Alcohol Use Disorders (AUDs) — sometimes collectively termed alcoholism — represent a costly and prevalent problem in the United States. The annual cost of alcohol dependence in the United States is over $150 billion dollars,  and about 100,000 people die annually due to alcohol-related causes.

People with alcohol-related medical illnesses have more frequent hospitalizations and longer hospital stays compared with individuals without alcoholism.  In fact, the price of healthcare resulting from AUDs in the United States is estimated at more than $26 billion per year.

Unfortunately, alcohol abuse and dependence are frequently under-diagnosed in the clinical setting, typically due to inadequate screening and the unreliability of self-reported alcohol use.  In one study, retrospective analysis demonstrated that less than 25% of patients admitted to hospital who screened positively for AUD received either inpatient alcohol intervention or a referral for outpatient alcohol treatment.

Alcoholism occurs when a person has developed dependence on alcohol and continues to use it, despite the problems it causes with that person’s job performance, academic performance, or relationships. The National Institute on Drug Abuse states that alcoholism is defined as a “chronic, relapsing brain disease” when the chronic use of a substance causes changes in the structure of the brain and how it works.

An Alcohol Use Disorder starts with drinking to excess on multiple occasions. This may include drinking alcohol to the point of feeling intoxicated or out of control in behavior.   A person can still develop a drinking problem when he or she drinks more than what is recommended for health and safety.

According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the following are the recommended Maximum Drinking Limits. People, with exceptions noted below, are advised to stay within these limits:

For healthy men up to age 65

  • No more than 4 drinks a day AND
  • No more than 14 drinks in a week

For healthy women (and healthy men over age 65)

  • No more than 3 drinks in a day AND
  • No more than 7 drinks in a week

Abstinence is advised to individuals who:

  • Take prescriptions or over-the-counter medications that may interact with alcohol
  • Have a health condition that may be exacerbated by alcohol
  • Are pregnant
  • Are considering becoming pregnant
  • Are younger than age 21

Signs of Alcoholism

The Diagnostic and Statistical Manual (DSM) is the classification system published by the American Psychiatric Association.  In 2013, the 5th edition was released.  It eliminated the terms Alcohol Abuse and Alcohol Dependence, and it created the broad category of Alcohol Use Disorders (AUD).  In order to meet the criteria for an AUD, a person must have at least two of the following symptoms:

  1. Alcohol is often taken in larger amounts or over a longer period than was intended.
  2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.
  3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.
  4. Craving, or a strong desire or urge to use alcohol.
  5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home.
  6. Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol.
  7. Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
  8. Recurrent alcohol use in situations in which it is physically hazardous.
  9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.
  10. Tolerance, as defined by either of the following: a) A need for markedly increased amounts of alcohol to achieve intoxication or desired effect b) A markedly diminished effect with continued use of the same amount of alcohol.
  11. Withdrawal, as manifested by either of the following: a) The characteristic withdrawal syndrome for alcohol (refer to criteria A and B of the criteria set for alcohol withdrawal) b) Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.

The presence of at least 2 of these symptoms indicates an alcohol use disorder (AUD). The severity of an AUD is either mild, moderate, or severe, depending on the number of symptoms.

Mild: The presence of 2 to 3 symptoms.
Moderate: The presence of 4 to 5 symptoms.
Severe: The presence of 6 or more symptoms.

Effects of Alcohol

Alcohol acts rapidly because it is very lipid soluble. Cell membranes, with their lipid bilayers, offer almost no impediment to it. Alcohol’s small size and lipid solubility make it pass the blood-brain barrier very quickly. Once in the brain, it stimulates some neurotransmitters and inhibits others. Alcohol’s effects on the gamma-aminobutyric acid (GABA) receptor are what leads to its psychoactive effects.

Though our knowledge of the neurobiology of alcohol is limited, we know plenty about its psychological effects. At low to moderate doses, alcohol creates relaxation and disinhibition. It is remarkably effective at reducing social anxiety, making it a staple at parties and earning it the nickname “the social lubricant.”

However, with greater consumption, alcohol’s effects penetrate to progressively deeper parts of the brain. The effects start on the surface, at the frontal lobes, where it relaxes the executive functions. As the blood alcohol level rises, it quiets the reticular activating system, which is what keeps us awake and alert to our surroundings, so sedation ensues. Next, the cerebellum is affected, which impacts coordination and causes staggering.

Ultimately, the brainstem is affected, which reduces the respiratory drive—at this point, we’ve reached the level of alcohol poisoning.

Thankfully, alcohol poisoning (overdose) is fairly rare: Since alcohol is a liquid, a person must consume a large amount to produce the alcohol level necessary to overdose, and the body will generally expel the alcohol through vomiting before reaching that level.

Depending on how much is taken and the physical condition of the individual, alcohol can cause:

  • Slurred speech
  • Drowsiness
  • Vomiting
  • Diarrhea
  • Upset stomach
  • Headaches
  • Breathing difficulties
  • Distorted vision and hearing
  • Impaired judgment
  • Decreased perception and coordination
  • Unconsciousness
  • Anemia (loss of red blood cells)
  • Coma
  • Blackouts (memory lapses, where the drinker cannot remember events that occurred while under the influence)

Alcohol Withdrawal

Each patient will experience differing severity of alcohol withdrawal, ranging from nonexistent to life-threatening. Predicting the likelihood of withdrawal is more art than science. In general, patients who have consumed larger amounts for longer periods of time on a consistent basis will have more severe withdrawal. Binge drinkers will rarely have withdrawal symptoms other than a bad hangover.

Early symptoms occur within a few hours after the last drink—although it may take 24–48 hours for symptoms to manifest—and usually last 48–72 hours. They include insomnia, nervousness, tremor, and sweating. Early withdrawal symptoms may subside on their own, although repeated episodes of alcohol withdrawal increase the likelihood of progression to worse withdrawal, also known as late withdrawal or delirium tremens.

Heavier drinkers and those who have experienced repeated early withdrawal may experience delirium tremens, which starts after development of early withdrawal has continued to progress, usually 48–72 hours after the last drink. Also known as “the DTs,” “the shakes,” and “rum fits,” symptoms of delirium tremens include worsening of the signs of early withdrawal, with serious altered mental status (hallucinations such as the famous “pink elephants”) and severe autonomic dysregulation manifested by rapid fluctuations in vital signs.

Development of delirium tremens carries a mortality of 5%, even when adequately treated. Because alcohol withdrawal can progress quickly and result in mortality, it is important to recognize and treat it early. Seizures are an early sign of alcohol withdrawal syndrome and can complicate management. Patients who present with an alcohol withdrawal– related seizure or with delirium tremens should be treated as a medical emergency and referred to the nearest emergency department for adequate medical monitoring and aggressive pharmacologic management to prevent significant morbidity and mortality.

Alcoholic hallucinosis is a condition that can resemble alcohol withdrawal syndrome. It presents with auditory and/or visual hallucinations, but not the autonomic dysregulation of alcohol withdrawal syndrome. Alcoholic hallucinosis is not life-threatening and is a consequence of intoxication, but not withdrawal. It often resolves with resolution of intoxication over time, or with pharmacologic treatment to prevent alcohol withdrawal syndrome.

Medication for Alcoholism

It may be appropriate to try a medication to stop drinking alcohol.

Therapy for Alcoholism

Cognitive Behavioral Therapy (CBT): A type of therapy most commonly used to treat depression and anxiety, but it has also been shown to be valuable in treating alcoholism and drug addiction, especially as part of an overall program of recovery. Cognitive-behavioral coping skills treatment is a short-term, focused therapeutic approach to helping drug-dependent people become abstinent by using the same learning processes the person used to develop alcohol and drug dependence initially.

Alternatives to AA

SMART Recovery: Alternative to AA with local and online meetings. It uses cognitive-behavioral approaches that help members recognize environmental and emotional factors for alcohol and other drug use (as well as other “addictive” behaviors) and then to respond to them in new, more productive ways. It also incorporates motivational interviewing concepts. Unlike some support groups whose principles remain static, SMART Recovery maintains a philosophy of evolving as scientific knowledge evolves. Although it is an abstinence-based program, SMART Recovery welcomes those who are ambivalent about quitting substance use.

Books on Alcoholism

What is Alcohol Use Disorder?

Before diving into the skills of diagnosing substance use disorders, it’s fair to take a step back and ask what a substance use disorder actually is. Is it a brain disease? Is it self-medication? Is it a life choice? The answer can be any of the above, or a combination, depending on the person and the substance. For the opioid addict with overwhelming cravings who is stealing money from her friends to buy her next fix, it is primarily a brain disease involving opiate receptors.

For the college student taking Adderall a couple of times a week—borrowed from friends—to study for exams and write papers, it may be a lifestyle choice (though it can devolve into neurochemical dependency if the habit becomes a daily one). For the man with social anxiety disorder who downs a few shots of vodka before going to a social event, it may be a form of self-medication. Like most disorders in medicine and psychiatry, substance use is multifactorial, and for this same reason, it can be treated in different ways.

Neurobiology of Addiction
While our knowledge of the neurobiology of addiction is limited, researchers are beginning to work out some of the mechanisms. One particular neurotransmitter, dopamine (DA), seems to play a central role for most addictions. Most psychiatrists are familiar with DA in the setting of psychosis. All antipsychotics block DA receptors, which implies that excessive DA can be a bad thing, as it may be one of the chemicals that can cause psychosis. However, there is another side of DA—it’s the primary neurotransmitter for the brain’s reward system.

Our brain releases high levels of DA during joyful events, like graduating from high school, winning a race, or enjoying a Thanksgiving dinner. Another experience that can cause a kind of “joy” is abusing drugs. Cocaine and methamphetamine cause the most DA release, leading the user to feel intensely exhilarated and powerful.

While a large release of DA can indeed produce positive emotions, the brain quickly institutes measures to maintain a stable internal environment, or homeostasis. One measure is to quickly clear the DA away, which the brain does by breaking the DA down with enzymes or recycling it. But when someone is consistently using drugs, there’s too much DA for this process to work.

Therefore, the brain alters itself to make the neurons a little less receptive to DA. This process is called “desensitization,” and it occurs in various ways biochemically, such as decreasing the number of DA receptors or slowing down receptor activation. As the brain desensitizes to DA, the drug user experiences this as tolerance, meaning the person does not experience the same high from a given dose.

If the dose is increased to compensate, the user will get high, but the brain will go through its homeostasis process again, forming tolerance to the higher dose. This is a simplistic neurobiological explanation of tolerance.

What about withdrawal—why does that happen? When there’s no external stimulation causing the brain to release DA, the user must depend on the old-fashioned process of the brain releasing DA as it normally would: that is, in response to the prosaic pleasurable events of life, like having a snack or watching a ball game.

But a brain that has gotten used to relying on high levels of DA has fewer DA receptors, and those receptors are less sensitive. Therefore, the normal amount of DA doesn’t produce much, if any, pleasure compared to what the addict experiences when getting a “fix.” When an addict’s drug of choice is taken away, a DA deficiency results. This is one reason withdrawal is so unpleasant, and why stimulant withdrawal causes depression. With a damaged reward circuit, it becomes very hard for a user to experience normal healthy behaviors as motivating. The temptation to use drugs is extreme, because the user now feels the drugs are needed simply to feel normal.

Genetics of addiction
Drug addiction often runs in families, though the strength of the development of addiction varies between substances. Familial transmission of substance abuse does not necessarily imply genetic involvement; however, there is in fact a large amount of evidence that genes play a role. One piece of evidence comes from studies of identical and fraternal twins.

The most interesting of these studies compares these two types of twins when they have been separated at birth and put up for adoption. If addiction had nothing to do with genes, but everything to do with upbringing, one might expect that the diagnostic concordance rate of identical and fraternal twins would be the same—but in fact the identical twin concordance rate is higher.

Using this kind of data, studies have estimated that the heritability of addiction to alcohol and drugs in general is 60%. This does not mean that a patient has a 60% chance of developing an addiction if one of the patient’s parents had an addiction, although this is a common misunderstanding. Instead, if a person becomes addicted, about 60% of the reason for that addiction will be genetic, while about 40% of it will be non-genetic—such as the effects of upbringing.

If genetics has so much to do with addiction, what are some of the possible genes that play a part, and how might they work? A number of genetic variants have been identified that might contribute to increasing a person’s vulnerability to addiction. For example, genes for certain subtypes of GABA-A receptors have an association with alcohol use disorder, and a different cluster of genes is associated with a higher risk for nicotine use disorder.

Other gene variants can protect against addiction. In several Asian populations, gene variants for alcohol dehydrogenase cause disulfiram-like reactions, making drinking very unpleasant. Overall, however, we’re still quite far from truly understanding the genetics of addiction, and there is no clinically useful genetic test for helping us predict who is likely to become addicted.


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Gabapentin Treatment for Alcohol Dependence:  A Randomized Controlled Trial

Activation of Melatonin Receptors Reduces Relapse-Like Alcohol Consumption

Alcohol and Caffeine:  The Perfect Storm

Sex Differences in the Genetic Risk for Alcoholism

Alcohol Dependence: The Importance of Neurobiology to Treatment

A Review of the Interactions between Alcohol and the Endocannabinoid System:  Implications for Alcohol Dependence and Future Directions for Research

The Alcohol Deprivation Effect Model for Studying Relapse Behavior:  A comparison between rats and mice