A Complex Interplay between Nutrition and Alcohol use Disorder: Implications for Breaking the Vicious Cycle

Abstract

Approximately 16.5% of the United States population met the diagnostic criteria for substance use disorder (SUD) in 2021, including 29.5 million individuals with alcohol use disorder (AUD). Individuals with AUD are at increased risk for malnutrition, and impairments in nutritional status in chronic alcohol users can be detrimental to physical and emotional well-being. Furthermore, these nutritional deficiencies could contribute to the never-ending cycle of alcoholism and related pathologies, thereby jeopardizing the prospects of recovery and treatment outcomes. Improving nutritional status in AUD patients may not only compensate for general malnutrition but could also reduce adverse symptoms during recovery, thereby promoting abstinence and successful treatment of AUD. In this review, we briefly summarize alterations in the nutritional status of people with addictive disorders, in addition to the underlying neurobiological mechanisms and clinical implications regarding the role of nutritional intervention in recovery from alcohol use disorder.

1. INTRODUCTION

Approximately 6% of the global population (age 15–64; 1 in every 17 people) was documented to be high in the past month [1]. In the United States alone, 57.8% of people age 12 and older (161.8 million people) were current users of illicit drugs, alcohol, or tobacco. including 133.1 million (47.5%) people who drank alcohol. Among these individuals, 29.5 million (8.6%) people met the diagnostic criteria for alcohol use disorder (AUD) [2]. Beyond addiction or substance use as a disease per se. drug overdose claimed 106,699 lives in the United States in 2021 [3]. While synthetic opioids and psychostimulants were responsible for many of the cases relevant to the illicit or prescription drugs category, alcohol-related deaths remain the fourth-leading preventable cause of death in the US. behind only tobacco use, poor diet, and physical inactivity [4]. In addition to the detrimental effect on health and well-being, a substantial economic and societal impact (e.g., healthcare expenses, property damage, motor vehicle accidents) is often associated with these addictive disorders, with AUD alone costing $249 billion [5].

Significant strides have been made in investigating the underlying neurobiological mechanisms of addictive disorders, which has paved the way for pharmacotherapeutics development [6–9]. However, a considerably higher relapse rate (40–60%) within the first year of abstinence remains a significant obstacle [10], demanding better therapeutics and effective strategies for the successful treatment of SUD [11]. In this regard, compromised nutritional status and disrupted dietary habits have been documented in patients with substance use disorder [12–15]. As a result, malnutrition is frequently reported in this population, which could substantially contribute to this relapsing disorder and related pathology [16, 17]. Evidence exists that addressing nutrition-related issues could help in recovery from addictive disorders [18, 19], yet other than injecting B Vitamins for Wernicke’s encephalopathy [20], proper nutrition and diet are often overlooked as important treatment components of AUD.

It is also apparent that feeding peptides (e.g., ghrelin. glucagon-like peptide-1) that control metabolic status can regulate brain reward circuitry and alter alcohol intake and alcohol-reinforced behaviors [21, 22]. Therefore, their dysregulation due to compromised nutritional status may contribute to escalated alcohol intake and various behavioral impairments observed in AUD patients. Interestingly, these patients display increased intake of highly palatable foods during recovery [23, 24]. Alcoholics Anonymous also recommends eating sweet-tasting food to reduce cravings [25]. It remains to be identified if increased palatable food consumption, in this case, is an effort to restore caloric deficits, alleviate the negative consequences of alcohol withdrawal, or both. However, none of the FDA-approved drugs for AUD target metabolic and nutritional impairments frequently present in patients with AUD. which could contribute to the chronic relapsing disorder [26]. Here, we review alterations in the nutritional status, potential neurobiological mechanisms, clinical implications, and recent studies assessing the role of nutrition, particularly in alcohol use disorder.

2. MALNUTRITION AND ALCOHOL USE DISORDER

Addiction is a chronic debilitating disease that is associated with a multitude of negative health effects, including impaired physiological, emotional, and nutritional status. SUD negatively impacts dietary intake, and people who misuse illicit substances have reported eating less frequently than healthy controls while favoring meals with lower nutritional value [15, 27–34]. In addition to directly impacting nutritional status, the socioeconomic impact of SUD could indirectly add to this complexity. For example, substance abuse negatively affects employment status and may result in periods of food insecurity or increased interpersonal stress [35], resulting in reduced food consumption altogether. These poor dietary choices, in combination with the reduction in nutritional intake, contribute to overall malnutrition (i.e., altered nutrient intake and/or body composition), reduced body weight, and body mass index (BMI), which are frequently observed in this population [27, 36–39]. While the appetite suppressant effects of substance use (e.g., cocaine) have been historically recognized as a contributing factor to this change in body composition [40], similar alterations have been documented in individuals who reported significantly higher nutritional intake compared to non-drug users [30]. It is also important to note that a relatively recent study reported no link between BMI and nutritional risk in opioid-dependent patients at a methadone-assisted treatment program [41], suggesting the incorporation of several other screening tools to assess nutrition status in these populations. In this regard, poor dietary choices and resultant reduced macro- and micro-nutrient intake are also reflected in the plasma nutrient profile, which could signify SUD-induced nutritional deficiencies. For example, significant abnormalities in the plasma concentration of macro-(e.g., hemoglobin, total protein, albumin) and micro-(e.g., Cu, Zn, K, Se, Na, Mg, P, Iron, and Vitamin A, C) nutrients have been registered in patients with SUD [28, 29, 32, 42, 43] and were comprehensively reviewed recently [27, 44].

Impaired nutritional status in people with AUD is unique from other SUDs due to the caloric content of alcohol. Alcohol, unlike other substances of abuse, contains calories, and nutritional impairments in AUD could be a result of direct/primary or indirect/secondary factors (Fig. 1. also reviewed in detail elsewhere) [32]. Direct malnutrition refers to the reduced nutritional intake observed in this population as a result of alcohol being substituted for proper nutritional intake [28, 45–47]. In moderate alcohol abuse, reductions in dietary carbohydrate intake to compensate for the increase in caloric intake from alcohol have been reported. As alcohol intake increases, dietary intake from carbohydrates, protein, and fat decreases further, which could directly contribute to deficiencies in essential nutrients [15, 48, 49]. On the other hand, indirect malnutrition is characterized by impairments in nutrient absorption and metabolism resulting from excessive alcohol consumption [50–54]. Therefore, impaired absorption/metabolism of macro and micro-nutrients adds to the nutritional deficiencies resulting from reductions in total caloric intake. Even in AUD patients with proper dietary habits, impairments in absorption/metabolism could create additional barriers to overall health [55–60].

Fig. (1).

Nutritional impact of alcohol use disorder.

In addition to the direct and indirect effects on ingested nutrients per se, alcohol can also impact the synthesis and secretion of some circulating proteins in the liver [61–66], which can contribute to AUD and related pathologies. For example, alcohol has been shown to reduce the synthesis/secretion of albumin [65–68], a highly abundant protein found in human plasma with varied physiological functions [69]. As a result, serum albumin levels are significantly lower in patients with AUD [64, 70–72], an effect documented in both males and females [62, 63]. Resultant hypoalbuminemia has important implications in several human pathological conditions, as lower serum albumin levels are associated with increased systemic inflammation, coronary artery disease, stroke, heart failure, thromboembolism, morbidity, and mortality [73–80]. Notably, several studies have reported low serum albumin levels as an independent predictor of myocardial infarction [81–83] and related cardiovascular complications [84–87]. Furthermore, serum albumin is an important component of the Naples Score (NS), which assesses the nutritional and inflammatory status for evaluating the prognostic outcomes of patients [88]. Studies have shown that Naples Score is independently associated with rehospitalization as well as long-term mortality in heart failure, peripheral artery disease, myocardial infarction, and cancer patients [88–93].

A significant body of evidence exists regarding sex differences in alcoholism [94]. Particularly, data exist documenting sex- and age-related differences in alcohol consumption, metabolism, and prevalence of AUD, as well as sex-specific neurobehavioral, neurobiological, and neuroanatomical alterations in AUD [94–106]. While men have been documented to drink more alcohol compared to women [94, 102], this gap may be narrowing, especially in the younger population [107]. Based on a recent national survey, the prevalence of past-month binge drinking was documented in 24.3% of males and 19.2% of females aged 12 or older [108]. Whereas underage (ages 12 to 20) past month binge drinking was slightly higher in females (8.9%) compared to males (7.5%) [109]. While the prevalence of alcohol use disorder was higher in males (12.6%; ages 12 and older) compared to females (8.5% ages 12 and older) [110], negative health consequences (e.g., alcoholic liver disease, breast cancer, cardiovascular, and psychiatric complications) of alcohol are significantly higher in females [94, 107, 111–117]. Recent studies further confirmed that women are more sensitive to alcohol-related liver disease and suffer dire health consequences than men [113, 118]. Interestingly, this higher susceptibility to alcohol-related liver disease in females is not due to any macro- and micro-nutrient intake differences when compared to men [119], ruling out any sex-specific nutrition differences contributing to the pathology of AUD.

Nevertheless, hazardous alcohol drinking levels are often associated with reduced fat mass, body weight, and BMI [120–123], and clinical observations (e.g.. BMI) could be a better indicator of malnutrition in individuals who are at risk for AUD-related pathology [124]. The nutritional deficiencies observed in individuals with AUD contribute not only to physiological impairments such as alcohol-related liver disease [16, 125] but also to the core symptoms of alcoholism, such as cognitive dysfunction [15, 126–129] and increased negative affect [130–132], thereby contributing to the vicious cycle of alcoholism and comorbidity.

3. ALCOHOL USE DISORDER: ALTERED NUTRITION AND NEUROBIOLOGICAL SUBSTRATES

AUD frequently co-occurs with feeding and eating disorders [133, 134], and a significant proportion of the college-aged population has been reported to engage in episodes of binge drinking and binge eating, an experience that puts them at greater risk for developing alcohol/drug abuse and numerous health concerns [135–137]. Interestingly, converging research evidence suggests some common neurobiological, behavioral, and physiological determinants of maladaptive eating and alcohol drinking [138–141]. For example, gut-brain peptides (e.g., ghrelin. glucagon-like peptide-1, etc.; nicely reviewed elsewhere) [139, 142] have increasingly gained attention as an important player in regulating alcohol intake and alcohol-seeking behavior [21, 143–146].

Glucagon-like peptide-1 (GLP-1), a gut-brain peptide produced in the intestine and hindbrain (nucleus tractus solitarius), is secreted in response to meal ingestion [147, 148]. By targeting its receptor (GLP-1R), it facilitates insulin secretion and normalizes plasma glucose, which forms the basis for the approval of GLP-1R agonists for the treatment of diabetes [149]. Besides as a key player in energy regulation, several preclinical studies have shown that GLP-1R agonists (e.g., Ex-4, liraglutide) reduce alcohol consumption and preference, motivation to consume alcohol and relapse-like alcohol drinking, effects potentially mediated via central GLP-1R [145, 150–157]. Consistent with the notion of gut-brain peptide interaction with the brain reward circuitry. GLP-1R agonists have been shown to block alcohol-mediated dopamine release in the nucleus accumbens [145, 151]. In addition, the beneficial effects of GLP-1R receptor stimulation in modulating alcohol withdrawal-induced anxiety-like behavior were also reported [158, 159]. In agreement with the preclinical data, reduced alcohol intake was observed in diabetic patients who were treated with liraglutide compared to patients treated with other non-GLP-1 drugs [160]. Similarly, another study documented a significant reduction in total alcohol intake and heavy drinking days in obese AUD patients, an effect absent in normal-weight individuals [161]. Furthermore, GLP-1R gene expression was found to be upregulated in the postmortem brain tissue (hippocampus and prefrontal cortex) of individuals with AUD compared to the healthy controls [162].

Ghrelin [acyl-ghrelin], often referred to as the hunger hormone, is another feeding peptide predominantly released in the stomach and is involved in appetite stimulation, feeding behavior, and several physiological processes via interaction with its receptor (GHSR) [163]. Both preclinical and clinical data support the role of the ghrelin system in AUD and related pathology [164, 165]. In this regard, numerous preclinical studies have documented reduced alcohol drinking behaviors (e.g., alcohol self-administration, relapse-like drinking) following GHSR antagonist administration [166–168]. Moreover, human genetics studies have revealed an association between polymorphism in the pre-pro-ghrelin gene and GHSR-la gene and problematic alcohol use [169–171]. Furthermore, alcohol consumption is reduced in GHSR knockout rodents compared to their wild-type controls [166, 172]. Similar to GLP-1, the effects of ghrelin on alcohol reward and alcohol intake are potentially mediated centrally [173], as alcohol-induced locomotor sensitization and dopamine release in the nucleus accumbens were abolished by genetic and pharmacological suppression of GHSR signaling [166, 174]. However, a positive association between plasma ghrelin and alcohol craving has also been documented [146, 175, 176]. In this regard, a human laboratory study reported reduced latency to initiation and increased alcohol self-administration following intravenous ghrelin administration in AUD patients [177], and GHSR inverse agonism reduced alcohol craving [178]. In short, while the role of central vs. peripheral ghrelin needs further exploration, the involvement of ghrelin receptor signaling in mediating alcohol reward has important clinical implications in the management of AUD.

Other feeding peptides implicated in the pathophysiology of addictive disorders are nicely reviewed elsewhere [139, 142]. Collectively, these preclinical and clinical studies highlight the involvement of gut-brain peptides in regulating alcohol reward and problematic alcohol drinking (refer to the studies [165, 179] for further detailed review). In addition, these peptides influence mood and emotional behaviors by interacting with brain corticostriatal-limbic circuitry [139, 180–182]. Furthermore, emotional dysregulation and drinking to cope, dictate the development and maintenance of AUD [183–185], and a positive association has been reported between anxiety-like behavior and ethanol consumption [186, 187]. Together, dysregulation in the gut-brain peptides due to excessive alcohol consumption and malnutrition could contribute to impaired physiological and emotional states observed in individuals with AUD.

4. ALTERED NUTRITION-RELATED BEHAVIOR IN ALCOHOL ABSTINENCE: CLINICAL IMPLICATIONS

While dietary changes and alterations in food preferences as a consequence of dysregulated drinking behavior are firmly established, very few studies have explored changes in nutrition-related behaviors during alcohol abstinence [23, 24, 188]. For example, a study exploring the role of dietary choices and the likelihood of abstinence among people with AUD reported a positive correlation between enhanced carbohydrate and sugar intake and staying sober longer [23]. Similarly, a significant increase in craving for and consumption of chocolate was observed in alcohol-dependent patients following alcohol detoxification. Importantly, these changes were not related to alcohol craving but had a temporary protective effect on alcohol relapse [24]. Whether this heightened preference for sweets/palatable foods is an attempt to restore caloric deficits, alleviate the negative consequences of alcohol withdrawal, or both is less clear.

Interestingly, a similar increase in sweet food consumption has been observed in patients recovering from other SUDs (e.g., opioids, nicotine) [32, 189–192]. Together, these data highlight that an increased preference for sweet food could serve as a substitute for drug use or regulate negative effects and cravings prevalent during early detoxification stages [188, 191]. This notion is also in alignment with the AUD recovery resource Alcoholics Anonymous, which recommends eating or drinking something sweet to allay the urge to drink [25],

This association between sweet/palatable food and relapse must be further explored clinically to address malnutrition and body weight-related issues, at least during early recovery from AUD. However, none of the FDA-approved drugs or clinical approaches targets compromised nutritional status in individuals with AUD, which may constitute a significant motivational factor that leads to relapse and poor treatment compliance. It is possible that improving nutritional status during abstinence would not only compensate for general malnutrition in AUD patients but also could serve to ameliorate some of the adverse symptoms observed during alcohol withdrawal, thereby enhancing prospects of recovery. Supporting this notion, a study evaluating the effects of nutrition therapy (modified menus and individualized nutrition counseling) reported a reduction in alcohol craving, significantly higher nutrient intakes, and greater abstinence in patients receiving nutritional therapy compared to the individuals who received only traditional therapy [19]. Therefore, nutrition education can positively influence recovery outcomes and should be a critical component of AUD/SUD treatment programs [18].

5. ADDRESSING NUTRITION IN AUD: TRANSLATIONAL ASPECTS

While substantial evidence supports the importance of addressing malnutrition in addictive disorders, the critical framework needed to evaluate its therapeutic potential remains to be identified. For example, what would be the most effective macro- or micro-nutrient composition of the recommended diets or food? How long should such a diet be administered/followed to promote long-term recovery? Considering the heterogeneity of AUD, could a generalized nutritional approach work for everyone? These critical parameters must be considered to address malnutrition in AUD and facilitate the recovery pathway.

In this regard, enhanced consumption of sugar/sweet food in individuals recovering from AUD and its potentially protective effect could shed some light [23, 24]. Eating sweets is also recommended by Alcoholics Anonymous to curb alcohol cravings [25]. In addition, preclinical studies have also shown reduced alcohol drinking following sucrose and saccharin consumption in both alcohol naive and alcohol-preferring P-rats [193, 194]. However, a recent human study that evaluated the effect of eating sweets on alcohol cravings did not support this popular belief [195]. Furthermore, studies have shown that consuming sweets in early recovery predicts increased alcohol cravings later [196].

Several clinical and preclinical studies have also evaluated the effect of a Ketogenic diet (KGD, a diet with a very high-fat proportion) on alcohol drinking [197–201]. In rodents, KGD (> 90.0% fat) was shown to reduce alcohol drinking and alcohol withdrawal symptoms [197–201]. A clinical study also reported reduced alcohol craving and withdrawal symptoms in individuals with AUD when given a KGD (80% fat) [197]. Notably, significantly increased body weight was observed in the animals receiving KGD compared to the standard diet group [199] This could be a concern as obesity and overweight are well-known risk factors for cardiovascular disease, mood disorders, impaired executive functioning, and higher all-cause mortality [202–205].

In this regard, preclinical studies from our lab have shown that intermittent access to a moderately high-fat diet (40% fat) significantly reduced alcohol drinking without impacting body weight [206–208]. Even acute intermittent access (twice a week for two weeks) of this nutritionally complete palatable diet (NPD) was effective enough to reduce alcohol drinking and attenuate relapse-like drinking behavior [207, 208]. Importantly, the NPD-induced effect on alcohol drinking was likely centrally mediated as selective changes in brain neurotransmitters gene expression and dopamine levels were observed in the brain reward circuitry of rats receiving NPD [208, 209]. We also found that similar acute intermittent access to a high-sugar diet and saccharin, a non-calorie sweetener, were equally effective in reducing alcohol drinking [207], suggesting palatability instead of a particular macronutrient responsible for these effects.

As mentioned above, people with AUD are also severely deficient in several micronutrients, which could adversely affect the disease state, recently reviewed elsewhere [210]. Therefore, any dietary approach addressing nutritional deficiency in AUD must include these essential micronutrients. For example, Vitamin Bl (thiamine) deficiency is known to cause Wernicke-Korsakoff syndrome, which could result in brain damage [211, 212] and could produce certain cardiovascular, psychiatric, and neurological complications [213, 214]. Furthermore, deficiency of certain micronutrients (e.g.. Zinc, Magnesium, Selenium, Folate, and Omega-3) has been documented to trigger negative emotional states (i.e., depression, anxiety, and suicidal ideations) [215–219] and could mediate alcohol toxic effects [220]. While the banana bag, standard care for hospitalized AUD patients, includes thiamine, multivitamins, and electrolytes, studies have challenged that improved formulation and additional supplementation are warranted [221, 222], which could help AUD-related pathology and facilitate recovery.

Ethanol-induced oxidative stress plays a critical role in AUD and related pathology. Certain micronutrients and antioxidant deficiencies commonly observed in AUD patients can further exacerbate this and could contribute to the development of alcohol dependence, alcoholic liver disease, and impaired emotional and cognitive controls [223–226]. Fruits, vegetables, and medicinal plants rich in antioxidants could have beneficial effects in this regard [227–233]. For example, Ginger (Zingiber officinale), traditionally used in cooking and herbal remedies, exhibits powerful antioxidant and hepatoprotective properties. Ginger has been shown to rescue alcohol-induced renal damage and impairments in antioxidant enzymes [234] and possesses hepatoprotective properties in models of alcoholic fatty liver disease [228], documenting its detoxifying and antioxidant potential. Carnitine is naturally produced in the body and has an important role in the metabolism and regulation of oxidative stress [235]. Carnitine supplementation was effective in reducing craving and relapse, improving negative emotional states and cognitive control in AUD [236–239]. Alcoholism can be conceptualized as a state of heightened brain stress systems and reduced reward functioning as a result of impaired central neurotransmissions (e.g., dopamine, opioids, serotonin, CRF) [240]. Studies examining the effects of certain amino acids (precursors for serotonin, dopamine, and glutamate neurotransmitter production) supplements found that using food supplements containing hydroxytryptophan, phenylalanine, and glutamine reduced alcohol withdrawal symptoms [241]. Emotional and cognitive improvements were also registered following tryptophan-rich food supplements [242, 243]. In addition, certain herbal supplements (e.g., Ashwagandha, Brahmi, St John’s Wort, Korean Red Ginseng) have also been shown to reduce ethanol withdrawal syndrome in rodents [244–246]. Therefore, in addition to macro and micro-nutrients, certain herbs and dietary supplementation summarized in Table 1 could provide positive effects outside of the implied benefits to overall emotional, physiological, and nutritional status in the AUD [233, 247–264] (Fig. 2).

Table 1.

Herbal and dietary supplements with beneficial effects in AUD.

Dietary Supplement	Effect on AUD	References
Polyunsaturated Fatty Acids
-	Reduced intake	[265]
	Reduced stress/anxiety	[266]
	Neuro-/Hepato-protective effects	[267, 268]
Amino Acids
-	Reduced withdrawal symptoms	[241]
	Improved emotional status	[242, 243]
	Improved cognitive functioning	[242]
	Hepatoprotective effects	[269]
Carnitine
-	Reduced cravings	[236]
	Improved emotional status	[237]
	Improved cognitive function	[238]
Vitamin Bl
-	Improved cognitive function	[126, 270]
Vitamin E
	Neuro-/Hepato-protective effects	[229, 269]
N-Acetylcysteine
-	Reduced craving	[271]
	Improved emotional status	[271]
	Improved cognitive function	[275]
	Reduced withdrawal symptoms	[276]
	Hepatoprotective effects	[272–274]
Korean Red Ginseng
-	Improved cognitive function	[246]
	Reduced withdrawal symptoms	[246]
	Reduced inflammation	[246]
	Reduced intake	[230]
	Hepatoprotective effects	[277]
	Gastric protection	[278]
Red Sage
-	Reduced intake	[230, 233, 279, 280, 282]
	Reduced withdrawal symptoms	[281]
	Hepatoprotective effects	[233]
Kudzu Root
-	Reduced intake	[230, 283–285]
	Decreased anxiety	[286]
	Hepatoprotective effects	[287]
St John’s wort
-	Reduced intake	[230,288–291]
	Reduced withdrawal symptoms	[245]
Brahmi
-	Reduced withdrawal symptoms	[244, 292]
Ashwagandha
-	Reduced withdrawal symptoms	[244, 292–294]
	Reduced intake	[294]
Ginger
-	Hepatoprotective effects	[228, 233, 234]

Fig. (2).

A complex interplay between nutrition and alcohol use disorder: Implications for breaking the vicious cycle. Excessive alcohol intake can result in impaired nutrient absorption and metabolism, in addition to reduced nutritional intake. This may then lead to general malnutrition and vital organ damage. These impairments contribute to dysregulation in the neuroendocrine system as well as in homeostasis regulation, triggering symptoms characteristic of AUD, such as negative emotional status, alcohol cravings, and dysregulated alcohol drinking. Improved nutritional interventions targeting both macro and micro-nutrients could treat general malnutrition and impaired emotional and cognitive controls observed in AUD, thereby increasing the recovery prospects. Specific dietary and herbal supplementations could help, along with nutritional education and patient counseling, to break the vicious cycle of alcoholism.

CONCLUSION

A great deal of effort has gone into documenting malnutrition in addictive disorders. Reduced intake, impaired absorption, and metabolism of nutrients in alcoholism could dysregulate gut-brain feeding peptides and thereby energy homeostatic and hedonic systems, which could contribute to AUD and related pathology. While general nutrition support exists for hospitalized AUD patients, concerns have been raised about its adequacy. Furthermore, altered nutrition-related behavior in detoxifying patients warrants further investigation for its potential beneficial effects in recovery. In addition. improved nutritional interventions targeting both macro and micro-nutrients are needed to address general malnutrition and impaired emotional and cognitive controls observed in AUD. Specific dietary and herbal supplementation could be beneficial in the due process. Finally, nutrition-related education and patient counseling beyond early detoxification stages could positively influence recovery outcomes. In summary, a complex interplay between malnutrition and alcohol use disorder further exacerbates AUD symptoms. Adequate nutrition, herbal and dietary supplementation, nutritional education, and mindfulness practices, along with prescription medications, could help to break this vicious cycle of alcoholism.

LIST OF ABBREVIATIONS

AUD

Alcohol Use Disorder

BMI

Body Mass Index

GLP-1

Glucagon-like Peptide-1

KGD

Ketogenic Diet

NS

Naples Score

SUD

Substance Use Disorder