Only a small percent of individuals with alcohol use disorder contribute to the greatest societal and economic costs ( 8 ). For example, in the 2015 National Survey on Drug Use and Health survey (total n = 43,561), a household survey conducted across the United States, 11.8% met criteria for an alcohol use disorder ( n = 5124) ( 6 ). Of these 5124 individuals, 67.4% ( n = 3455) met criteria for a mild disorder (two or three symptoms, based on DSM-5), 18.8% ( n = 964) met criteria for a moderate disorder (four or five symptoms, based on DSM-5), and only 13.8% ( n = 705) met criteria for a severe disorder (six or more symptoms) ( 6 ). There is a large treatment gap for alcohol use disorder, arising from the fact that many individuals with alcohol use disorder do not seek treatment. Those with a mild or moderate alcohol use disorder may be able to reduce their drinking in the absence of treatment ( 9 ) and have a favorable course; but it is those with more severe alcohol use disorder who most often seek treatment and who may experience a chronic relapsing course ( 10 ).
Near the end of the 18th century, the Pennsylvania physician Benjamin Rush described the loss of control of alcohol and its potential treatments ( 11 ). His recommendations for remedies and case examples included practicing the Christian religion, experiencing guilt and shame, pairing alcohol with aversive stimuli, developing other passions in life, following a vegetarian diet, taking an oath to not drink alcohol, and sudden and absolute abstinence from alcohol. Through the 1800s and early 1900s, the temperance movement laid the groundwork for mutual help organizations, and the notion of excessive alcohol use as a moral failing. During the same period, inebriate asylums emerged as a residential treatment option for excessive alcohol use, although the only treatment offered was forced abstinence from alcohol ( 12 ). The founding of Alcoholics Anonymous (A.A.) in the 1930s ( 13 ) and the introduction of the modern disease concept of alcohol use disorder (previously called “alcoholism”) in the 1940s ( 14 ) laid the groundwork for many of the existing treatment programs that remain widely available today. Over the past 80 years, empirical studies have provided support for both mutual support [A.A. and other support groups, such as SMART (Self-Management and Recovery Training)] and medical models of treatment for alcohol use disorder, as well as the development of new pharmacological and behavioral treatment options. In addition, there are several public health policy initiatives (e.g., taxation, restrictions on advertising, and outlet density) and brief intervention programs (e.g., social norms interventions) that can be effective in reducing prevalence of alcohol use disorder and alcohol-related harms ( 1 ).
Alcohol use disorder is characterized by loss of control over alcohol drinking that is accompanied by changes in brain regions related to the execution of motivated behaviors and to the control of stress and emotionality (e.g., the midbrain, the limbic system, the prefrontal cortex, and the amygdala). Mechanisms of positive and negative reinforcement both play important roles with individual drinking behavior being maintained by positive reinforcement (rewarding and desirable effects of alcohol) and/or negative reinforcement mechanisms (negative affective and physiological states that are relieved by alcohol consumption) ( 15 , 16 ). At the neurotransmitter level, the positive reinforcing effects of alcohol are primarily mediated by dopamine, opioid peptides, serotonin, γ-aminobutyric acid (GABA), and endocannabinoids, while negative reinforcement involves increased recruitment of corticotropin-releasing factor and glutamatergic systems and down-regulation of GABA transmission ( 16 ). Long-term exposure to alcohol causes adaptive changes in several neurotransmitters, including GABA, glutamate, and norepinephrine, among many others. Discontinuation of alcohol ingestion results in the nervous system hyperactivity and dysfunction that characterizes alcohol withdrawal ( 15 , 16 ). Acting on several types of brain receptors, glutamate represents one of the most common excitatory neurotransmitters. As one of the major inhibitory neurotransmitters, GABA plays a key role in the neurochemical mechanisms involved in intoxication, tolerance, and withdrawal. This brief review can offer only a very simplified overview of the complex neurobiological basis of alcohol use disorder. For deeper, more detailed analysis of this specific topic, the reader is encouraged to consult other reviews ( 15 , 16 ).
Alcohol withdrawal symptoms may include anxiety, tremors, nausea, insomnia, and, in severe cases, seizures and delirium tremens. Although up to 50% of individuals with alcohol use disorder present with some withdrawal symptoms after stopping drinking, only a small percentage requires medical treatment for detoxification, and some individuals may be able to reduce their drinking spontaneously. Medical treatment may take place either in an outpatient or, when clinically indicated, inpatient setting. In some cases, clinical monitoring may suffice, typically accompanied by supportive care for hydration and electrolytes and thiamine supplementation. For those patients in need of pharmacological treatment, benzodiazepines (e.g., diazepam, chlordiazepoxide, lorazepam, oxazepam, and midazolam) are the most commonly used medications to treat alcohol withdrawal syndrome. Benzodiazepines work by enhancing the effect of the GABA neurotransmitter at the GABA A receptor. Notably, benzodiazepines represent the gold standard treatment, as they are the only class of medications that not only reduces the severity of the alcohol withdrawal syndrome but also reduces the risk of withdrawal seizures and/or delirium tremens. Because of the potential for benzodiazepine abuse and the risk of overdose, if benzodiazepine treatment for alcohol withdrawal syndrome is managed in an outpatient setting, careful monitoring is required, particularly when combined with alcohol and/or opioid medications ( 17 ).
a-2 agonists (e.g., clonidine) and β-blockers (atenolol) are sometimes used as an adjunct treatment to benzodiazepines to control neuro-autonomic manifestations of alcohol withdrawal not fully controlled by benzodiazepine administration ( 18 ). However, because of the lack of efficacy of a-2 agonists and β-blockers in preventing severe alcohol withdrawal syndrome and the risk of masking withdrawal symptoms, these drugs are recommended not as monotherapy, but only as a possible adjunctive treatment.
Of critical importance to a successful outcome is the fact that alcohol withdrawal treatment provides an opportunity for the patient and the health care provider to engage the patient in a treatment program aimed at achieving and maintaining long-term abstinence from alcohol or reductions in drinking. Such a treatment may include pharmacological and/or psychosocial tools, as summarized in the next sections.
U.s. food and drug administration–approved pharmacological treatments.
Development of novel pharmaceutical reagents is a lengthy, costly, and expensive process. Once a new compound is ready to be tested for human research use, it is typically tested for safety first via phase 0 and phase 1 clinical studies in a very limited number of individuals. Efficacy and side effects may then be further tested in larger phase 2 clinical studies, which may be followed by larger phase 3 clinical studies, typically conducted in several centers and are focused on efficacy, effectiveness, and safety. If approved for use in clinical practice, this medication is still monitored from a safety standpoint, via phase 4 postmarketing surveillance.
Only three drugs are currently approved by the U.S. Food and Drug Administration (FDA) for use in alcohol use disorder. The acetaldehyde dehydrogenase inhibitor disulfiram was the first medication approved for the treatment of alcohol use disorder by the FDA, in 1951. The most common pathway in alcohol metabolism is the oxidation of alcohol via alcohol dehydrogenase, which metabolizes alcohol to acetaldehyde, and aldehyde dehydrogenase, which converts acetaldehyde into acetate. Disulfiram leads to an irreversible inhibition of aldehyde dehydrogenase and accumulation of acetaldehyde, a highly toxic substance. Although additional mechanisms (e.g., inhibition of dopamine β-hydroxylase) may also play a role in disulfiram’s actions, the blockade of aldehyde dehydrogenase activity represents its main mechanism of action. Therefore, alcohol ingestion in the presence of disulfiram leads to the accumulation of acetaldehyde, resulting in numerous related unpleasant symptoms, including tachycardia, headache, nausea, and vomiting. In this way, disulfiram administration paired with alcohol causes the aversive reaction, initially proposed as a remedy for alcohol use disorder by Rush ( 11 ) in 1784. One challenge in conducting a double-blind, placebo-controlled alcohol trial of disulfiram is that it is easy to break the blind unless the “placebo” medication also creates an aversive reaction when consumed with alcohol, which would then provide the same mechanism of action as the medication (e.g., the placebo and disulfiram would both have the threat of an aversive reaction). Open-label studies of disulfiram do provide support for its efficacy, as compared to controls, with a medium effect size ( 19 ), as defined by Cohen’s d effect size ranges of small d = 0.2, medium d = 0.5, and large d = 0.8 ( 20 ). The efficacy of disulfiram largely depends on patient motivation to take the medication and/or supervised administration, given that the medication is primarily effective by the potential threat of an aversive reaction when paired with alcohol ( 21 ).
The next drug approved for treatment of alcohol use disorder was acamprosate; first approved as a treatment for alcohol dependence in Europe in 1989, acamprosate has subsequently been approved for use in the United States, Canada, and Japan. Although the exact mechanisms of acamprosate action are still not fully understood, there is evidence that it targets the glutamate system by modulating hyperactive glutamatergic states, possibly acting as an N -methyl- d -aspartate receptor agonist ( 22 ). The efficacy of acamprosate has been evaluated in numerous double-blind, randomized controlled trials and meta-analyses, with somewhat mixed conclusions ( 23 – 26 ). Although a meta-analysis conducted in 2013 ( 25 ) indicated small to medium effect sizes in favor of acamprosate over placebo in supporting abstinence, recent large-scale trials conducted in the United States ( 27 ) and Germany ( 28 ) failed to find effects of acamprosate distinguishable from those of a placebo. Overall, there is evidence that acamprosate may be more effective in promoting abstinence and preventing relapse in already detoxified patients than in helping individuals reduce drinking ( 25 ), therefore suggesting its use as an important pharmacological aid in treatment of abstinent patients with alcohol use disorder. The most common side effect with acamprosate is diarrhea. Other less common side effects may include nausea, vomiting, stomachache, headache, and dizziness, although the causal role of acamprosate in giving these side effects is unclear.
A third drug, the opioid receptor antagonist naltrexone, was approved for the treatment of alcohol dependence by the FDA in 1994. Later, a monthly extended-release injectable formulation of naltrexone, developed with the goal of improving patient adherence, was also approved by the FDA in 2006. Naltrexone reduces craving for alcohol and has been found to be most effective in reducing heavy drinking ( 25 ). The efficacy of naltrexone in reducing relapse to heavy drinking, in comparison to placebo, has been supported in numerous meta-analyses ( 23 – 25 ), although there is less evidence for its efficacy in supporting abstinence ( 25 ). Fewer studies have been conducted with the extended-release formulation, but its effects on heavy drinking, craving, and quality of life are promising ( 29 , 30 ). Common side effects of naltrexone may include nausea, headache, dizziness, and sleep problems. Historically, naltrexone’s package insert has been accompanied by a risk of hepatotoxicity, a precaution primarily due to observed liver toxicity in an early clinical trial with administrating a naltrexone dosage of 300 mg per day to obese men ( 31 ). However, there is no published evidence of severe liver toxicity at the lower FDA-approved dosage of naltrexone for alcohol use disorder (50 mg per day). Nonetheless, transient, asymptomatic hepatic transaminase elevations have also been observed in some clinical trials and in the postmarketing period; therefore, naltrexone should be used with caution in patients with active liver disease and should not be used in patients with acute hepatitis or liver failure.
Disulfiram, acamprosate, and naltrexone have been approved for use in Europe and in the United States. Pharmacologically similar to naltrexone, nalmefene was also approved for the treatment of alcohol dependence in Europe in 2013. Nalmefene is a m- and d-opioid receptor antagonist and a partial agonist of the k-opioid receptor ( 32 ). Side effects of nalmefene are similar to naltrexone; compared to naltrexone, nalmefene has a longer half-life. Meta-analyses have indicated that nalmefene is effective in reducing heavy drinking days ( 32 ). An indirect meta-analysis of these two drugs concluded that nalmefene may be more effective than naltrexone ( 33 ), although whether a clinically relevant difference between the two medications really exists is still an open question ( 34 ). Network meta-analysis and microsimulation studies suggest that nalmefene may have some benefits over placebo for reducing total alcohol consumption ( 35 , 36 ). The approval of nalmefene in Europe was accompanied by some controversy ( 37 ); a prospective head-to-head trial of nalmefene and naltrexone could help clarify whether nalmefene has added benefits to the existing medications available for alcohol use disorder. Last, nalmefene was approved in Europe as a medication that can be taken “as needed” (i.e., on days when drinking was going to occur). Prior work has also demonstrated the efficacy of taking naltrexone only on days that drinking was potentially going to occur ( 38 ).
In addition to these drugs, a GABA B receptor agonist used to treat muscle spasms, baclofen, was approved for treatment of alcohol use disorder in France in 2018 and has been used off label for alcohol use disorder for over a decade in other countries, especially in other European countries and in Australia ( 39 , 40 ). Recent human laboratory work suggests that baclofen may disrupt the effects of an initial priming dose of alcohol on subsequent craving and heavy drinking ( 41 ). Meta-analyses and systematic reviews examining the efficacy of baclofen have yielded mixed results ( 35 , 39 , 42 ); however, there is some evidence that baclofen might be useful in treatment of alcohol use disorder among individuals with liver disease ( 43 , 44 ). Evidence of substantial heterogeneity in baclofen pharmacokinetics among different individuals with alcohol use disorder ( 41 ) could explain the variability in the efficacy of baclofen across studies. The appropriate dose of baclofen for use in treatment of alcohol use disorder remains a controversial topic, and a recent international consensus statement highlighted the importance of tailoring doses based on safety, tolerability, and efficacy ( 40 ).
Numerous other medications have been used off label in the treatment of alcohol use disorder, and many of these have been shown to be modestly effective in meta-analyses and systematic reviews ( 23 , 24 , 26 , 35 ). Systematic studies of these medications suggest promising findings for topiramate, ondansetron, gabapentin, and varenicline. The anticonvulsant drug topiramate represents one of the most promising medications in terms of efficacy, based on its medium effect size from several clinical trials [for a review, see ( 45 )], including a multisite clinical study ( 46 ). One strength of topiramate is the possibility of starting treatment while people are still drinking alcohol, therefore serving as a potentially effective treatment to initiate abstinence (or to reduce harm) rather than to prevent relapse in already detoxified patients ( 45 ). Although not approved by the FDA, it is worth noticing that topiramate is a recommended treatment for alcohol use disorder in the U.S. Department of Veterans Affairs ( 47 ). A concern with topiramate is the potential for significant side effects, especially those affecting cognition and memory, warranting a slow titration of its dose and monitoring for side effects. Furthermore, recent attention has been paid on zonisamide, another anticonvulsant medication, whose pharmacological mechanisms of actions are similar to topiramate but with a better tolerability and safety profile ( 48 ). Recently published and ongoing research focuses on a potential pharmacogenetic approach to treatment in the use of topiramate to treat alcohol use disorder, based on the possibility that both efficacy and tolerability and safety of topiramate may be moderated by a functional single-nucleotide polymorphism (rs2832407) in GRIK1, encoding the kainate GluK1 receptor subunit ( 49 ). Human laboratory studies ( 50 ) and treatment clinical trials ( 51 ) have also used a primarily pharmacogenetic approach to testing the efficacy of the antinausea drug ondansetron, a 5HT 3 antagonist, in alcohol use disorder. Overall, these studies suggest a potential role for ondansetron in alcohol use disorder, but only in those individuals with certain variants of the genes encoding the serotonin transporter 5-HTT and the 5-HT 3 receptor. The anticonvulsant gabapentin has shown promising results in human laboratory studies and clinical trials ( 52 – 54 ), although a more recent multisite trial with an extended-release formulation of the medication did not have an effect of gabapentin superior to that of a placebo ( 55 ). Although the latter findings might be related to potential pharmacokinetic issues secondary to the specific formulation used, it is nonetheless possible that gabapentin may be more effective in patients with more clinically relevant alcohol withdrawal symptoms ( 52 ). Several human laboratory studies support a role for varenicline, a nicotinic acetylcholine receptor partial agonist approved for smoking cessation, in alcohol use disorder [for a review, see ( 56 )], and two of three clinical trials also support its efficacy on alcohol outcomes ( 57 – 59 ), especially in heavy drinkers who are males ( 59 ) and in male and female alcohol-dependent individuals who are also smokers ( 60 ). Additional details on the FDA-approved medications and other medications tested in clinical research settings for the treatment of alcohol use disorder are summarized in Table 2 .
FDA, U.S. Food and Drug Administration; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NMDA, N -methyl- d -aspartate; PO, per os (oral); IM, intramuscular; HT, serotonin.
| ||
Acamprosate (PO) | 1998 mg per day | Unclear—it has been suggested that acamprosate is a modulator of hyperactive glutamatergic states, possibly as an NMDA receptor agonist |
Disulfiram (PO) | 250–500 mg per day | Inhibition of acetaldehyde dehydrogenase |
Naltrexone (PO) | 50 mg per day | m-opioid receptor antagonist |
Naltrexone (IM) | 380 mg once a month | m-opioid receptor antagonist |
Baclofen (PO) | 30–80 mg per day | GABA receptor agonist |
Approved in France by the National Agency for the Safety of Medicines and Healthcare Products | ||
Gabapentin (PO) | 900–1800 mg per day | Unclear—the most likely mechanism is blockade of voltage-dependent Ca channels. Although it is a GABA analog, gabapentin does not seem to act on the GABA receptors |
Nalmefene (PO) | 18 mg per day | m- and d-opioid receptor antagonist and k-opioid receptor partial agonist |
Approved in Europe by the European Medicines Agency | ||
Ondansetron (PO) | 0.5 mg per day (fixed dose) or up to 36 mcg/kg per day | 5HT antagonist |
Prazosin/doxazosin (PO) | Up to 16 mg per day | a-1 receptor antagonists |
Topiramate (PO) | Up to 300 mg per day | Topiramate is an anticonvulsant with multiple targets. It increases GABA -facilitated neuronal activity and simultaneously antagonizes AMPA and kainate glutamate receptors. It also inhibits l-type calcium channels, limits the activity of voltage-dependent sodium channels and facilitates potassium conductance. Furthermore, it is a weak inhibition of the carbonic anhydrase isoenzymes, CA-II and CA-IV |
Varenicline (PO) | 2 mg per day | Nicotinic acetylcholine receptor partial agonist |
The medications and targets described above have shown promising results in phase 2 or phase 3 medication trials. However, owing to the development of novel neuroscience techniques, a growing and exciting body of data is expanding the armamentarium of targets currently under investigation in animal models and/or in early-phase clinical studies. Pharmacological approaches with particular promise for future drug development include, but are not limited to the following [for recent reviews, see, e.g., ( 56 , 61 – 68 )]: the antipsychotic drug aripiprazole, which has multiple pharmacological actions (mainly on dopamine and serotonin receptors), the antihypertensive alpha-1 blocker drugs prazosin and doxazosin, neurokinin-1 antagonism, the glucocorticoid receptor blocker mifepristone, vasopressin receptor 1b antagonism, oxytocin, ghrelin receptor antagonism, glucagon-like peptide-1 agonism, and pharmacological manipulations of the nociception receptor (We are intentionally using a general pharmacological terminology for the nociceptin receptor, given that it is unclear whether agonism, antagonism, or both may represent the best approach.). New medications development is particularly important for the treatment of comorbid disorders that commonly co-occur among individuals with alcohol use disorder, particularly affective disorders, anxiety disorders, suicidality, and other substance use disorders. This aspect of alcohol use disorder is relevant to the fact that addictive disorders often present with significantly more severe symptoms when they coexist with other mental health disorders ( 69 ). Likewise, there is evidence that pharmacotherapy is most effective when implemented in conjunction with behavioral interventions ( 70 ), and all phase 2 and phase 3 medication trials, mentioned above, have included a brief psychosocial behavioral treatment in combination with medication.
Evidence-based treatments.
A wide range of behavioral and psychological treatments are available for alcohol use disorder, and many treatments are equally effective in supporting abstinence or drinking reduction goals ( 71 – 74 ). Treatments with the greatest evidence of efficacy range from brief interventions, including motivational interviewing approaches, to operant conditioning approaches, including contingency management and the community reinforcement approach, to cognitive behavioral treatments, including coping skills training and relapse prevention, and to acceptance- and mindfulness-based approaches. Twelve-step facilitation, which was designed specifically to connect individuals with mutual support groups, has also been shown to be effective ( 75 ). In addition, harm reduction treatments, including guided self-control training and controlled drinking interventions, have been successful in supporting drinking reduction goals ( 70 ).
Meta-analyses and systematic reviews have found that brief interventions, especially those based on the principles of motivational interviewing, are effective in the treatment of alcohol use disorder. These interventions can include self-monitoring of alcohol use, increasing awareness of high-risk situations, and training in cognitive and behavioral techniques to help clients cope with potential drinking situations, as well as life skills training, communication training, and coping skills training. Cognitive behavioral treatments can be delivered in individual or group settings and can also be extended to the treatment of families and couples ( 72 , 73 ).
Acceptance- and mindfulness-based interventions are increasingly being used to target alcohol use disorder and show evidence of efficacy in a variety of settings and formats, including brief intervention formats ( 76 ). Active ingredients include raising present moment awareness, developing a nonjudgmental approach to self and others, and increasing acceptance of present moment experiences. Acceptance- and mindfulness-based interventions are commonly delivered in group settings and can also be delivered in individual therapy contexts.
Computerized, web-based, and mobile interventions have also been developed, incorporating the principles of brief interventions, behavioral and cognitive behavioral approaches, as well as mindfulness and mutual support group engagement; many of these approaches have demonstrated efficacy in initial trials ( 77 – 79 ). For example, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) has developed the Take Control computerized intervention that includes aspects of motivational interviewing and coping skills training and was designed to provide psychosocial support (particularly among those assigned to the placebo medication) and also to increase adherence and retention among individuals enrolled in pharmacotherapy trials ( 80 ).
Mutual support group (e.g., A.A. and SMART) attendance and engagement have been shown to be associated with recovery from alcohol use disorder, even in the absence of formal treatment ( 81 ). However, selection biases (e.g., people selecting to attend these groups) raise difficulties in assessing whether other factors that are associated with treatment effectiveness may be the active ingredients for improving outcomes among those who attend mutual support groups. For example, individuals who are highly motivated to change might be more likely to attend mutual support groups. Likewise, mutual support groups often provide individuals with increased social network support for abstinence ( 82 ). Motivation to change and having a social network that supports abstinence (or reductions in drinking) are both factors that are associated with greater treatment effectiveness ( 83 ).
As noted above, most behavioral and psychological treatments are equally effective with small effect size differences [Cohen’s d = 2.0 to 0.3 ( 20 )] between active treatments ( 84 – 88 ). Behavioral interventions have also been shown to be as effective as pharmacotherapy options, with a 16-week cognitive behavioral intervention shown to be statistically equivalent to naltrexone in reducing heavy drinking days in a large randomized trial ( 27 ). One of the challenges of examining behavioral interventions in randomized trials is that intervention blinding and placebo controls cannot be implemented in most contexts, other than in computerized interventions. Furthermore, the general therapeutic factors common to most behavioral interventions (e.g., therapist empathy and supportive therapeutic relationship) in treatment of alcohol use disorder are as powerful as the specific therapeutic targets of specific behavioral interventions (e.g., teaching skills in a cognitive behavioral treatment) in facilitating behavioral change ( 89 ).
With respect to behavioral treatments, there are numerous opportunities for the development of novel mobile interventions that could provide treatment and recovery support in near real time. This mobile technology may also extend the reach of treatments to individuals with alcohol use disorder, particularly in rural areas. On the basis of a contextual self-regulation model of alcohol use ( 90 ), it is critical to address the immediate situational context alongside the broader social, environmental, and familial context in which an individual experiences the world and engages in momentary decision-making. Ambulatory assessment, particularly tools that require only passive monitoring (e.g., GPS, heart rate, and skin conductance) and real-time support via mobile health, could provide immediate environmental supports and could extend the reach of medications and behavioral treatments for alcohol use disorder. For example, a mobile device could potentially signal a high-risk situation by indicating the geographic location (near a favorite drinking establishment) and the heart rate (increased heart rate when approaching the establishment). The device could provide a warning either to the individual under treatment and/or to a person supporting that individual’s recovery. In addition, developments in alcohol sensing technology (e.g., transdermal alcohol sensors) could greatly increase rigor of research on alcohol use disorder and also provide real-time feedback on alcohol consumption levels to individuals who are attempting to moderate and/or reduce their alcohol use.
Recent advances in neuromodulation techniques may also hold promise for the development of novel treatments for alcohol use disorder. Deep brain stimulation, transcranial magnetic stimulation, transcranial electrical stimulation (including transcranial direct current stimulation and transcranial alternating current stimulation), and real-time neurofeedback have recently been tested as potential treatments for addiction, although evidence in favor of these treatments is currently uncertain and focused mostly on intermediate targets (e.g., alcohol craving) ( 91 ). These techniques attempt to directly target specific brain regions and addiction-related cognitive processes via surgically implanted electrodes (deep brain stimulation), electrical currents or magnetic fields applied to the scalp (transcranial electrical and magnetic stimulation, respectively), or individual self-generated modulation via feedback (neurofeedback). Although robust large scale trials with double-blind, sham controls, and long-term follow-ups of alcohol behavior change and relapse have not been conducted ( 91 ), the heterogeneity of alcohol use disorder suggests that targeting one specific neural region may be insufficient to treat such a complex disorder, with its multiple etiologies and diverse clinical courses ( 92 ).
Numerous models have examined factors that predict treatment readiness, treatment engagement, and treatment outcomes for alcohol use disorder. The transtheoretical model of change proposes that an individual’s own readiness to change his or her drinking behavior may have an impact on treatment engagement and effectiveness ( 93 ). The dynamic model of relapse proposes the involvement of multiple interacting biological, psychological, cognitive, emotional, social, and situational risk factors that are static and dynamic in their association with treatment outcomes ( 83 ). Neurobiological models of addiction focus on the brain reward and stress system dysfunction that contributes to the development and maintenance of alcohol use disorder, that is, the “addiction cycle” ( 15 , 16 ). The alcohol and addiction research domain criteria (AARDoC) ( 92 ), which have been operationalized in the addictions neuroclinical assessment ( 94 ), focus on the following three domains that correspond to particular phases in the addiction cycle: incentive salience in the binge/intoxication phase, negative emotionality in the withdrawal/negative affect phase, and executive function in the preoccupation/anticipation phase. Within each domain of the AARDoC, the addictions neuroclinical assessment proposes constructs that can be measured at multiple levels of analysis, such as craving in the incentive salience domain, negative affect and emotion dysregulation in the negative emotionality domain, and cognitive impairment and impulsivity in the executive function domain. The AARDoC acknowledge that environmental and contextual factors play a role in alcohol use disorder and treatment outcomes. Moreover, because of the heterogeneity of alcohol use disorder, the significance of these domains in causing alcohol use disorder and alcohol-related problems will vary among individuals.
Each of the abovementioned theoretical models proposes factors that may affect treatment effectiveness; however, many of the constructs proposed in each of these models are overlapping and likely contribute to the effectiveness of alcohol use disorder treatment across a range of populations and settings. A heuristic model combining components from each of these models is shown in Fig. 1 . Specifically, this model highlights the precipitants of alcohol use that are influenced by the neurobiological adaptations proposed in the addiction cycle (indicated by bold font) and additional contextual factors (regular font) that decrease or increase the likelihood of drinking in context, depending on whether an individual uses effective coping regulation in the moment. The domains supporting alcohol use/coping regulation (negative emotionality, executive function, incentive salience, and social environment) may interact to predict alcohol use or coping regulation in the moment. For example, network support for abstinence could improve decision-making and decrease likelihood of drinking. Conversely, experiences of physical pain are associated with increases in negative affect and poorer executive function, which could both increase likelihood of drinking. Both of these examples require environmental access to alcohol and a desire to drink alcohol. Treatment effectiveness will depend on the extent to which a particular treatment targets those risk factors that are most likely to increase or decrease the likelihood of drinking for each individual, as well as the personal resources that each individual brings to treatment and/or that could be enhanced in treatment. A functional analysis of contextual risk and protective factors can be critically important in guiding treatment.
Risk factors proposed in the AARDoC, including incentive salience, negative emotionality, executive function, and social environmental factors, are shown in black bold font encircling alcohol use. Contextual risk factors, including decision-making, self-efficacy, pain, craving, etc., are shown in black font in colored boxes. Risk and protective factors overlap with alcohol use and interact in predicting coping regulation and alcohol use among individual patients.
For example, there is considerable heterogeneity in treatment response to naltrexone, which may vary in efficacy in some individuals. Recent studies conducted to determine whether certain patients may benefit more from naltrexone have yielded mixed findings ( 95 ). Promising evidence suggests that individuals with the OPRM1 A118G G (Asp40) allele may have a better response to naltrexone ( 96 – 98 ); however, a prospective study of medication response among individuals stratified by presence of the Asp40 allele did not provide support for the genotype by treatment interaction ( 99 ), and recent human laboratory studies have not confirmed the hypothesized mechanisms underlying the pharmacogenomic effect ( 100 ). Initial evidence suggests that naltrexone may be more effective in reducing heavy drinking among smokers ( 101 ) and among those with a larger number of heavy drinkers in their social networks ( 102 ). With respect to reinforcement typologies, recent work has found that naltrexone may be more effective among those who tend to drink alcohol for rewarding effects ( 103 ), and acamprosate may also be more effective for individuals who drink to relieve negative affect ( 104 ).
Heterogeneity of individuals with alcohol use disorder.
This review has briefly summarized the treatments currently available for alcohol use disorder that are relatively effective, at least in some patients. Many new treatments are also being developed, and some of them seem promising. Nevertheless, numerous gaps in scientific knowledge remain. Notably, most people who drink alcohol do not develop an alcohol use disorder, most people with alcohol use disorder do not seek treatment, and most of those who do not seek treatment “recover” from alcohol use disorder without treatment ( 2 ). Very little is known about factors, particularly neurobiological, genetic, and epigenetic factors, that predict the transition from alcohol use to alcohol use disorder, although basic science models suggest that a cycle of neuroadaptations could be at play ( 15 , 16 ). We also lack a basic understanding of how individuals recover from alcohol use disorder in the absence of treatment and what neurobiological, psychological, social, and environmental factors are most important for supporting recovery from alcohol use disorder. Gaining a better understanding of recovery in the absence of treatment, particularly modifiable psychological, neurobiological, and epigenetic factors, could provide novel insights for medications and behavioral treatment development. Among many other factors, special attention is needed in future studies to shed light on the role of sex and gender in the development and maintenance of alcohol use disorder and on the response to pharmacological, behavioral, and other treatments.
The heterogeneity of alcohol use disorder presents a major challenge to scientific understanding and to the development of effective treatments for prevention and intervention ( 92 ). For example, a DSM-5 diagnosis of alcohol use disorder requires 2 or more symptoms, out of 11, over the past year. That requirement equates to exactly 2048 potential symptom combinations that would meet the criteria of alcohol use disorder. An individual who only meets criteria for tolerance and withdrawal (i.e., physiological dependence) likely requires a very different course of treatment from an individual who only meets the criteria for failure to fulfill role obligations and use of alcohol in hazardous situations. Gaining a better understanding of the etiology and course of alcohol use disorder, as well as identifying whether different subtypes of drinkers may respond better to certain treatments ( 103 , 104 ), is critical for advancing the science of alcohol use disorder prevention and treatment. Alternative conceptualizations of alcohol use disorder may also aid in improving our understanding of the disorder and reducing heterogeneity. For example, the pending International Classification of Diseases , 11th edition, will simplify the diagnosis of alcohol dependence to requiring only two of three criteria in the past 12 months: (i) impaired control over alcohol use; (ii) alcohol use that dominates over other life activities; and (iii) persistence of alcohol use despite consequences. The diagnosis will be made with or without physiological dependence, as characterized by tolerance, withdrawal, or repeated use to prevent or alleviate withdrawal ( 105 ). It remains to be seen whether simplification of the criteria set will narrow our conceptualization or potentially increase heterogeneity of this disorder among those diagnosed with alcohol dependence.
An additional challenge to development of pharmacological treatments for alcohol use disorder is the high placebo response rates seen in drug trials ( 106 ). The tendency for individuals to have a good treatment response when assigned to placebo medication reflects both the high probability of recovery without treatment and the heterogeneity in the disorder itself. Many people who enter treatment are already motivated to change behavior, and receiving a placebo medication can help these individuals continue the process of change. Gaining a better understanding of which kinds of individuals respond to placebo and of the overall physiological and behavioral complexities in the placebo response is critical to identifying those individuals who will benefit the most from active medication. More generally, very little is understood about how motivation to change drinking behavior may influence the efficacy of active medications, particularly via adherence mechanisms. Additional research on targeted (i.e., as needed) dosing of medications, such as nalmefene and naltrexone ( 32 , 38 ), would be promising from the perspective of increasing adherence to medications and also raising awareness of potentially heavy drinking occasions.
In addition to gaining a better understanding of the disorder and who benefits from existing treatments, the examination of molecular targets for alcohol use disorder could open up multiple innovative directions for future translational research on the treatment of alcohol use disorder. Recent research has identified many targets that might be important for future medication trials ( 67 ). For example, most of the medication development efforts in past decades have focused on pathways and targets typically related to reward processing and positive reinforcement. While important, this approach ignores the important role of stress-related pathways (e.g., corticotropin release factor and other related pathways) in negative reinforcement and in the later stages of alcohol use disorder, which is often characterized by physical dependence, anxiety, and relief drinking [for reviews, see ( 15 , 16 )]. Furthermore, it is also becoming more and more apparent that other promising targets may be identified by looking at the brain not as an isolated system but rather as an organ with bidirectional interactions with peripheral systems. Examples of the latter approach include the growing evidence suggesting a potential role of inflammation and neuroinflammation and of the gut-liver-brain axis in the neurobiological mechanisms that regulate the development and/or maintenance of alcohol use disorder ( 107 – 109 ). Moving medications development from phase 1 to phase 2 and 3 trials has also been a difficulty in the field. Future directions that might improve translation of basic science into clinical practice include the broader use of human laboratory models and pilot clinical trials ( 110 ), as well as expanding the outcomes that might be targeted in phase 2 and phase 3 trials to include drinking reduction outcomes ( 111 , 112 ).
New directions for behavioral treatment development include a greater focus on identifying effective elements of behavioral treatments and on the components of treatment that are most critical for successful behavior change ( 89 , 113 ). Studies investigating the effects of specific treatment components are critical for refining treatment protocols to more efficiently target the symptoms of alcohol use disorder. Continued development of mobile health interventions will also help with disseminating treatment to a wider range of individuals struggling with alcohol use disorder.
Last, but not the least, there is also a critical need for more research on dissemination and implementation, given the fact that many treatment programs still do not incorporate evidence-based practices, such as cognitive behavioral skills training, mindfulness-based interventions, and medications. Both pharmacological and behavioral treatments for alcohol use disorder are markedly underused; the recent Surgeon General’s report Facing Addiction in America ( 114 ) highlights the fact that only about 1 in 10 people with a substance use disorder receives any type of specialty treatment. Therefore, basic science and human research efforts will need to be accompanied by translational approaches, where effective novel medications and precision medicine strategies are effectively translated from research settings to clinical practice. Greater integration of alcohol screening and medication in primary care and other clinical settings, as well as research on best methods for implementation, has great potential for expanding access to effective treatment options ( 115 ). Because the heterogeneity of alcohol use disorder makes it highly unlikely that one single treatment will work for all individuals, it is important to provide a menu of options for pharmacological and behavioral therapies to both clinicians and patients. Reducing the stigma of alcohol use disorder and moving toward a public health approach to addressing this problem may further increase the range of acceptable treatment options.
Funding: This research was supported by a grant from NIAAA (R01 AA022328) awarded to K.W. (principal investigator). R.Z.L. is funded by NIAAA. L.L. is jointly funded by NIAAA and the National Institute on Drug Abuse (NIDA) (ZIA-AA000218). The content of this review does not necessarily represent the official views of the funders. Author contributions: K.W. wrote the first draft of the manuscript. K.W., R.Z.L., and L.L. provided additional text and edits. All authors approved the final draft. Competing interests: The authors declare that they have no competing interests. Data and materials availability: All data needed to evaluate the conclusions in the paper are present in the paper and/or in the materials cited herein. Additional data related to this paper may be requested from the authors.
Alcohol use disorder is a pattern of alcohol use that involves problems controlling your drinking, being preoccupied with alcohol or continuing to use alcohol even when it causes problems. This disorder also involves having to drink more to get the same effect or having withdrawal symptoms when you rapidly decrease or stop drinking. Alcohol use disorder includes a level of drinking that's sometimes called alcoholism.
Unhealthy alcohol use includes any alcohol use that puts your health or safety at risk or causes other alcohol-related problems. It also includes binge drinking — a pattern of drinking where a male has five or more drinks within two hours or a female has at least four drinks within two hours. Binge drinking causes significant health and safety risks.
If your pattern of drinking results in repeated significant distress and problems functioning in your daily life, you likely have alcohol use disorder. It can range from mild to severe. However, even a mild disorder can escalate and lead to serious problems, so early treatment is important.
Alcohol use disorder can be mild, moderate or severe, based on the number of symptoms you experience. Signs and symptoms may include:
Alcohol use disorder can include periods of being drunk (alcohol intoxication) and symptoms of withdrawal.
The National Institute on Alcohol Abuse and Alcoholism defines one standard drink as any one of these:
If you feel that you sometimes drink too much alcohol, or your drinking is causing problems, or if your family is concerned about your drinking, talk with your health care provider. Other ways to get help include talking with a mental health professional or seeking help from a support group such as Alcoholics Anonymous or a similar type of self-help group.
Because denial is common, you may feel like you don't have a problem with drinking. You might not recognize how much you drink or how many problems in your life are related to alcohol use. Listen to relatives, friends or co-workers when they ask you to examine your drinking habits or to seek help. Consider talking with someone who has had a problem with drinking but has stopped.
Many people with alcohol use disorder hesitate to get treatment because they don't recognize that they have a problem. An intervention from loved ones can help some people recognize and accept that they need professional help. If you're concerned about someone who drinks too much, ask a professional experienced in alcohol treatment for advice on how to approach that person.
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Genetic, psychological, social and environmental factors can impact how drinking alcohol affects your body and behavior. Theories suggest that for certain people drinking has a different and stronger impact that can lead to alcohol use disorder.
Over time, drinking too much alcohol may change the normal function of the areas of your brain associated with the experience of pleasure, judgment and the ability to exercise control over your behavior. This may result in craving alcohol to try to restore good feelings or reduce negative ones.
Alcohol use may begin in the teens, but alcohol use disorder occurs more frequently in the 20s and 30s, though it can start at any age.
Risk factors for alcohol use disorder include:
Alcohol depresses your central nervous system. In some people, the initial reaction may feel like an increase in energy. But as you continue to drink, you become drowsy and have less control over your actions.
Too much alcohol affects your speech, muscle coordination and vital centers of your brain. A heavy drinking binge may even cause a life-threatening coma or death. This is of particular concern when you're taking certain medications that also depress the brain's function.
Excessive drinking can reduce your judgment skills and lower inhibitions, leading to poor choices and dangerous situations or behaviors, including:
Drinking too much alcohol on a single occasion or over time can cause health problems, including:
Early intervention can prevent alcohol-related problems in teens. If you have a teenager, be alert to signs and symptoms that may indicate a problem with alcohol:
You can help prevent teenage alcohol use:
Alcohol use disorder care at Mayo Clinic
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Alcohol is a chemical substance derived from the fermentation or distillation of various fruits, grains, or other natural sources. It is commonly consumed in the form of alcoholic beverages and is known for its psychoactive effects. Alcohol, specifically ethanol, acts as a central nervous system depressant, affecting brain function and altering behavior.
The origin and history of alcohol can be traced back to ancient civilizations. The earliest evidence of alcohol production dates back to around 7000 to 6600 BCE in China, where fermented beverages made from rice, honey, and fruit were consumed. Similarly, in the Middle East, evidence of alcoholic beverages made from barley dates back to around 5400 to 5000 BCE. Throughout history, alcohol has played a significant role in various cultures and societies. It was often associated with religious rituals, social gatherings, and medicinal purposes. The Ancient Egyptians, Greeks, and Romans had a wide variety of alcoholic beverages, and the art of brewing and distillation spread through trade routes. During the Middle Ages, monasteries in Europe became centers of brewing and distillation, and the production of alcoholic beverages became more organized. In the 18th and 19th centuries, the Industrial Revolution led to the mass production of alcohol, contributing to social issues related to alcohol abuse.
Alcohol has both short-term and long-term effects on the body and mind. In the short term, alcohol acts as a depressant, slowing down the central nervous system and affecting coordination, judgment, and reaction time. It can cause relaxation, euphoria, and lowered inhibitions. However, excessive consumption can lead to negative effects such as impaired judgment, blurred vision, slurred speech, and increased risk-taking behavior. Long-term alcohol use can have detrimental effects on various organs and systems. Prolonged heavy drinking can damage the liver, leading to conditions such as cirrhosis and alcoholic hepatitis. It can also weaken the immune system, increase the risk of cardiovascular diseases, and contribute to the development of certain types of cancer. Alcohol misuse and addiction can have profound social and psychological consequences. It can strain relationships, lead to financial difficulties, and contribute to mental health disorders such as depression and anxiety. Additionally, excessive alcohol consumption is associated with an increased risk of accidents, injuries, and even fatalities. It is important to note that moderate alcohol consumption can have some potential health benefits, such as a reduced risk of heart disease. However, these potential benefits must be balanced with the risks and individual circumstances, and it is always advisable to consume alcohol responsibly and in moderation.
Public opinion about alcohol varies greatly depending on cultural, social, and individual factors. It is a complex and multifaceted topic that elicits diverse perspectives. Some individuals and societies view alcohol consumption as an acceptable and enjoyable part of social gatherings and celebrations. They may see it as a way to relax, socialize, and enhance the enjoyment of certain experiences. In these contexts, alcohol is often seen as a normal and integral aspect of everyday life. On the other hand, there are those who hold more cautious or negative views towards alcohol. They may emphasize the potential risks and harms associated with its use, such as addiction, health problems, and impaired judgment. Concerns about alcohol-related accidents, violence, and addiction can shape public opinion and lead to stricter regulations and policies. Public opinion on alcohol is also influenced by cultural and religious beliefs, as well as personal experiences and values. Some individuals may have witnessed the negative consequences of alcohol misuse and therefore hold more critical views. Others may have positive associations with alcohol and view it as a benign or enjoyable substance when consumed responsibly.
Alcohol is a frequently depicted substance in various forms of media, including movies, television shows, music, and advertising. Its portrayal in media can range from positive and glamorous to negative and cautionary, reflecting the diverse perspectives and attitudes towards alcohol. In some media representations, alcohol is shown as a symbol of sophistication, celebration, and socializing. It is often associated with luxury and enjoyment, depicted in glamorous settings where characters are seen drinking champagne, cocktails, or wine. This positive representation can be found in movies like "The Great Gatsby" and TV shows like "Mad Men," where characters are shown indulging in alcohol as a part of their lifestyle. However, media also portrays the negative consequences and risks associated with alcohol consumption. Films like "Leaving Las Vegas" and "Flight" depict the destructive effects of alcohol addiction, showcasing the devastating impact it can have on individuals and their relationships. Such portrayals serve as cautionary tales and highlight the potential dangers of excessive alcohol use. Furthermore, there are public service announcements and campaigns that aim to raise awareness about responsible drinking and the harmful effects of alcohol abuse. These messages often depict the negative consequences of alcohol-related accidents, impaired judgment, and addiction.
1. According to the World Health Organization (WHO), alcohol is responsible for more than 3 million deaths worldwide each year. This includes deaths from alcohol-related diseases, accidents, and violence. It is a significant public health concern that requires attention and prevention efforts. 2. A study published in the journal Addiction revealed that alcohol consumption is a leading risk factor for disease burden and premature death globally. It ranked as the seventh leading risk factor for both death and disability-adjusted life years (DALYs) in 2016, highlighting the significant impact of alcohol on population health. 3. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) reports that alcohol-related problems cost the United States economy an estimated $249 billion in 2010. These costs include healthcare expenses, lost productivity, and criminal justice costs associated with alcohol-related incidents. This statistic emphasizes the economic burden of alcohol misuse on society.
Alcohol is an important topic to explore in an essay due to its widespread use and the complex implications it has on individuals, society, and public health. Understanding the various aspects of alcohol, including its history, effects, public opinion, and representation in media, can provide valuable insights into its impact on individuals and communities. By delving into the history of alcohol, one can examine its cultural, social, and economic significance throughout different time periods and regions. Exploring the effects of alcohol on the human body and mind helps shed light on the risks and potential consequences associated with its consumption. Analyzing public opinion allows for an understanding of societal attitudes, perceptions, and debates surrounding alcohol use and abuse. Furthermore, the representation of alcohol in media and popular culture plays a significant role in shaping public perceptions and behaviors. Investigating how alcohol is portrayed in films, advertisements, and literature can reveal underlying messages and narratives about its consumption.
1. Babor, T. F., Higgins-Biddle, J. C., Saunders, J. B., & Monteiro, M. G. (2001). AUDIT: The Alcohol Use Disorders Identification Test: Guidelines for use in primary care (2nd ed.). World Health Organization. 2. Dawson, D. A., Goldstein, R. B., Saha, T. D., & Grant, B. F. (2015). Changes in alcohol consumption: United States, 2001–2002 to 2012–2013. Drug and Alcohol Dependence, 148, 56–61. 3. Grant, B. F., & Dawson, D. A. (2017). Alcohol and drug use disorder: Diagnostic criteria for use in general health care settings. National Institute on Alcohol Abuse and Alcoholism. 4. Gual, A., Segura, L., Contel, M., & Heather, N. (2013). AUDIT-3 and AUDIT-4: Effectiveness of two short forms of the Alcohol Use Disorders Identification Test. Alcohol and Alcoholism, 48(5), 565–565. 5. Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217–238. 6. Rehm, J., Mathers, C., Popova, S., Thavorncharoensap, M., Teerawattananon, Y., & Patra, J. (2009). Global burden of disease and injury and economic cost attributable to alcohol use and alcohol-use disorders. The Lancet, 373(9682), 2223–2233. 7. Roerecke, M., & Rehm, J. (2010). Alcohol consumption, drinking patterns, and ischemic heart disease: A narrative review of meta-analyses and a systematic review and meta-analysis of the impact of heavy drinking occasions on risk for moderate drinkers. BMC Medicine, 8(1), 1–23. 8. Room, R., Babor, T., & Rehm, J. (2005). Alcohol and public health. The Lancet, 365(9458), 519–530. 9. Schuckit, M. A. (2014). Alcohol-use disorders. The Lancet, 383(9929), 988–998. 10. World Health Organization. (2018). Global status report on alcohol and health 2018. World Health Organization.
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Physiology and psychology of addiction, prescription drug abuse, depressants, hallucinogens.
Drug and substance abuse is an issue that affects entirely all societies in the world. It has both social and economic consequences, which affect directly and indirectly our everyday live. Drug addiction is “a complex disorder characterized by compulsive drug use” (National Institute on Drug Abuse, 2010).
It sets in as one form a habit of taking a certain drug. Full-blown drug abuse comes with social problems such as violence, child abuse, homelessness and destruction of families (National Institute on Drug Abuse, 2010). To understand to the impact of drug abuse, one needs to explore the reasons why many get addicted and seem unable pull themselves out of this nightmare.
Many experts consider addiction as a disease as it affects a specific part of the brain; the limbic system commonly referred to as the pleasure center. This area, which experts argue to be primitive, is affected by various drug substances, which it gives a higher priority to other things. Peele (1998) argues that alcoholism is a disease that can only be cured from such a perspective (p. 60). Genetics are also seen as a factor in drug addiction even though it has never been exclusively proven.
Other experts view addiction as a state of mind rather than a physiological problem. The environment plays a major role in early stages of addiction. It introduces the agent, in this case the drug, to the abuser who knowingly or otherwise develops dependence to the substance. Environmental factors range from violence, stress to peer pressure.
Moreover, as an individual becomes completely dependent on a substance, any slight withdrawal is bound to be accompanied by symptoms such as pain, which is purely psychological. This is because the victim is under self-deception that survival without the substance in question is almost if not impossible. From his psychological vantage point, Isralowitz (2004) argues that freedom from addiction is achievable provided there is the “right type of guidance and counseling” (p.22).
A doctor as regulated by law usually administers prescription drugs. It may not be certain why many people abuse prescription drugs but the trend is ever increasing. Many people use prescription drugs as directed by a physician but others use purely for leisure. This kind of abuse eventually leads to addiction.
This problem is compounded by the ease of which one can access the drugs from pharmacies and even online. Many people with conditions requiring painkillers, especially the elderly, have a higher risk of getting addicted as their bodies become tolerant to the drugs. Adolescents usually use some prescription drugs and especially painkillers since they induce anxiety among other feelings as will be discussed below.
Stimulants are generally psychoactive drugs used medically to improve alertness, increase physical activity, and elevate blood pressure among other functions. This class of drugs acts by temporarily increasing mental activity resulting to increased awareness, changes in mood and apparently cause the user to have a relaxed feeling. Although their use is closely monitored, they still find their way on the streets and are usually abused.
Getting deeper into the biochemistry of different stimulants, each has a different metabolism in the body affecting different body organs in a specific way. One common thing about stimulants is that they affect the central nervous system in their mechanism. Examples of commonly used stimulants include; cocaine, caffeine, nicotine, amphetamines and cannabis. Cocaine, which has a tremendously high addictive potential, was in the past used as anesthetic and in treatment of depression before its profound effects were later discovered.
On the streets, cocaine is either injected intravenously or smoked. Within a few minutes of use, it stimulates the brain making the user feel euphoric, energetic and increases alertness. It has long-term effects such as seizures, heart attacks and stroke. Cocaine’s withdrawal symptoms range from anxiety, irritability to a strong craving for more cocaine.
Cannabis, also known as marijuana , is the most often abused drug familiar in almost every corner of the world, from the streets of New York to the most remote village in Africa. Although its addiction potential is lower as compared to that of cocaine, prolonged use of cannabis results to an immense craving for more.
It produces hallucinogenic effects, lack of body coordination, and causes a feeling of ecstasy. Long-term use is closely associated with schizophrenia, and other psychological conditions. From a medical perspective, cannabis is used as an analgesic, to stimulate hunger in patients, nausea ameliorator, and intraocular eye pressure reducer. Insomnia, lack of appetite, migraines, restlessness and irritability characterize withdrawal symptoms of cannabis.
Unlike stimulants, depressants reduce anxiety and the central nervous system activity. The most common depressants include barbiturates, benzodiazepines and ethyl alcohol. They are of great therapeutically value especially as tranquilizers or sedatives in reducing anxiety.
Depressants can be highly addictive since they seem to ease tension and bring relaxation. After using depressants for a long time, the body develops tolerance to the drugs. Moreover, body tolerance after continual use requires one use a higher dose to get the same effect. Clumsiness, confusion and a strong craving for the drug accompany gradual withdrawal. Sudden withdrawal causes respiratory complications and can even be fatal.
Narcotics have been used for ages for various ailments and as a pain reliever pain. They are also characterized by their ability to induce sleep and euphoria. Opium, for instance was used in ancient China as a pain reliever and treatment of dysentery and insomnia. Some narcotics such as morphine and codeine are derived from natural sources.
Others are structural analogs to morphine and these include heroin, oxymorphone among others. Narcotics are highly addictive resulting to their strict regulation by a majority of governments. Narcotics act as painkillers once they enter the body.
They are used legally in combination with other drugs as analgesics and antitussives but are abused due to their ability to induce a feeling of well being. Their addiction potential is exceptionally high due to the body’s tolerance after consistent use, forcing the user to use and crave for more to get satisfaction. Increase in respiration rate, diarrhea, anxiety, nausea and lack of appetite are symptoms common to narcotic withdrawal. Others include; running nose, stomach cramps, muscle pains and a strong craving for the drugs.
Hallucinogens affect a person’s thinking capacity causing illusions and behavioral changes especially in moods. They apparently cause someone to hear sounds and see images that do not exist. Lysergic acid diethylamide (LSD), which commonly abused hallucinogen, has a low addiction potential because it does not have withdrawal effects. They also affect a person’s sexual behavior and other body functions such as body temperature. There are no outright withdrawal symptoms for hallucinogens.
Isralowitz, R. (2004). Drug use: a reference handbook . Santa Barbara, Clif.: ABC-CLIO. Print.
National Institute on Drug Abuse. (2010). NIDA INfoFacts: Understanding Drug Abuse and Addiction . Web.
Peele, S. (1998). The meaning of Addiction : Compulsive Experience and its Interpretation . San Francisco: Jossey-Bass.
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Cholesterol gallstones and long-term use of statins: is gut microbiota dysbiosis bridging over uncertainties.
Graphical Abstract
2. materials and methods, 2.1. research participant approach, 2.2. gsd diagnostic methodology, 2.3. gs classification and analysis, 2.4. dyslipidemia diagnostic methodology, 2.5. diabetes mellitus diagnostic methodology, 2.6. microbiological and sequencing assessment of stools, 4. discussion, limitations, 5. conclusions, supplementary materials, author contributions, institutional review board statement, informed consent statement, data availability statement, conflicts of interest.
Demographic Data | Statin (+) | Statins (−) | CON | p | p | p |
---|---|---|---|---|---|---|
Age | 60.92 ± 14.85 | 58.36 ± 11.76 | 57.77 ± 10.52 | 0.1781 | 0.0850 | 0.7089 |
Gender F/M | 52/48 | 51/49 | 54/46 | 0.8878 | 0.7774 | 0.6718 |
Urban residency | 70% | 62% | 71% | 0.2336 | 0.8771 | 0.1786 |
Working/retired | 45%55/% | 51%/49% | 52/48% | 0.3969 | 0.3232 | 0.8878 |
Biological Workups | Statin (+) | Statins (−) | p | p | p | |
---|---|---|---|---|---|---|
Hemoglobin (g/dL) | 13.306 ± 1.395 | 13.279 ± 0.745 | 13.433 ± 1.451 | 0.1538 | 0.6128 | 0.2081 |
Leukocytes/mm | 8.775 × 10 ± 3.017 × 10 | 8.750 × 10 ± 2.985 × 10 | 7.983 × 10 ± 2.627 × 10 | 0.7275 | 0.0712 | 0.0660 |
Platelets/mm | 264.71 × 10 ± 48.37 × 10 | 256.06 × 10 ± 69.79 × 10 | 257.35 × 10 ± 32.72 × 10 | 0.3096 | 0.2090 | 0.8660 |
CRP (U/L) | 0.86 ± 0.57 | 0.94 ± 0.30 | 0.65 ± 0.43 | 0.2157 | 0.0037 | <0.0001 |
ALT (IU/L) | 21.92 ± 5.14 | 22.43 ± 4.09 | 21.62 ± 4.17 | 0.4384 | 0.6509 | 0.1617 |
Conjugated Bilirubin (mg/dL) | 0.36 ± 0.26 | 0.39 ± 0.25 | 0.37 ± 0.12 | 0.4066 | 0.7273 | 0.4716 |
Amylase (U/L) | 20.43 ± 5.96 | 20.03 ± 5.26 | 19.56 ± 3.46 | 0.6154 | 0.2083 | 0.4562 |
FPG (mg/dL) | 102.36 ± 9.57 | 99.03 ± 7.45 | 92.36 ± 4.57 | 0.0066 * | <0.0001 * | <0.0001 * |
Creatinine (mg/dL) | 0.706 ± 0.254 | 0.703 ± 0.145 | 0.69 ± 0.211 | 0.0449 | 0.7597 | 0.6924 |
LDL cholesterol | 100.22 ± 2.81 | 172.81 ± 12.64 | 95.54 ± 2.81 | <0.0001 * | <0.0001 * | <0.0001 * |
Triglycerides | 109.76 ± 2.31 | 114.96 ± 3.01 | 101.42 ± 2.11 | <0.0001 * | <0.0001 * | <0.0001 * |
Gut dysbiosis | 35% | 54% | 3% | 0.0070 * | <0.0001 * | <0.0001 * |
Clinical Spectra | Statin (+) | Statins (−) | p |
---|---|---|---|
Admission by ER | 41% | 45% | 0.5688 |
Smoking history | 48% | 45% | 0.6714 |
Alcohol consumption history | 39% | 28% | 0.1002 |
Dyslipidemia duration (years) | 14.25 ± 1.3 | 13.25 ± 1.2 | <0.0001 * |
Family history of GSD | 23% | 35% | 0.0621 |
Female postmenopausal estrogen replacement therapy | 17% | 11% | 0.2226 |
DM/IGT | 35% | 29% | 0.3643 |
Metformin treatment | 9% | 4% | 0.1526 |
Obesity | 45% | 38% | 0.3163 |
Hypertension | 22% | 17% | 0.3734 |
Other CV conditions | 30% | 21% | 0.1453 |
IBS | 2% | 4% | 0.4083 |
NAFLD | 42% | 36% | 0.3856 |
GSD | 5% | 14% | 0.0304 * |
Cholecystectomy | 1% | 3% | 0.3136 |
Good in-hospital outcome | 85% | 80% | 0.3533 |
Alterations to Microbiota in Dysbiotic Patients | Statin (+) | Statin (−) | p |
---|---|---|---|
Dysbiosis severity | 1.42 ± 0.60 | 2.05 ± 0.65 | <0.0001 * |
Biodiversity Shannon–Wiener H index | 2.68 ± 0.51 | 2.21 ± 0.23 | <0.0001 * |
Enterotype 1 | 14/35 (40%) | 36/54 (66.66%) | 0.013 * |
Enterotype 2 | 13/35 (37.14%) | 12/54 (22.22%) | 0.1282 |
Enterotype 3 | 7/35 (20%) | 4/54 (7.4%) | 0.0793 |
Enterotype unclassified | 1/35 (2.85%) | 2/54 (3.7%) | 0.8290 |
Increased LPS (+) bacteria | 21/35 (60%) | 48/54 (88.88%) | 0.0148 * |
Decreased mucin-degrading microbiota | 22/35 (62.85%) | 45/54 (83.33%) | 0.0296 * |
Decreased mucosa-protective microbiota | 23/35 (65.71%) | 47/54 (87.03%) | 0.0171 * |
Decreased butyrate-producing microbiota | 24/35 (68.57%) | 47/54 (87.03%) | 0.0352 * |
Age | 59.40 ± 2.30 | 59.43 ± 1.74 | 0.9772 | |
Females | 4 | 9 | 0.5275 | |
Males | 1 | 5 | 0.5278 | |
Symptoms and signs | asymptomatic | 3 | 5 | 0.3580 |
dyspepsia | 1 | 5 | 0.5278 | |
jaundice | 0 | 1 | 0.5508 | |
Murphy’s sign | 1 | 3 | 0.9481 | |
US GS features | <1 cm | 3 | 2 | 0.05 * |
1–3 cm | 1 | 11 | 0.0233 * | |
>3 cm | 0 | 1 | 0.5508 | |
multiple | 4 | 11 | 0.9478 | |
solitary | 1 | 3 | 0.9481 | |
Cholecystectomy | 1 | 2 | 0.7694 | |
GS composition | cholesterol-rich | 2 | 5 | 0.1224 |
Code | ν | ν * | ν | ν | ν | ν * | ν | ν * |
Cholesterol, CH | 3429.1 (±0.9) | - | 2931.1 (±0.6) | 2900.7 (±0.1) | 2866.8 (±0.2) | - | 1671.1 (±0.3) | - |
Gallstone GS1 | 3435.9 (±3.5) | 3272.9 (±0.2) | 2933.4 (±0.2) | 2897 (±0.2) | 2864 (±0.2) | 1699.2 (±0.7) | - | 1651.5 (±0.3) |
Gallstone GS2 | 3430.1 (±0.6) | 3276 (±1.5) | 2933 (±0.3) | 2898.2 (±1.3) | 2865 (±0.3) | 1699.7 (±0.8) | 1662.3 (±0.8) | 1649.3 (±3.5) |
Gallstone GS3a | 3395.4 (±1.3) | - | 2931.8 (±0) | 2899.7 (±0.2) | 2866.3 (±0.1) | 1699.7 (±1.7) | 1667.1 (±0.6) | 1649.5 (±2.2) |
Gallstone GS3b | 3396.1 (±0.9) | - | 2931.1 (±0.3) | 2900.7 (±0.1) | 2866.6 (±0.2) | 1699.8 (±0.3) | 1667.8 (±0.8) | - |
Code | ν * | ν | δ1 | δ2 | δ | δ | δ1 * | δ |
Cholesterol, CH | - | 1463.7 (±0.1) | 1437.8 (±1.8) | 1372.8 (±3.4) | 1334.1 (±0.8) | 1315.5 (±1) | - | 1273.5 (±0.6) |
Gallstone GS1 | 1572.4 (±0) | 1461.4 (±0.2) | 1444.1 (±0.2) | 1368.4 (±0.1) | 1330.1 (±0.1) | - | 1281.4 (±0.2) | - |
Gallstone GS2 | 1572.5 (±0.7) | 1462.4 (±0.3) | 1442.7 (±1.6) | 1368.5 (±1.8) | 1332.3 (±0.7) | - | 1280.9 (±2) | - |
Gallstone GS3a | 1574.1 (±0.2) | 1463.4 (±0.1) | 1440.1 (±0.2) | 1371 (±0.3) | 1335.1 (±0.4) | - | - | 1274.1 (±0.7) |
Gallstone GS3b | 1571.1 (±0.3) | 1463.8 (±0.2) | 1438 (±0.9) | 1375.6 (±3.5) | 1334.9 (±1) | - | - | 1272.3 (±0.5) |
Code | δ * | δ | ν | δ | δ | δ | δ | δ |
Cholesterol, CH | - | 1236.2 (±0.7) | 1191 (±0.2) | 1168.1 (±1.4) | 1131.8 (±0.9) | 1107.3 (±0.1) | 1054.2 (±0.1) | 1022.7 (±0.1) |
Gallstone GS1 | 1250.1 (±0.1) | 1235.1 (±0.2) | 1196.6 (±0.1) | 1169.6 (±0.2) | 1135.8 (±0.1) | 1109.4 (±0.1) | 1048 (±0.1) | 1020.2 (±0.1) |
Gallstone GS2 | 1250.7 (±0.8) | 1235.8 (±0.9) | 1195.5 (±0.2) | 1169.3 (±0.8) | 1135.1 (±0) | 1109.1 (±0.3) | 1050 (±0.7) | 1021.5 (±0.8) |
Gallstone GS3a | 1250.4 (±1) | 1236.8 (±0.2) | 1192.3 (±0.2) | 1167.1 (±0.7) | 1133.3 (±0.1) | 1107.7 (±0.1) | 1053.2 (±0) | 1022.2 (±0) |
Gallstone GS3b | 1252.5 (±0.6) | 1236.7 (±0.4) | 1191.1 (±0.2) | 1169.2 (±1.4) | 1130.5 (±0.4) | 1107.2 (±0.1) | 1054.5 (±0.2) | 1022.7 (±0.2) |
Code | δ | δ | δ | δ | ν | δ | δ | δ |
Cholesterol, CH | 985.9 (±0) | 955 (±1.3) | 927.5 (±1) | 883.4 (±0.6) | 839.4 (±0.6) | 800.1 (±0.5) | 739 (±1.5) | 699.5 (±0.5) |
Gallstone GS1 | 983.7 (±0) | 954.4 (±0.1) | 929.6 (±0.1) | 883.4 (±0) | 839.6 (±0.1) | 798.6 (±0.1) | 736.3 (±0.1) | 700 (±0.8) |
Gallstone GS2 | 984.9 (±0.6) | 954.6 (±0.4) | 928.8 (±2.2) | 883.4 (±0.1) | 839.3 (±0.1) | 798.6 (±0.9) | 737.1 (±0.6) | 699.9 (±0.3) |
Gallstone GS3a | 985.5 (±0.1) | 955.5 (±0.1) | 929.7 (±0.4) | 882 (±0.3) | 839.2 (±0.2) | 800.1 (±0) | 737.6 (±0.1) | 698.5 (±0.5) |
Gallstone GS3b | 986.3 (±0.4) | 955.7 (±0.2) | 927.6 (±1.4) | 883.1 (±0.3) | 839.7 (±0.5) | 800.1 (±0.3) | 738.6 (±0.8) | 699.6 (±0) |
Table Analyzed | GSD_ Multiple Linear Regression | |||||||
---|---|---|---|---|---|---|---|---|
Dependent variable | GSD | |||||||
Regression type | Least-squares | |||||||
Model | ||||||||
Analysis of Variance | SS | DF | MS | F (DFn DFd) | p value | |||
Regression | 8.428 | 7 | 1.204 | F (7 92) = 15.91 | p < 0.0001 | |||
DZ/IGT | 0.2563 | 1 | 0.2563 | F (1 92) = 3.386 | p = 0.0690 | |||
Obesity | 0.3728 | 1 | 0.3728 | F (1 92) = 4.926 | p = 0.0289 | |||
Alcohol | 0.2106 | 1 | 0.2106 | F (1 92) = 2.783 | p = 0.0986 | |||
Smoking | 0.257 | 1 | 0.257 | F (1 92) = 3.397 | p = 0.0685 | |||
Hypertension | 0.2352 | 1 | 0.2352 | F (1 92) = 3.109 | p = 0.0812 | |||
NAFLD | 0.1022 | 1 | 0.1022 | F (1 92) = 1.351 | p = 0.2482 | |||
DB | 3.707 | 1 | 3.707 | F (1 92) = 48.98 | p < 0.0001 | |||
Residual | 6.962 | 92 | 0.07567 | |||||
Total | 15.39 | 99 | ||||||
Parameter estimates | Variable | Estimate | Standard error | 95% CI (asymptotic) | |t| | p value | p value summary | |
β0 | Intercept | 0.02957 | 0.05979 | −0.08918 to 0.1483 | 0.4945 | 0.6221 | ns | |
β1 | DZ/IGT | 0.1198 | 0.06513 | −0.009499 to 0.2492 | 1.84 | 0.069 | ns | |
β2 | Obesity | 0.1361 | 0.0613 | 0.01431 to 0.2578 | 2.22 | 0.0289 | * | |
β3 | Alcohol | −0.1041 | 0.0624 | −0.2280 to 0.01983 | 1.668 | 0.0986 | ns | |
β4 | Smoking | −0.1066 | 0.05785 | −0.2215 to 0.008275 | 1.843 | 0.0685 | ns | |
β5 | Hypertension | −0.1124 | 0.06375 | −0.2390 to 0.01421 | 1.763 | 0.0812 | ns | |
β6 | NAFLD | 0.07831 | 0.06738 | −0.05551 to 0.2121 | 1.162 | 0.2482 | ns | |
β7 | DB | 0.4417 | 0.0631 | 0.3163 to 0.5670 | 6.999 | <0.0001 | **** |
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Georgescu, D.; Lighezan, D.-F.; Ionita, I.; Hadaruga, N.; Buzas, R.; Rosca, C.-I.; Ionita, M.; Suceava, I.; Mitu, D.-A.; Ancusa, O.-E. Cholesterol Gallstones and Long-Term Use of Statins: Is Gut Microbiota Dysbiosis Bridging over Uncertainties? Diagnostics 2024 , 14 , 1234. https://doi.org/10.3390/diagnostics14121234
Georgescu D, Lighezan D-F, Ionita I, Hadaruga N, Buzas R, Rosca C-I, Ionita M, Suceava I, Mitu D-A, Ancusa O-E. Cholesterol Gallstones and Long-Term Use of Statins: Is Gut Microbiota Dysbiosis Bridging over Uncertainties? Diagnostics . 2024; 14(12):1234. https://doi.org/10.3390/diagnostics14121234
Georgescu, Doina, Daniel-Florin Lighezan, Ioana Ionita, Nicoleta Hadaruga, Roxana Buzas, Ciprian-Ilie Rosca, Mihai Ionita, Ioana Suceava, Diana-Alexandra Mitu, and Oana-Elena Ancusa. 2024. "Cholesterol Gallstones and Long-Term Use of Statins: Is Gut Microbiota Dysbiosis Bridging over Uncertainties?" Diagnostics 14, no. 12: 1234. https://doi.org/10.3390/diagnostics14121234
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The Healthcare Professional's
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Helping your patients with alcohol-related problems, what to know, ask, and offer.
Alcohol contributes to more than 200 health conditions and about 178,000 deaths in the U.S. each year. Yet alcohol-related risks often go unaddressed in healthcare settings. The Core Resource on Alcohol provides evidence-based content to help healthcare professionals:
"This resource is a good way to increase your confidence when you see patients with alcohol-related concerns , which you're going to see often." — Primary care practitioner
Learn how to apply the Core Resource in clinical practice.
View the 14 Core articles below in any order and earn CME/CE credit for as many or as few as you wish. Each article provides instructions at the end for earning credit, which is available for physicians, physician assistants, nurses, pharmacists, and psychologists, as well as other healthcare professionals whose licensing boards accept APA or AMA credits. Others may earn a certificate of completion. The CME/CE system will keep a history of the articles you have completed for credit.
See also the Additional Links for Patient Care for many helpful alcohol-related healthcare resources for different types of providers. Learn more about the Core Resource on Alcohol.
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Our analysis of the data.
F EW RICH countries have taken to legal weed quite like America. Although federal regulation remains tight, the drug is legal for recreational use in 24 states and for medical use in 38. One in six American adults now uses marijuana at least monthly, according to the National Survey on Drug Use and Health ( NSDUH ); nearly one in 20—about 11m people—gets high every day. A recent paper by Jonathan Caulkins of Carnegie Mellon University estimates that the number of “daily or near-daily” marijuana users—defined as those who report getting high on at least 21 of the past 30 days—surpassed the number of daily alcohol users in 2022.
That finding grabbed headlines. It does not mean that weed is a bigger health risk than alcohol, but it does have some worrying implications.
The first point to note is that a lot more Americans drink alcohol than get high from cannabis; drinking is a lot more dangerous. Around two-thirds of American adults have had a drink in the past year, compared with a fifth who have had a toke. More than half imbibe at least once a month. The Centres for Disease Control and Prevention reckons that the number of deaths in America that can be attributed to alcohol, either in full or in part, is now nearly 180,000 per year. The mortality risk from marijuana is virtually nil. The main danger comes from driving under the influence.
But weed users tend to indulge their habit more often. One in five marijuana users gets high every day (before legalisation by some states the figure was around one in ten). By our calculations, disregarding “near-daily users” the number of daily tokers surpassed the number of daily drinkers in 2018. Their habit may not be harmless.
Studies have shown that people who use cannabis regularly may develop schizophrenia and other psychotic disorders earlier than they might otherwise have done. Heavy users may also have an increased risk of cardiovascular diseases, including heart attacks and strokes. In an article for the Washington Monthly Mr Caulkins explained that heavy use may also harm short-term memory, concentration and motivation, resulting in “lost opportunities in schools and the workplace”. Our analysis appears to back this up. Data from the NSDUH survey show that in 2022 just 42% of daily or near-daily marijuana users said they had “very good” or “excellent” health, compared with 53% of monthly users and 56% of yearly ones (see chart 2). Those differences remain even after controlling for demographic characteristics such as age, race and education, and excluding people who use marijuana for medical purposes. Daily pot users also tend to report worse mental health, with a larger share saying that they suffered an episode of depression in the past year.
On measures of employment the findings are less stark. Serious stoners fare only slightly worse in the workplace than more casual pot users. Working-age adults who use marijuana every day or nearly every day are only slightly less likely to be employed than are monthly users. They work roughly the same number of hours, too. But the data also show that heavy marijuana users tend to skip work more often than do casual users and non-users. They also earn less (see chart 3).
Correlation is not causation. It may be that people with lower incomes and poorer health are more inclined to become heavy pot users; or that some third factor causes all three outcomes. Whatever the explanation, the number of daily smokers could rise as legalisation becomes more common. As many as five states could legalise recreational use of the drug in 2024. Voters in Florida and South Dakota are already set to vote on the issue in November. ■
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The president’s son, who was convicted of three felonies, could face a stiffer sentence if he is convicted in a separate tax case scheduled for September.
By Eileen Sullivan
Hunter Biden, the president’s son, was found guilty on three felony counts related to buying a gun while he was in the throes of drug addiction. On Oct. 12, 2018, he filled out the required federal background check form, marking “no” to a question about his drug use.
His lawyers argued that the special counsel who brought the case, David C. Weiss, had no evidence that Mr. Biden used drugs the day of his purchase or in the surrounding period.
Before deciding to convict him on all three charges, the jury heard about Mr. Biden’s spiraling addiction to crack cocaine from women in his life, as well as in Mr. Biden’s own words, which the prosecution shared by using excerpts from the audiobook of his memoir.
Here are some takeaways.
The verdict in Mr. Biden’s trial came just weeks after former President Donald J. Trump was convicted in a Manhattan courtroom of falsifying business records to cover up a hush-money payment to a porn star. Both trials were surrounded by partisan dynamics and questions about the criminal justice system’s ability to operate without regard to politics.
Mr. Biden’s trial was held in the Biden family’s hometown, in the middle of a presidential campaign and amid intense pressure from Republicans to find criminality by Hunter Biden. The fact that juries have now convicted both the presumptive Republican presidential nominee and the son of his opponent, the sitting president, will not end debate about politics and the courts. But it might keep the issue from becoming further inflamed.
In his 2021 memoir, Hunter Biden laid bare his unrelenting abuse of crack cocaine. Witness testimony and text messages added to the damaging portrait of the president’s son, a stark reminder of his yearslong troubles at a time when his father is in a close re-election race.
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