Emerging Treatments for Alcohol Use Disorder (AUD)

Emerging Treatments for Alcohol Use Disorder (AUD)

Social and other media platforms are buzzing with words like the “microbiome”, “peptides”, and “fibermaxxing” lately. Should we pay attention to the hype? It turns out, these concepts are relevant to the field of treatment and recovery. Interventions that address gut health, whether through oral supplementation, enema, or another approach, show promise for supporting symptoms and conditions associated with alcohol use disorder (AUD). While not psychological in nature, below, I will describe some of the latest evidence on medical interventions that may also affect behavioral outcomes. Trigger warning: Please do note that some unconventional concepts are explored in this article, including treatments related to stool, which can make some readers squeamish.

Though generalized*, the term microbiome can be used to describe the colonies of diverse non-human organisms—including but not limited to bacteria, yeasts, fungi, and their genomes (3;19)—that live in and on our bodies in a symbiotic relationship (7). Within a healthy gastrointestinal tract alone there are tens of thousands of microbial organisms. When in balance, our gut microbiome supports us in maintaining health through various actions, such as breaking down dietary fiber, producing beneficial nutrients (e.g., short chain fatty acids), and by influencing signaling activities—like those that control the immune response and affect neurotransmitter production (7;19). However, along with genetic and environmental causes, lifestyle choices, like eating ultra-processed foods or food-like products (mass-produced hot dogs or chemically-derived candies, for example [17]), consuming drugs (prescription or illicit) and/or alcohol (acute or chronic use) (9) can negatively alter the gastrointestinal microbiome significantly, leading to dysbiosis—or imbalanced/dysregulated colonies of microorganisms (15).

Dysbiosis plays a role in the development of drug tolerance, withdrawal symptoms (11), and mental health disorders (5). Gut microbial imbalances are associated with a variety of disease states, including alcohol-induced liver disease (1). Through fecal sample evaluation, researchers from the UC, San Diego found that patients with alcohol-induced hepatitis (inflammation of the liver) had Enterococus faecalis, a strain known to cause life-threatening infections (23), 2,700-fold more than those in the non-AUD control group (18). When the researchers transplanted human stool containing E. faecalis into mice, it caused severe liver disease. When the researchers trialed bacteriophage therapies (the use of viruses to infect and kill bacteria) targeting E. faecalis, less liver inflammation and injury was present in the treated group than in the mice of the control group. The impact of this new targeted bacteriophage approach on humans is yet unknown.

Dysbiosis may also drive alcohol craving and consumption behaviors via the gut-brain axis—that bi-directional communication system between the gastrointestinal tract and the brain (15). Therefore, by increasing specific taxa of microbiota in the gut as a treatment, messages that travel through the gut-brain axis can be altered in a way that has been shown to reduce alcohol craving and consumption (20). Both animal and human study outcomes suggest that fecal matter transplants (FMTs), rich in specific health-supporting non-human organisms, such as Ruminococcaceae-centered communities—which tend to be lower in those who excessively consume alcohol (20)— offer a unique complementary treatment pathway for people with alcohol-induced dysbiosis by allowing for the reintroduction of beneficial colonies of organisms that make up a healthy microbiome. Fecal matter transplants—the use of the stool from a healthy individual to support microbial diversity in another—have been used throughout history (9). Today, there are stool collection facilities that screen donor material for infectious diseases and other concerns, though there is not yet a precise infectious screening nor processing protocol established. Routes of stool transfer from one person to another include oral, nasogastric tube administration, rectal enema and others, which are informed by the type of medical condition or therapeutic need.

Researchers Bajaj et al. (2021) enrolled 20 men meeting criteria for both “problem drinking” (AUDIT-10 >8) and alcohol-related cirrhosis (end stage liver disease) in a double-blind, randomized, placebo-controlled clinical trial to assess safety and tolerability of FMT via enema. They also identified the impact of the treatment on short-term alcohol craving and consumption, microbial function and composition, and other measures. All participants were similar at baseline in status of cirrhosis, alcohol consumption, unsuccessful alcohol rehabilitation treatment attempts, cognitive performance, diet, medication, and quality of life (QOL) measures. All subjects were screened for stool and plasma markers of microbial diversity before the trial and 15 days later. At day 16, 90% (n =9) of the subjects in the FMT arm reported reduced craving for alcohol (ACQ-SF) versus 30 % (n =3) in the placebo group. Participants receiving the FMT enema also had positive changes in their microbial diversity while no changes were present in the microbiota of the placebo group. Long-term follow-up indicated alcohol misuse occurred in more of the placebo group patients than those assigned FMT.

Other treatments focused on restoring or contributing to microbial homeostasis are showing promise for symptom treatment for alcohol use disorder, too. Psychobiotic interventions, defined as “beneficial bacteria (probiotics) or support for such bacteria (prebiotics) that influence bacteria-brain relationships” (19) have been demonstrated to prevent alcohol-induced dysbiosis in several animal and human studies (as described here), though more human data is needed to fully understand the mechanisms and limitations. Sarkar et al. (2016) illustrate that psychobiotics increase the release of gut peptide hormones, including ‘innate’ satiety peptides—specifically, glucagon-like peptide-1 (GLP-1)—which may suppress alcohol craving, possibly due to modulation of the brain’s reward pathway (12;14).

Peptides are short chains of amino acids that serve specific functions in the body (24). Our bodies combine peptides to, for example, build proteins. When we consume food, endogenous GLP-1 is secreted from cells in the small intestine, as well as synthesized in other areas of the body, and released as a neurotransmitter in parts of the brain associated with reward and addiction (13; 24). Synthetic GLP-1s, or GLP-1 receptor agonists (GLP-1RAs), are medications designed to mimic our natural peptides and are approved to treat diabetes and obesity, as they can suppress glucagon secretion and control appetite. They are marketed under brand names or peptide analogs such Ozempic, liraglutide, semaglutide and exenatide (list not exhaustive). The American Medical Association shares that while approved injectable peptides like insulin and GLP-1RAs have been around for years, newer injectables marketed by social media/wellness influencers as anti-aging or muscle growth hacks are not FDA approved (2). Still, a variety of GLP-1RAs are currently being evaluated for use disorders, a multitude of disease symptoms, and medical conditions (24).

In one trial, participants with obesity receiving once-per-week GLP-1 semaglutide injections had larger reductions in alcohol consumption over the period of one month compared to controls (13) and also reported reduced craving. Through secondary analysis, of a previous study (14) evaluating the impact of an extended-release (ER) form of exenatide (Bydureon®, once‐weekly injections) on alcohol consumption in 30 people (9 females, 21 males) with comorbid obesity, Jensen et al. (2025) found patients with obesity may experience a delayed, yet notable reduction in alcohol consumption, compared to patients taking placebo. Delayed response mechanisms and longer-term impacts are yet unclear. Research also has yet to elucidate the mechanisms and the impact of ER semaglutide on non-binary-sexed persons with comorbid AUD and obesity, or people with AUD and normal weight.

While there are risks associated with fecal matter transplants (possible transmission of infectious disease, diarrhea, etc. [9]) and psychobiotic supplementation, especially for people with weak immune systems or other conditions (6), “Fibermaxxing”, or eating abundant quantities of diverse, fiber-rich, whole plant foods (animal foods do not contain fiber) may be a complementary approach for addressing alcohol-induced dysbiosis. Studies exploring fiber-rich diets specifically for AUD in humans are sparse, though a scoping review by Lewis et al. (2025) finds fiber-focused diets may support recovery for those with SUDs in other ways (e.g., increased resilience and self-esteem). According to K. Snell, a grad student in the Department of Nutrition and Integrative Physiology at the University of Utah, fibermaxxing, which can be defined as eating upwards of 50 grams of fiber or more, does not align with recommended dietary guidelines of approximately 14 grams of fiber per 1,000 calories consumed; however, “there is no official upper limit” (22). A “low and slow” approach to increasing fiber—low number of grams of fiber increased gradually over an extended period of time—can help individuals reduce uncomfortable side effects of fiber consumption, like gas and bloating while working toward “optimal” fiber goals (4; 22).

Fiber directly affects both satiety and the constitution of the microbiome—which, as described above, may ultimately influence alcohol craving and consumption behaviors. Diet is the most influential factor within our control to directly shape gut microbial composition and function (21). Where the Standard American Diet (SAD), rich in fried, ultra-processed, packaged foods contributes to dysbiosis, plant-forward eating patterns (e.g., Mediterranean-style diets; whole-foods, plant-based diets) that include a variety of leafy greens, vegetables, whole grains, fruits, seeds, nuts, legumes, herbs, spices, and fermented foods like sauerkraut or kimchi promote favorable microbial diversity (4; 21).

Despite most humans having broad overlaps, every individual ultimately has a microbiome as unique as a snowflake (8). Thus, before making dietary pattern, supplementation, medication, or other lifestyle changes, and certainly before using FMT, it’s important to discuss your plan with your licensed medical provider(s). Please note that some of the treatments described above may or may not yet be available in your area, especially for purposes related to use disorders.

Author Bio: Dixie Schexnaildre (she/her) earned her Doctor of Health Science (DHSc ) degree and a Master of Science in Complementary and Integrative Health with a concentration in Integrative Addiction Therapies from Drexel University’s College of Nursing and Health Professions, as well as a Graduate Certificate in Mind, Brain & Learning from Drexel’s School of Education. She completed her didactic Substance Use Disorder Counselor certificate programming at UCSD Extended Studies and holds multiple integrative health certifications, such as RYT-500, Clinical Nutrition, and is a National Acupuncture Detoxification Association (NADA) Acudetox Specialist.

A proud GODA (Grandchild of Deaf Adults), Dr. Dixie also has more than 25 years of experience as a professional American Sign Language (ASL)/English interpreter, primarily in educational settings (EIPA >4.0: K–12). Her work is driven by a commitment to equitable access to education and healthcare. She has published with Nova Science Publishers, the Online Learning Journal, the Journal of Interprofessional Education & Practice, JDARA, and others. Her writings serve as entertainment/education only, and are not intended as a replacement for medical advice, nor to diagnose, treat, prevent, or cure disease.

*Researchers Guzzo et al. (2022) provide more nuanced terminology to differentiate nonbacterial microbes here: https://academic.oup.com/ibdjournal/article/28/7/1112/6517341

 References

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