Why do more than 14 million American adults suffer from some form of alcohol use disorder (AUD)?


The statistics are sobering. More than 14 million American adults suffer from some form of alcohol use disorder (AUD), a chronic inability to stop or control alcohol use despite the negative consequences.

This is according to the National Institute on Alcohol Abuse and Alcoholism, a part of the National Institutes of Health.

The causes of AUD are complex and can include a mix of genetic, environmental, and social factors, including a family history of alcoholism. This familial effect, however, may be more complicated than first assumed.

New research published in the journal Psychological Science has uncovered a previously unrecognized family connection to AUD: the drinking habits of a person’s in-laws.

This study suggests that marriage to a spouse who as a child was exposed to parental alcohol misuse increases that person’s likelihood of developing AUD, even if the spouse does not have a drinking disorder.

“Our goal here was to examine whether a spouse’s genetic makeup influences risk for AUD,” said Jessica Salvatore, an assistant professor of psychology at Virginia Commonwealth University, and lead author on the paper.

“In a somewhat surprising twist, we found that it wasn’t the spouse’s genetic makeup that influenced AUD risk. Rather, it was whether the spouse was raised by an AUD-affected parent.”

The researchers analyzed marital information on more than 300,000 couples in Swedish national population registries, finding that marriage to a spouse with a predisposition toward alcohol use disorder increased risk for developing AUD.

This increased risk was not explained by socioeconomic status, the spouse’s AUD status, nor contact with the spouse’s parents. Instead, the researchers found that, rather than genetics, this increased risk reflected the psychological consequences of the spouse having grown up with an AUD-affected parent.

“Growing up with an AUD-affected parent might teach people to act in ways that reinforce a spouse’s drinking problem,” said Salvatore. “For example, taking care of a spouse when they have a hangover.”

The study’s findings underscore the pernicious and long-lasting impact of growing up with a parent with AUD, extending even to the spouses of their adult children.

“It demonstrates the long reach that parental alcohol problems have on the next generation,” Salvatore said. “It’s not just the offspring of affected parents who are at risk, it’s the people those offspring end up marrying, too.”

The findings are consistent with evidence from other research labs, she said, which suggests that those who grow up with a parent with an alcohol use disorder may be at particularly high risk of using alcohol as a “tool” to improve their marital interactions.

“These kinds of processes may inadvertently lead a spouse down the path of alcohol misuse,” she said.

“To be clear, my guess is that these processes are out of people’s conscious control. No one wants to ‘give’ their spouse an alcohol problem.”

The study’s findings are an important contribution to a burgeoning area of research on social genetic effects, or the effects of a social partner’s genetic makeup, Salvatore said.

Conclusions from previous studies of social genetic effects were limited by the fact that people’s genotypes were correlated with their rearing environments. In other words, in prior studies it was difficult to say whether effects were attributable to the partner’s genes versus how they were raised because their parents provided both their genes and their home lives.

“What we were able to do in our study was tease apart the effects of the social partner (spouse’s) genes and the rearing environment,” she said. “And when we did that, what we found surprised us: It’s something about the spouse being raised by a parent with a drinking problem, rather than the spouse’s genetic makeup, that influences a person’s risk for developing an alcohol problem.”

The study’s findings could prove valuable when it comes to treating couples struggling with alcohol.

The findings reinforce the idea that interventions for substance-use disorders should be administered at the level of a couple or the family (for those who have a partner) rather than at the individual level, Salvatore said.

This study is part of Salvatore’s larger body of research that seeks to understand “how the people we love shape the way we drink.”

“In the best-case scenario, spouses can be one of our first defenses against poor health—they bug us to schedule our annual exams, and they’re among the first to notice if we’re feeling blue or tipping too many drinks back.

But spouses can also be a liability for poor health,” she said. “The results from this study underscore how a spouse’s experiences in his/her family of origin can be a risk factor for the development of alcohol problems.”

Alcohol (EtOH), in one form or another, is the most commonly consumed, mood-altering substance worldwide [1].

The World Health Organization (2014) estimates that 3.3 million deaths are attributed to alcohol use disorder (AUD). In the United States, nearly 88,000 Americans die annually directly related to AUD, making it the third leading preventable cause of mortality with tobacco use first and poor
diet and sedentary lifestyle second [2].

AUD carries a sizeable economic burden to the nation at $223.5 billion annually. The health consequences of AUD are directly linked to over 200 diseases, such as anemia, cancer, cardiovascular disease, cardiomyopathy, cirrhosis of the liver, dementia, depression, seizures, gout, hypertension, suppressed immune function, neuropathy, and pancreatitis [3].

According to Swift and Aston (2015), “Alcohol use disorder is a heterogeneous illness with a complex biology that is controlled by many genes and gene-by-environment interactions” [4]. AUD is prevalent in 10–20% of hospitalized patients [5]. Trauma patients have a significantly higher prevalence at 31–70% [5].

When hospitalized, without access to alcohol, AUD patients can develop acute alcohol withdrawal syndrome (AWS) [6]. According to Maldonado., et al. (2015), AWS occurs in the abrupt cessation of alcohol, resulting in a wide range of symptoms: confusion, agitation, ag- gressive behaviors, seizures, delirium tremens, hallucinations, permanent cognitive dysfunction, psychosis, surgical complications, and prolonged hospitalizations [7].

Thus, recognizing the pathophysiology, progression, assessment and treatment (PPAT) of AWS can help patients, affected family members, public health policymakers, and healthcare providers cope with, screen for, and treat AWS better.

AUD is infrequently identified until alcohol withdrawal symptoms appear in the AUD-patient. If the initial signs and symptoms of AWS go undetected, more severe – even life-threatening – complications can result. A more severe symptom of AWS (e.g., violent behavior) can put patients and hospital staff at risk.

Patient-restraint is utilized at this stage of AWS. The severely affected patient—exhibiting continu- ous agitation or delirium tremens (DTs)—might be transferred to the intensive care unit (ICU) for observation and treatment [8,9].

Pathophysiology and progression of alcohol withdrawal syndrome (AWS)

AWS occurs due to a cascade of neurobiological events, primarily by the disruption of healthy neurotransmitter equilibrium. According to Saitz (1998), long-term alcohol consumption alters the gamma-aminobutyric acid (GABA) inhibitory pathway.

This pathway alteration decreases endogenous GABA and receptors; excitatory N-methyl-D-aspartate (NMDA) concentrations increase [10]. Thus, in AWS, there is neurotransmitter excitation and hyperactivity that run persistently and unimpeded [11].

According to Lautieri (2020), alcohol withdrawal side effects and symptoms can be divided into three stages, as follows :

  • Stage 1: Anxiety, insomnia, nausea, and abdominal pain characterize this stage, which appear 8 hours after the last drink.
  • Stage 2: High blood pressure, increased body temperature, atypical heart rate, and confusion occur at this stage, which appear 24–72 hours after the last drink.
  • Stage 3: Hallucinations, fever, seizures, and agitation occur at this stage, which appear 2–4 days after the last drink.

Note: All symptoms tend to decrease within 5–7 days, barring any complications or comorbidities [12].

Assessment of AUD to prevent or ameliorate AWS

In a retrospective study involving trauma patients, Hosking., et al. (2007) discovered that patient histories (including AUD detection) were performed in just 7.3% of the patients [13]. However, there are a variety of screening tools and approaches used to detect AUD (see the links in the Supplemental Information section):

  • Alcohol Use Disorders Identification Test-Piccienlli Consumption (AUDIT-PC)
  • CAGE questionnaire tool, the Alcohol Use Disorders Identification Test (AUDIT)
  • Prediction of Alcohol Withdrawal Severity Scale (PAWSS)
  • DSM-IV-TR Mini-International Neuropsychiatric Interview (MINI)

Wong., et al. (2015) noted that each (above) detection method is useful in the early identification of AUD and, thus, limits the progres- sion to AWS [14]. Biomarkers from laboratory findings aid in identifying chronic alcohol abuse and AUD; however, such biomarkers are not predictive for AUD-patients progressing to AWS [15].

Alcohol withdrawal risk assessmentPerformed in all adult patients at time of admission using Alcohol Use Disorders Identification Test-Piccinelli Consumption (AUDIT-PC)11   If score is ≥ 5, perform CIWA-Ar
CIWA-ArAssessment to determine level of severity of alcohol withdrawal syndrome
Precautions algorithmFollowed when CIWA-Ar score is ≤ 8
Treatment algorithmFollowed when CIWA-Ar score is ≥ 9
Physician order setInitiated for patients with alcohol withdrawal syndrome
Sedation Agitation ScaleAdministered before each medication dose
Table 1: Components of the Alcohol Withdrawal Symptom Management Care Guideline.
CIWA-Ar: Revised Clinical Institute Withdrawal Assessment of Alcohol Scale.
Note: Table 1 reproduced from Improving Alcohol Withdrawal Outcomes in Acute Care [15].

Salottolo., et al. (2017) noted that AUD is calibrated by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) as follows:

  • In women, consuming greater than one drink daily or greater than three drinks on a given occasion, or greater than seven drinks per week.
  • In men, consuming greater than two drinks daily or greater than four drinks on a given occasion, or greater than fourteen drinks per week.

Note: A standard drink is defined as a beverage containing 14 grams of alcohol (i.e., a 12-ounce beer, 5-ounce glass of wine, or 1.5-ounce shot of hard liquor) [16]. (For more information, follow the link to NIAAA: https://www.niaaa.nih.gov/).

Hasin., et al. (2013) noted that alcohol abuse, dependence, and withdrawal criteria are defined by the American Psychiatric Association in the Diagnostic and Statistical Manual, Fifth Edition (DSM-5) as follows:

  • Meeting two of the eleven criteria within a 12-month timeframe, used to pick up cyclic remissions.
  • The severity of AUD being dependent upon the number of criteria met (e.g., mild, moderate, or severe) [17].

Note: The DSM-5 lists diagnosis criteria for AWS is based upon a patient with a cessation or reduction of alcohol after heavy and pro- longed drinking, meeting two of eight symptom criteria (see the link in the Supplemental Information section).

Treatment of AUD and AWS

In the early 1900s, lumbar puncture, electroconvulsive therapy, chloroform, digitalis, and insulin coma were employed to treat AWS [18]. In the 1950s, treatments included paraldehyde (for seizures) and promazine. In the1960s, chlorpromazine, chlordiazepoxide, and hydroxyzine were added as drug treatment for AWS; most of the drugs had antipsychotic properties. In the 1970s, diazepam and barbitu- rates were added as treatments for AWS [19].

According to Franck (2013), the current pharmacologic interventions for AWS are as follows:

  • Benzodiazepines are the first-line treatment for AWS, although there is debate over which type is most effective.
  • Clonidine is also being applied for the alpha-2 agonist effects of elevated heart rate and hypertension.
  • Dexmedetomidine, like clonidine, is an alpha-2 agonist, which has been shown effective in some patients in acute DTs.
  • Baclofen, a muscle relaxant, has shown promise as a GABA-B agonist as well as traditional barbiturates for their GABA-B-ago- nistic effects.
  • Propofol and dexmedetomidine are used in intensive care settings with anesthesia [14]. However, if propofol or dexmedetomi- dine is needed, the patient will require intubation and mechanical ventilation. Propofol is used in those patients that are refrac- tory to large doses of benzodiazepines [20].
Figure 1: A graphic representation of the PPAT of AWS. Note. Concept and design by Nicholas
A Kerna and Mitchell G Jomsky (2020).

Supplementary Information

  • Alcohol Use Disorders Identification Test-Piccienlli Consumption (AUDIT-PC); see Pecoraro., et al. (2014), “Using the AUDIT-PC to predict alcohol withdrawal in hospitalized patients” (https://www.ncbi.nlm.nih.gov/pubmed/23959745) [20].
  • Prediction of Alcohol Withdrawal Severity Scale (PAWSS); see Maldonado., et al. (2015), “Prospective Validation Study of the Prediction of Alcohol Withdrawal Severity Scale (PAWSS) in Medically Ill Inpatients: A New Scale for the Prediction of Compli- cated Alcohol Withdrawal Syndrome” (https://www.ncbi.nlm.nih.gov/pubmed/25999438) [7].
  • DSM-IV-TR diagnostic criteria for alcohol abuse and dependence with a specific section of the Mini International Neuropsychiat- ric Interview (MINI); see Francis., et al. (2015), ”Validation of the MINI (DSM IV) Tool for the Assessment of Alcohol Dependence among Young People in Northern Tanzania Using the Alcohol Biomarker Phosphatidylethanol (PEth)” (https://www.ncbi.nlm. nih.gov/pmc/articles/PMC4661629/) [23].

For the leading mode of AUD assessment in the emergency ward, see Richoux., et al. (2011) “Alcohol use disorders in the emergen-  cy ward: choice of the best mode of assessment and identification of at-risk situations” (https://www.ncbi.nlm.nih.gov/pmc/articles/ PMC3125196/) [24].


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More information: Jessica E. Salvatore et al, Disentangling Social-Genetic From Rearing-Environment Effects for Alcohol Use Disorder Using Swedish National Data, Psychological Science (2020). DOI: 10.1177/0956797620931542


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