the genetic predisposition to alcohol addiction initially develops is still being studied to help reduce the risk of those with genetic traits associated with addiction.

Alcohol Addiction and Neurobiology

There may be a neurobiological component to the risk of developing addiction. Scientists report differences in how the reward circuit pathways in the brain of those with alcohol use disorder (AUD) differ from those without addiction or before addiction. This means the brain of an individual with AUD processes the chemical activation of alcohol differently than others. Researchers are unable to conclude what the cause of this neurobiological difference is, only that it can be observed.17

This observed change in neurobiological functioning may be part of why once AUD develops, many individuals required alcohol addiction treatment to become and stay sober.

If you feel concerned about your alcohol use or need alcohol addiction treatment, call 800-948-8417 Question iconCalls are forwarded to these paid advertisers to speak to an addiction treatment specialist about available services.


  1. American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Association Publishing.
  2. Lewis, M. J. (1996). Alcohol reinforcement and neuropharmacological therapeutics. Alcohol & Alcoholism, 31(1), 17-25.
  3. Di Chiara, G. (1997). Alcohol and dopamine. Alcohol health and research world, 21(2), 108.15704345.
  4. Van Ree J. M. (1996). Endorphins and experimental addiction. Alcohol (Fayetteville, N.Y.), 13(1), 25–30.
  5. Baghayeri, M., Nodehi, M., Veisi, H., Tehrani, M. B., Maleki, B., & Mehmandost, M. (2019). The role of pramipexole functionalized MWCNTs to the fabrication of Pd nanoparticles modified GCE for electrochemical detection of dopamine. Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 27(2), 593–603.
  6. McLeod, S. (2016). Albert Bandura’s Social Learning Theory. SimplyPsychology.
  7. Bragulat, V., Cox, C., Davidson, D., Dzemidzic, M., Kareken, D.A., O’Conner, S.J., & Talvage, T. (2010). Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers. NeuroImage, 50(1), 267-276.
  8. Bradshaw, S., Story Chavez, M., Hawkins, L., Mullet, N., Shumway, S. & Zielinski, M. (2019, May 15). Codependency and Prefrontal Cortex Functioning: Preliminary Examination of Substance Use Disorder Impacted Family Members. The American Journal on Addictions, 28(5), 367-375.
  9. Wood, M. D., Read, J. P., Palfai, T. P., & Stevenson, J. F. (2001). Social influence processes and college student drinking: the mediational role of alcohol outcome expectancies. Journal of Studies on Alcohol, 62(1), 32-43.
  10. Roberson, A. A., McKinney, C., Walker, C., & Coleman, A. (2018). Peer, social media, and alcohol marketing influences on college student drinking. Journal of American college health: J of ACH, 66(5), 369–379.
  11. Caspi, A., Dickson, R., Milne, B.J., Moffitt, T.E., Nagin, D.S., Odgers, C.L., Piquero, A. R., Poulton, R. & Slutske, W.S. (2008, October 01). Is It Important to Prevent Early Exposure to Drugs and Alcohol Among Adolescents? Psychological Science, 19(10), 1037-1044.
  12. Wang, R., Hausknecht, K. A., Shen, Y. L., Haj-Dahmane, S., Vezina, P., & Shen, R. Y. (2018). Environmental enrichment reverses increased addiction risk caused by prenatal ethanol exposure. Drug and alcohol dependence, 191, 343–347.
  13. Tabakoff, B., Cornell, N., & Hoffman, P. L. (1986). Alcohol tolerance. Annals of emergency medicine, 15(9), 1005-1012.
  14. Bayard, M., Mcintyre, J., Hill, K., & Woodside, J. (2004). Alcohol withdrawal syndrome. American family physician, 69(6), 1443-1450.15053409
  15. Becker, H. C. (2008). Alcohol dependence, withdrawal, and relapse. Alcohol Research & Health, 31(4), 348–361.23584009
  16. Enoch MA, Goldman D. (2001). The genetics of alcoholism and alcohol abuse. Current Psychiatry Reports, 3(2),144-51.
  17. Ferraguti G, Pascale E, Lucarelli M. (2015). Alcohol addiction: a molecular biology perspective. Current Medical Chemistry, 22(6), 670-84.
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