Douglas D. DeGeeter
California College of Ayurveda
Clinical Ayurvedic Medicine
Introduction
“We shall now explain the Treatment on Alcoholism. Thus said Lord Atreya.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 1–2
Alcoholism is a worldwide health concern. It spans the breadth of moderate to chronic and can lead to a wide variety of serious health conditions if allowed to go untreated, often growing in severity due to the addictive qualities of both a mental and physical nature. In the United States alone, 88,000 deaths a year are associated with the consumption of alcohol (1). Though the problem of identifying and diagnosing individuals with Alcohol Use Disorder (AUD) is not the theme of this discussion, it needs mentioning that a large segment of the population goes undiagnosed due to a lack of screening among health care professionals (1). AUD is defined as “a problematic pattern of alcohol use accompanied by clinically significant impairment or distress” (1). Diagnosis is based on standards outlined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). DSM-5 defines AUD as a chronic inability to stop alcohol use despite adverse social, occupational, and health consequences, with severity graded according to the number of diagnostic criteria an individual meets (2).
Severe alcoholism comes with serious health risks with a history of difficulties in both diagnosis and treatment. The downstream health consequences of untreated AUD affect the individual, family, and community alike, with 7.4% of emergency room visits consisting of alcohol-related conditions and 29.5 million people aged 12 and over suffering from AUD in some degree of severity (2). Though AUD is a major health issue and the most commonly diagnosed substance abuse disorder, only about 7.6% of the afflicted population receives treatment (2).
Western medicine has developed extensive and reliable diagnostic tools; however, training and implementation are not deployed at scale within the medical community, resulting in only 1 in 6 adults reporting being asked about their drinking by a health care professional when visiting a health care provider (1). Despite the fact that Western medicine has developed sophisticated diagnostic tools and FDA-approved pharmacotherapies—including disulfiram, naltrexone, and acamprosate—AUD remains notoriously difficult to treat (1). It is not uncommon for patients to experience relapse. Additionally, the existing pharmacological interventions address only a portion of the disorder’s underlying drivers, leaving considerable room for complementary approaches that address the condition from a holistic health and wellness perspective (1).
The physical and mental health consequences of alcohol use are extensive and well documented in the medical literature. Nearly every major organ system of the body is affected by chronic alcohol exposure, producing progressive liver disease that can advance to cirrhosis and hepatocellular carcinoma, cardiovascular strain and cardiomyopathy, pancreatic injury, and profound neurological damage including peripheral neuropathy and memory-impairing Wernicke-Korsakoff syndrome. Alcohol can also directly compromise immune function, leaving affected individuals at greater risk of infection and slower to recover from illness and injury (1,2). Apart from these physical sequelae, AUD carries a heavy psychological burden, often complicated by co-occurring depression, anxiety, and in advanced cases psychosis and dementia (1,2). It is precisely this confluence of interconnected mind-body factors that adds to the complications in treating AUD, adds to the difficulties in seeking treatment, and lends to the sense of hopelessness many in need of treatment feel, setting the stage for relapse.
This review is an examination of the biomedical research into AUD-related sequelae, their manifestation processes and treatments, and by extension an examination of complementary treatment protocols documented in classical Ayurvedic medical texts and complementary treatment therapies adapted from the Yoga Sutras of Patanjali. Long before the development of modern diagnostic tools and categories, the classical medical tradition of Ayurveda identified and systematically classified conditions closely resembling what is now termed AUD. This condition is known as Madatyaya and is addressed at length in the twenty-fourth chapter of the Chikitsa Sthana of the Caraka Samhita, one of the foundational texts of Ayurvedic medicine (3). This chapter sits deliberately following the chapter on poisoning (Vishachikitsa), nor does it appear insignificant that the chapter following addresses wounds and ulcers (Vrana).
Madatyaya is classified according to the predominance of the three doshas—Vata, Pitta, Kapha—producing distinct symptom presentations: a Vataja subtype that “causes the obstruction of the movement of vayu in the channels of circulation” (31), a Pittaja subtype marked by heat, thirst, and burning sensations (32), a Kaphaja subtype addressed through treatment that promotes digestion, reduces ama, and cleanses the circulatory channels (33), and a Sannipataja subtype in which all three doshas are vitiated simultaneously, producing the most severe presentation (34). The Caraka Samhita goes beyond recognition of the physical needs of AUD and addresses simultaneously the mental health aspects of AUD treatment through understanding the importance of treating the mind—Manovaha Srotas (the pathway of the mind)—which is closely related to treating and recognizing mental health disorders. This psychological dimension appears in the classical text’s identification of Tamas and Rajas as drivers of an individual’s proclivity toward excessive drinking; the Sattvic individual, by contrast, is inherently resistant to it and understands moderation (3).
This paper undertakes a review of the existing literature—both classical Ayurvedic texts and contemporary peer-reviewed research—to examine the major physical and mental health sequelae associated with chronic alcohol use, and to demonstrate that Ayurvedic chikitsa (therapeutic management) offers clinically actionable, constitutionally individualized approaches that are increasingly supported by published Western research. It is not proper or useful to position Ayurvedic and Western biomedical understandings of AUD in opposition to each other, but instead to treat them as complementary systems directed at the same underlying pathology. This is especially beneficial in that the consumption of high-proof alcoholic spirits was not in use at the time of the early chronicles of Ayurvedic medicine—this early system did not have to contend with the potential severity of modern withdrawal symptoms, while simultaneously the modern biomedical system lacks the tools to address the integrated physical, mental, and spiritual complexities of chronic alcoholism and addiction. Where modern medicine excels in precision diagnostics, pharmacological intervention, and the management of acute life-threatening complications, Ayurvedic medicine offers a constitutionally tailored framework for long-term restoration of health through Rasayana therapies aimed at rebuilding the vital reserves known as Ojas in Ayurvedic medicine. The sequelae this review addresses in association with AUD are: liver disease and cirrhosis, cardiovascular disease and stroke, Ayurvedic chikitsa, neurological damage including Wernicke-Korsakoff syndrome, alcohol withdrawal syndrome, mental health conditions including depression and anxiety, and yoga as therapy.
Defining the Condition and Treatment
“For all living beings, food is the sustainer of life, but when taken inappropriately, it causes death.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 58–60
AUD, Alcohol Use Disorder, is defined as “a problematic pattern of alcohol use leading to clinically significant impairment or distress” (4), as manifested by at least 2 of 11 criteria occurring within a 12-month period. Severity is classified by the number of criteria met: mild (2–3 criteria), moderate (4–5 criteria), severe (6 or more criteria). To further define and classify AUD, the 11 criteria are grouped into four clusters:
- Impaired control: Drinking more or longer than intended; persistent desire or unsuccessful efforts to cut down; spending a great deal of time obtaining, using, or recovering from alcohol; craving.
- Social impairment: Failure to fulfill major role obligations; continued use despite persistent social or interpersonal problems; giving up or reducing important social, occupational, or recreational activities.
- Risky use: Recurrent use in physically hazardous situations; continued use despite knowledge of a persistent physical or psychological problem likely caused or exacerbated by alcohol.
- Pharmacological: Tolerance (needed for markedly increased amounts to achieve effect, or markedly diminished effect with continued use of the same amount) and withdrawal (characteristic withdrawal syndrome, or alcohol taken to relieve/avoid withdrawal symptoms) (4).
Hand in hand with a detailed diagnostic system is a codified system of treatment built around an interdisciplinary team; in the US model, the treatment of addiction is incorporated within hepatology care integrated with social workers, psychiatrists, therapists, and hepatologists (2).
In the Caraka Samhita, alcoholism is not identified in the modern sense of a chronic use disorder, though there is overlap; instead it seeks to identify the point at which the drinking of alcohol stops behaving as a substance of pleasure and connection in service of constitution and in harmony with sattvic qualities, and starts behaving as a disease process with a samprapti (pathogenesis) of its own doshic-driven progression culminating in a sannipataja, tridoshic condition. Madatyaya appears as ten qualities—the ten qualities contained in alcohol—in direct opposition to the ten qualities of Ojas: where alcohol is light, hot, sharp, dry, and expansive, Ojas is heavy, cold, soft, unctuous, and dense (3). Because the heart (Hridaya) is understood as the seat of Ojas, Buddhi (intellect), and Manas (mind) alike, alcohol’s direct assault on Ojas at this site explains why Madatyaya produces not merely physical intoxication but the progressive mental distortion—moha, or delusion—that Caraka describes as its most dangerous complication (3).
There is growing interest in understanding ways in which Western medical modalities and Ayurvedic medicine can be applied in conjunction with each other, advancing our cumulative knowledge of patient care. Addiction, and specifically the treatment of AUD, offers such an opportunity based on the current medical literature and documented cases. Western medicine’s strongest asset is its ability to safely treat severe AUD withdrawal; however, each of the FDA-approved medications for treating AUD comes with its own set of limitations. Moreover, outside of stabilizing patients in a state of severe withdrawal that has life-threatening consequences, the Western medical approach has little to offer. To get comprehensive care, an individual suffering from AUD needs to see multiple specialists (1). In answer to this fragmentation, Ayurvedic medicine offers a single, constitutionally tailored framework capable of addressing AUD’s full range of physical and psychological manifestations within one clinical relationship—a capacity demonstrated concretely in a 2024 case report documenting the integrated Ayurveda and Yoga management of chronic alcoholism sequelae, in which doshic– and srotas-based assessment guided the simultaneous treatment of neurological, cognitive, and psychological complications within a single therapeutic protocol combining Satvavajaya Chikitsa, Yoga, Rasayana therapy, and procedures including Shirodhara and Nasya, resulting in measurable improvement on the Glasgow Coma Scale, a standard biomedical outcome measure (5).
Physical Health Sequelae and Ayurvedic Chikitsa
Liver Disease and Cirrhosis
“All the types of madatyaya are caused by the vitiation of all three doshas. In the beginning, treatment should be made of the most prominent dosha. Then the treatment should generally be started from the location of Kapha, followed by that of Pitta, and lastly that of Vayu.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 107–111
Alcohol-associated liver disease (ALD) displays one of the clearest points of convergence between Western and Ayurvedic pharmacology. Chronic alcohol use, as the leading cause of advanced hepatic disease and liver-related mortality, demonstrates a well-documented progression from steatosis and steatohepatitis to progressive fibrosis, cirrhosis, and hepatocellular carcinoma (HCC), including alcohol-associated hepatitis (AH) and the possibility of developing acute-on-chronic liver failure (ACLF). This pathology is discussed by Caraka as the condition known as Yakridhalayudara (liver disease) alongside conditions of Plihodara (spleen). In chapter 13 of the Caraka Samhita, Chikitsa Sthana, Yakridhalayudara is described as a condition of inflammation with Ranjaka Pitta lodging in the Rakta Dhatu and Raktavaha Srotas. From here, Pitta vitiation pushes secondary Kapha vitiation, causing scarring and nodular formation in the same tissue and channel; finally, the late stage ends with weight loss and depleted Ojas indicative of Vata vitiation (8).
Liver transplant and abstinence from alcohol appear to be the only options the Western medical system has to offer; no FDA-approved pharmacotherapy exists for ALD in its advanced stages (6). Ayurvedic pharmacology has within its repertoire of herbal remedies demonstrated effectiveness in alleviating liver damage. In one study, researchers gave rats alcohol every day for 45 days—enough to reliably damage the liver, confirmed by measuring several standard blood/liver chemistry markers. After 30 days, with liver damage already underway, researchers administered Picroliv, a purified active compound extracted from Picrorhiza kurroa (Kutki), to some of the rats alongside the alcohol for the final 15 days of the study. The rats that got Picroliv showed less liver damage on those blood markers compared to rats that got alcohol alone. Though Picroliv didn’t prevent alcohol exposure, it did measurably reduce alcohol-induced liver harm (7). As the condition progresses into its late, Vata-dominant stage, Caraka prescribes Guduchi, Aloe Vera, and Amalaki as the primary rejuvenative herbs, tonifying hepatic tissue and rebuilding Ojas where earlier heat-clearing measures are no longer sufficient (8). Recent studies support these ancient applications, with results showing that administration of Tinospora cordifolia extract restored normal intestinal nutrient absorption and improved the liver’s capacity to retain those nutrients, correcting the multivitamin deficiency associated with alcohol consumption (9).
Cardiovascular Disease and Stroke Risk
“The stability of Ojas is counteracted by the pervasiveness of alcohol.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 29–36
Hrdroga is the Sanskrit word used to refer to diseases of the heart and cardiac disorders. It also refers to heartburn, the emotional pain of the heart, and, in poetic usage, love (10,11). From the Ayurvedic perspective, the heart is not only the central mechanism of the cardiovascular system but also the seat of Ojas and the emotional center of the mind (13). This view gives Ayurvedic medicine a dynamic approach to treating disorders of the heart, one that assesses not only the physical health of the organ but its emotional and spiritual health as well. Western cardiology’s primary interventions are diagnostic, surgical, and pharmaceutical, with lifestyle counseling comparatively secondary and inconsistently delivered (12).
Ayurveda’s Hrdroga management, by contrast, is structured around daily conduct (Dinacharya), diet, and emotional regulation as first-line therapy, not an afterthought to pharmacology (14). Ayurveda is well known for its lifestyle-based treatment approach and extensive body therapies, Panchakarma among them. With this in mind, the approach here is to focus on the pharmacological and physiological dimension of that model—the herbs, compounds, and clinical actions Ayurveda brings to specific alcohol-related conditions—while lifestyle and behavioral protocols such as Dinacharya remain part of the broader Ayurvedic framework, addressed here only in principle rather than in detail.
Western research has clarified much of the mechanism by which alcohol damages the heart, even as key questions remain open. Ethanol has a direct effect on heart tissue: it damages heart muscle, causes oxidative stress, and stimulates the renin-angiotensin system. Alcohol-induced cardiomyopathy is defined as dilated cardiomyopathy from heavy drinking—typically more than 80g of alcohol per day for five or more years, with other causes of dilated cardiomyopathy ruled out.
As ethanol breaks down, it produces acetaldehyde, which is known to damage mitochondria and impair the actin-myosin system, the proteins that allow heart muscle to contract. The same research shows that “repeated episodes of acute heavy drinking…are a risk factor for myocardial infarction and stroke” (15). Further studies show ethanol affecting the heart on two timescales: a single heavy-drinking episode can trigger arrhythmias, while long-term chronic use can lead to heart failure. In both cases, the underlying molecular mechanisms are “incompletely understood,” and current research is pursuing emerging treatment approaches not yet standardized into clinical practice (16).
It is in this gap—mechanisms identified but treatment still experimental—that Ayurvedic medicine has the potential to contribute. A substantial body of Ayurvedic herbology research already speaks directly to it. Ancient Indian physicians used powdered Arjuna bark to treat angina (hritshool) and other cardiovascular conditions, with records of its use tracing back to the Atharva Veda, the text from which Ayurvedic medicine originates. Arjuna carries the properties and qualities of sweet, acrid, cooling and heating, aphrodisiac, expectorant, tonic, styptic, anti-dysenteric, and purgative/laxative, and has traditionally been used beyond cardiac conditions for urinary discharge, strangury, leucoderma, anaemia, hyperhidrosis, asthma, and tumors. Its active compounds—glycosides, flavonoids in large quantity, tannins, and minerals—map onto the mechanisms described above: flavonoids act as antioxidants, anti-inflammatories, and lipid-lowering agents, directly addressing the oxidative stress driven by ethanol metabolism, while glycosides are cardiotonic, strengthening heart muscle contraction where acetaldehyde impairs it.
Clinical study of Arjuna dates back as early as 1909. An early study from 1951 found that Arjuna bark decoction produced clinical improvement in patients with congestive heart failure, essential hypertension, and liver cirrhosis in 42%, 62%, and 40% of cases, respectively. Later experimental studies have demonstrated a range of pharmacological actions:
- Significant inotropic effect (strengthening of heart muscle contraction)
- Hypotensive effect (lowering of blood pressure)
- Increased coronary artery blood flow
- Protection of heart muscle against ischemic damage
- Mild diuretic and anti-thrombotic activity
- Enhanced prostaglandin E2 (a compound involved in vascular regulation)
- Hypolipidaemic activity
- Reduction of LDL cholesterol oxidation and reperfusion ischemic injury
The authors of this study conclude that Arjuna “can be considered a useful drug for coronary artery disease, hypertension, and ischemic cardiomyopathy” (17).
Ayurvedic Chikitsa
“If a person who has stopped drinking alcohol suddenly takes to drinking in excess, he suffers from two diseases, viz., dhvamsaka and viksaya. Since such a person is already emancipated because of [their] earlier drinking habit, these two diseases appearing…are very difficult to cure. Their signs, symptoms, and treatment will not be described appropriately.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 199–205
We looked at the damage AUD does to some of the major organ systems, demonstrating Western medical and correlative Ayurvedic approaches to treating disease. In truth, chronic alcohol consumption creates more than just isolated health conditions; instead it vitiates whole systems of the body, creating a matrix of integrated health issues including gut dysfunction, compromised immune function, degenerative nerve conditions, and a variety of serious mental health issues. This section turns to that broader matrix, examining how chronic alcohol exposure compromises gut health and immune function, drives neurological degeneration, and produces a range of serious mental health sequelae—conditions that, in Ayurvedic terms, rarely appear in isolation from one another. It has been shown that 46% of individuals with AUD develop peripheral neuropathy. The direct cause is unknown; this is “likely attributable to the complex range of physiological derangements that come with chronic alcohol abuse” (18), making it difficult to trace the exact origin. Three competing explanations exist—poisoning due directly to the alcohol, nutritional deficiencies (vitamin B/thiamine), or unknown causes—which researchers are unable to confirm (18).
Ayurvedic medicine, by its internal logic and reasoning process, is effective at integrating the “complex range” (18) of pathologies often associated with AUD. A case study conducted at the College of Ayurveda & Research Centre, Pimpri, Pune, India, demonstrated Ayurvedic medicine’s ability in “transforming health through the cumulative effects of Rasayana medicines, Panchakarma, and yoga” (19). The case report’s own diagnosis presents a clear case of Madatyaya Upadrava, also known as Vikshay. Vikshay in this article is differentiated from Madatyaya as “severe pain in the body and head, obstruction in the heart (chest) and throat, severe delusion, cough, thirst, vomiting, and fever” (20). Caraka defines Vikshay as “cardiac disorder, throat disorder, unconsciousness, vomiting, pain in the limbs, fever, morbid thirst, cough, headache” (21). In this case, all three doshas were vitiated with a Vata predominance, consistent with the patient’s presentation of confusion, aphasia, severe pain, and neurological disturbances. The pathology chain included a pathological disturbance of Annavaha Srotas leading to Agnimandya and malabsorption in Samana Vayu, creating thiamine (vitamin B) deficiency (19).
Treatment proved highly effective, running on three distinct paths: Satvavajaya Chikitsa, Shamana Chikitsa, and Shodhana Chikitsa (19). Satvavajaya Chikitsa is a psychic or mind-regulation therapy directed at reducing cravings for alcohol as well as alcohol-associated triggers, a treatment decision made to address both the mental and physical dependence on alcohol. Shamana Chikitsa focused on herbal pacification therapy with an herbal Rasayana formulation comprised of Guduchi, Gokshura, and Amalaki for rejuvenation, and Ashwagandha for stress and cognitive support.
Yashtyadi Churna (Yashti, Pippali, Vacha, Aakarkarambh) was formulated to target aphasia, with Shreikhandasava given for alcohol-related toxicity, and finally Ekangaveer Rasa to assist with broader neurological symptoms (19). For cleansing Ama, Shodhana Chikitsa was performed, incorporating Snehan and Swedan as preparatory oleation and fomentation, Nasya was performed with Bala Taila to address neurological presentations via the facial and nasal route, and Matra Basti with 80ml of Bala Taila for Vata pacification and to support thiamine synthesis compromised by malabsorption. Finally, Shirodhara with Jatamansi Taila was performed for its calming effects, and Nabhipuran with Bala Taila again to relieve Udana Vayu, the sub-dosha governing speech and vitiated due to excessive physical labor (19).
To support the herbal and performative therapies, Yoga and Pranayama therapies were indicated, with 45-minute daily sessions. Each session consisted of Anulom Vilom, Ujjayi, Bhramari, asana, and meditation with Om chanting (19). These treatments did significant work in reducing alcoholic cravings, producing measurable results as indicated by the Present Alcohol Craving Scale falling from 15–20 to 1 over the eight-week treatment period (19). Through the course of treatment, the case showed documented improvement in pain, cognition (MMSE 18–23 to 28/30), fever, speech, craving, and consciousness level (GCS 13 to 15), with a modest rise in thiamine (1 to 2 µg/dL) (19). What is extraordinary in this case report is the demonstrated multi-domain nature of the improvements, indicating that a single integrated treatment regimen can move several sequelae at once.
Alcohol Withdrawal Syndrome
“Feeling as if the body is covered with grass, ash, creepers, leaves, and dust; and dashing of birds over the body because of bewilderment.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 101–106
Of the conditions caused by extreme alcohol consumption, it is critical that the patient experiencing withdrawal symptoms seek professional help. In such cases, the cessation of drinking must be done under careful supervision. Symptoms can be acute, with death a real concern in extreme cases. Western pharmacology offers real solutions for at-risk patients with access to medical treatment. The sudden discontinuation of alcohol use in heavy/chronic drinkers, leading to Alcohol Withdrawal Syndrome (AWS), occurs in 8% of individuals hospitalized with AUD (22). Symptoms of AWS include tremor, anxiety, sweating, nausea, tachycardia, and in severe cases hallucinations, seizures, and delirium tremens; untreated, symptoms can be fatal. The AWS symptoms described are very similar to those described by Caraka in chapter 24 of the Caraka Samhita, Chikitsa Sthana. As a depressant acting on the central nervous system, alcohol produces euphoria and behavioral excitation via an increase in glutamate binding to N-methyl-D-aspartate (NMDA) receptors; at high concentrations, acute intoxication is the result of potentiation of GABA effects (22).
Tolerance develops with prolonged alcohol use and often leads to dependence. Research suggests this may be tied to the downregulation of GABA receptors and the upregulation of NMDA receptors. The abrupt absence of alcohol in the system exposes these changes, resulting in glutamate-driven CNS excitation, producing autonomic overactivity, delirium, and seizures. Western medical treatment calls for hydration and resuscitation, with pharmacological treatment centered around benzodiazepines (lorazepam, chlordiazepoxide, oxazepam, diazepam) as the first line of treatment. These drugs act as GABA-A agonists, increasing chloride channel opening frequency, resulting in an inhibitory effect mimicking ethanol’s own action. Though effective in stabilizing AWS symptoms, risks include dependency and withdrawal symptoms, increased risk of falling, respiratory failure, cognitive impairment, depressive mood, sleep disorders, and increased impulsivity potentially leading to suicidal behaviors (22). Given these risks, these drugs are not suitable for every patient and must be administered under medical supervision, demonstrating a need for safer pharmacologic agents.
Ashwagandha and Brahmi offer a real solution to these limitations. “Ashwagandha and Brahmi, with their GABA agonist activity, may have the potential to control alcohol withdrawal symptoms” (22). These herbs have been in use within Ayurvedic medicine for centuries to promote longevity and vitality. To back these claims, Ashwagandha in preclinical studies has been shown to possess “anticonvulsant, antidepressant, antianxiety, and hepatoprotective effects” (22). “Glycowithanolides withaferin-A and sitoindosides VII–X isolated from Ashwagandha significantly reversed ibotenic acid-induced cognitive defects in [an] Alzheimer’s disease model…chronic oral administration of withanoside attenuated axonal, dendritic, and synaptic losses and memory deficits induced by amyloid peptide Aβ (25-35) in mice, [and] can modulate GABAergic, cholinergic, and oxidative systems in [the] CNS” (22). Bacopa monnieri (Brahmi) is a well-known Ayurvedic nootropic, with the principal chemical unit being Bacoside-A, producing a nootropic effect along with “other neuromodulatory, hepatoprotective, and antioxidant activities,” with other studies showing improvements in learning and memory (22). “Brahmi potentiates a therapeutic effect by reversing the alterations in general GABA, GABA-A, GABA-B receptor binding, GABA-A receptor subunits, GAD, and CREB gene expression that occur during epilepsy, resulting in increased GABA-mediated inhibition in the overstimulated cerebral cortex neurons” (22). These GABA agonist activities corroborate Ayurvedic usage and indicate “potential to control alcohol withdrawal symptoms” (22).
Experimental findings support these mechanistic claims. In a rodent model of alcohol withdrawal, animals treated with Ashwagandha and Brahmi, alone or in combination, showed significantly reduced agitation scores and stereotypic behavior compared to the untreated ethanol withdrawal group, with the combined extract producing the most consistent effect, remaining significant at both the second and sixth hour of testing (22). On the elevated plus maze, a standard measure of anxiety-like behavior, the combination treatment likewise preserved a higher percentage of entries into the open arms relative to untreated animals, indicating an anxiolytic effect consistent with the herbs’ GABAergic activity (22). Open field testing showed the treated groups maintained more normalized locomotor activity, in contrast to the hyperactivity characteristic of untreated withdrawal (22). Most notably, in the pentylenetetrazol (PTZ) kindling test, a measure of seizure threshold, 100% of untreated ethanol-withdrawal animals developed convulsions, while animals treated with diazepam, Ashwagandha, Brahmi, or the combination showed 0% convulsions, indicating that these herbal extracts conferred seizure protection equivalent to standard benzodiazepine treatment (22). Together, these results demonstrate that Ashwagandha and Brahmi do not merely offer a plausible mechanism but produce measurable withdrawal-mitigating effects comparable to first-line pharmacologic treatment, lending empirical support to their traditional Ayurvedic use.
Yoga As Therapy
“Alcohol does not cause alcoholism without causing agitation of the mind and causing morbidity in the body. Therefore, to a patient suffering from alcoholism, therapeutic measures (psycho-therapy) for the cheerfulness of the mind should be administered.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 194
The twentieth-century mystic Sri Aurobindo’s life’s work centered on a system of spiritual awareness and development he called Integral Yoga; though not an Ayurvedic or Vedic text, he was nonetheless an accomplished yogi and scholar of Sanskrit and the classical spiritual philosophy and literature of India. The relevance of his work for the modern reader struggling with AUD and addiction at large lies in the belief that the spiritual path, and the benefits it bestows, are accessible to everyone in the modern world regardless of position in life. There are many complications associated with managing the physical/material plane, including managing our lives, managing our health, as well as the stresses of career and relationships, and the struggles of navigating compulsions. This is a realm we are all familiar with. The aim of Yoga is as much a conditioning of the physical and mental states of being as it is the spiritual. Perfection in the physical and mental plane is a key aspect of Yoga. Health, then, flows from the body once the ego self comes into harmony with the higher self, once the little self of ego listens to the voice of our higher self (23). In the recovery process this paper attempts to address, outer transformation is not inseparable from inner transformation.
“Yoga is the ultimate skill to calm down the mind…(mana prashamanopayah yoga ityabhidhiyate)…achieved through…practicing the principles of yama/niyama and through yogic breathing techniques,” so states the Yoga Vashista (24). That claim has since been tested empirically: recent studies report yoga’s measurable effects on depression and mental health (24). Randomized controlled trials conducted on individuals with Major Depressive Disorder (MDD), older women, college students, pregnant women, breast cancer patients, and women with PMS have shown that practicing yoga reduces depression scores.
Patanjali expounds upon the first two of the eight limbs of yoga in his Sutras: “Non-killing, truthfulness, non-stealing, continence, and non-receiving are called Yama…Internal and external purification, contentment, mortification, study, and worship of God are the Niyamas” (26). The restorative mechanisms of Yama/Niyama remain largely self-reported through practitioners’ own accounts, framed through classical concepts rather than clinical measurement. The other three limbs, grounded in the definitions of Patanjali, fare differently: meditation, Pranayama, and Asana have each been studied under clinical conditions. In the Yoga Sutras of Patanjali, at the beginning of the first chapter, meditation is described: “Yoga is restraining the mind-stuff (Chitta) from taking various forms (Vrttis).” In chapter 2, Pranayama is described as a “seat being conquered, the dualities do not obstruct. Controlling the motion of exhalation and inhalation follows after this,” and Asana is described as “that which is firm and pleasant. By slight effort and meditating on the unlimited, posture becomes firm and pleasant” (25).
Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis, triggering a cascade of corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH), and cortisol release, alongside sympathetic nervous system activation and catecholamine release. This same cascade also triggers pro-inflammatory cytokines—interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor alpha (TNF-α)—which impair serotonin transport and production, contributing to the onset of depression (24).
At several positions along this chain, yoga intervenes. It reduces ACTH and, in turn, cortisol secretion, and lowers phenylethanolamine N-methyltransferase (PNMT) activity, reducing catecholamine formation. Yoga raises plasma serotonin while lowering monoamine oxidase, the enzyme responsible for breaking serotonin down. It reduces the inflammatory markers implicated in the same cascade—NK (natural killer) cell activity, IL-6 (interleukin-6), TNF-α (tumor necrosis factor-alpha), and hs-CRP (high-sensitivity C-reactive protein)—while suppressing NF-κB (nuclear factor kappa B) transcription of pro-inflammatory cytokines at the source. Beyond this direct opposition to the cascade, yoga affects several other markers attributed to mood: one cited study found a roughly 65% increase in dopamine availability, attributed to reduced striatal receptor binding. Meditation has been found to raise melatonin, and noradrenaline is enhanced even as adrenaline is lowered. Yoga also increases BDNF (brain-derived neurotrophic factor), linked to lower cortisol and improved heart rate variability. Yoga has been shown to raise Sirt1 (Sirtuin 1) expression, a gene associated with antidepressant effects (24).
It is these exact biomedical factors that demonstrate the effectiveness of yoga therapy as applied in the earlier case study of a 71-year-old male with chronic AUD in Section V, Ayurvedic Chikitsa. In this case study, meditation, Pranayama, and Asana, in conjunction with other Ayurvedic treatment modalities, are credited with restoring mental balance (5). Asanas were credited with helping the patient manage his emotions through stress reduction, relaxation, and greater awareness of body sensations and an understanding of his emotional and physical states; Pranayama was responsible for calming the patient’s mind while increasing blood circulation to the brain and strengthening the patient’s self-regulation ability and impulse control. “Yoga was used as Satvavajaya Chikitsa, which emphasizes the principle of ‘Chitta Vritti Nirodha,’ meaning controlling the mind from different unwanted thoughts” (5). Here is a man who consumed alcohol from the age of 14, who made an attempt to quit only to resume drinking heavier than before (5). With the help of intentionally targeted yoga therapy, this patient was not only able to quit drinking and restore his health, but to do so while also reducing alcoholic craving from 15–20 down to 1 on the Present Alcohol Craving Scale (5).
Conclusion
“Intake of alcohol in appropriate manner will not give rise to diseases caused by [excessive intake of] alcohol.” — Caraka Samhita, Vol. IV, Ch. XXIV, Vrs. 199–205
Reviewing the available medical literature, we see that Ayurvedic medicine, applied toward the treatment of AUD, has effective applications both as an independent source of care and in conjunction with allopathic medicine. In chapter 24 of the Caraka Samhita, Caraka explicitly states the dangers of alcohol abuse and its depleting effect on Ojas through the ten attributes of alcohol counteracting the ten attributes of Ojas (27). The depletion of Ojas is a common link among the disorders discussed in conjunction with AUD. Caraka’s answer to this depletion is twofold: Rasayana dravyas that rebuild Ojas through diet and herbal medicine, and Achara Rasayana, which rebuilds Ojas through conduct and the discipline of mind. Many of the herbs described in this review fall under a category of herbs called Rasayanas, which are described in the opening commentary of chapter 1:1, Vol. III of the Caraka Samhita as “drugs, diet, and regimens which promote longevity by preventing aging and diseases” (30).
Achara Rasayana is a practice described by Caraka as a behavioral rejuvenation code of conduct (27). This code was created for the development of mental, physical, social, and spiritual well-being. He goes on to state, “A person undergoing rejuvenation therapy attains longevity, memory, intellect, freedom from disease, youth, excellence of luster, complexion, and voice, excellent potentiality of the body and the sense organs, Vak-Siddhi (i.e., what he says comes true), respect, and brilliance. The means by which one gets the excellence of Rasa is known as Rasayana, or rejuvenation therapy” (28). These principles are designed to “enhance the Sattva Guna in a person” (29). These principles work not by altering Prakriti, a concept Caraka holds as fixed, but by increasing Sattva Guna, “the aim of following Achara Rasayana” (29). This is the same opposition the paper opened with: alcohol being light, hot, sharp, dry, and expansive against Ojas with its heavy, cold, soft, unctuous, and dense qualities. Every intervention this review has traced—herbal, behavioral, and yogic therapy—works to rebuild that opposition by rebuilding what Madatyaya depletes.
Endnotes
1. Henry R. Kranzler and Michael Soyka, “Diagnosis and Pharmacotherapy of Alcohol Use Disorder: A Review,” JAMA 320, no. 8 (2018): 815–824, at 815.
2. Sara M. Nehring, Richard J. Chen, and Andrew M. Freeman, “Alcohol Use Disorder: Screening, Evaluation, and Management,” in StatPearls [Internet] (Treasure Island, FL: StatPearls Publishing, 2026), last updated March 16, 2024.
3. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24 (Madatyaya Chikitsa Adhyaya).
4. American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, 5th ed. (Washington, DC: American Psychiatric Publishing, 2013).
5. Aqsa Zarin Khan, Jibi Varghese, Shweta Kodre, Mohini Niware, Snehal Pansare, Shreya Bhatia, Samkit Shah, and Manna Mathew, “Ayurveda and Yoga Management of Chronic Alcoholism Sequelae—A Case Report,” Journal of Ayurveda and Integrative Medicine 15, no. 1 (2024): article 100862.
6. Lauren L. Jophlin, Ashwani K. Singal, Ramon Bataller, Robert J. Wong, Bryan G. Sauer, Norah A. Terrault, and Vijay H. Shah, “ACG Clinical Guideline: Alcohol-Associated Liver Disease,” American Journal of Gastroenterology 119, no. 1 (2024): 30–54, at 30.
7. Ravi Rastogi, Seema Saksena, Narendra Kumar Garg, Narinder Kumar Kapoor, Dharam Pal Agarwal, and Bhola Nath Dhawan, “Picroliv Protects Against Alcohol-Induced Chronic Hepatotoxicity in Rats,” Planta Medica 62, no. 3 (1996): 283–285, at 283.
8. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 13, verses 74–89 (vol. 3).
9. Bhawana Sharma and Rajesh Dabur, “Protective Effects of Tinospora cordifolia on Hepatic and Gastrointestinal Toxicity Induced by Chronic and Moderate Alcoholism,” Alcohol and Alcoholism 51, no. 1 (2016): 1–10.
10. V. S. Apte, The Practical Sanskrit-English Dictionary, rev. and enl. ed. (Poona: Prasad Prakashan, 1957–1959), s.v. “hṛdroga.”
11. “Hridroga, Hṛdroga, Hrid-roga: 18 Definitions,” Wisdom Library, accessed September 30, 2026, https://www.wisdomlib.org/definition/hridroga.
12. K. Muniasamy, N. K. Chander, N. Gudapati, S. Pradeep, E. Raman, R. Saranya, N. S. Babu, and K. Srinidhi, “Cardiologists’ Knowledge and Implementation of Lifestyle Counselling for Cardiovascular Disease Prevention: A National Survey,” Bioinformation 20, no. 12 (2024): 1948–1953, at 1948.
13. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Sutra Sthana, chapter 30, verse 7.
14. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 26, verses 77–103.
15. Fernando Domínguez, Eric Adler, and Pablo García-Pavía, “Alcoholic Cardiomyopathy: An Update,” European Heart Journal 45, no. 26 (2024): 2294–2305, at 2294.
16. Julian Mustroph, Simon Lebek, Lars S. Maier, and Stefan Neef, “Mechanisms of Cardiac Ethanol Toxicity and Novel Treatment Options,” Pharmacology & Therapeutics 197 (2019): 1–10.
17. Shridhar Dwivedi, “Terminalia arjuna Wight & Arn.—A Useful Drug for Cardiovascular Disorders,” Journal of Ethnopharmacology 114, no. 2 (2007): 114–129.
18. Thomas Julian, Nicholas Glascow, Roxana Syeed, and Panagiotis Zis, “Alcohol-Related Peripheral Neuropathy: A Systematic Review and Meta-Analysis,” Journal of Neurology 266, no. 12 (2019): 2907–2919, at 2907.
19. Khan et al., “Ayurveda and Yoga Management of Chronic Alcoholism Sequelae.” (See note 5.)
20. Rashmi Choudhary, S. R. Inchulkar, and Prafulla, “A Critical Review on Madatyaya (Alcoholism),” International Ayurvedic Medical Journal 6, no. 11 (2018): 2502–2508, at 2506.
21. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24 (Madatyaya Chikitsa Adhyaya), verses 199–205.
22. Ijasul M. Haque, Akhilesh Mishra, Bhupinder Singh Kalra, and Shalini Chawla, “Role of Standardized Plant Extracts in Controlling Alcohol Withdrawal Syndrome—An Experimental Study,” Brain Sciences 11, no. 7 (2021): article 919.
23. Marc Halpern, Principles of Ayurvedic Medicine, 13th ed. (California: Harmony in Health Press, 2020), 5.
24. R. Padmavathi, A. P. Kumar, K. S. Dhamodhini, et al., “Role of Yoga in Stress Management and Implications in Major Depression Disorder,” Journal of Ayurveda and Integrative Medicine 14, no. 5 (2023): article 100767.
25. Patanjali, Yoga Sutras, trans. and commentary Swami Vivekananda, in Raja Yoga (1896; e-book ed.), chapter 1, verse 2; chapter 2, verses 46–49.
26. Patanjali, Yoga Sutras, trans. and commentary Swami Vivekananda, in Raja Yoga (1896; e-book ed.), chapter 2, verses 30, 32.
27. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), vol. III, chapter 1, Pada 4, verses 30–36.
28. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), vol. III, chapter 1, Pada 1, verses 7–8.
29. Ganga N, Anusha Baburaj, and Abhishek S. L., “Achara Rasayana: A Substantial Reference That Can Determine Character Formation in Children,” Journal of Ayurveda and Integrated Medical Sciences 8, no. 3 (2023): 73–79, at 77.
30. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), vol. III, chapter 1, Pada 1, verses 1–2.
31. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24, verses 117–120.
32. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24, verses 144–145.
33. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24, verses 177–179.
34. Agnivesa, Caraka Samhita: Text with English Translation and Critical Exposition Based on Cakrapani Datta’s Ayurveda Dipika, trans. Ram Karan Sharma and Vaidya Bhagwan Dash, Chowkhamba Sanskrit Studies 94 (Varanasi: Chowkhamba Sanskrit Series Office, 2024 reprint), Chikitsa Sthana, chapter 24, verses 98–100.
Abstracts
Copies of the abstracts of the research article sources used in this paper, as required by the program’s research paper guidelines. Three sources (marked below) are paywalled beyond the abstract page itself; for these, the PubMed link to the full, free abstract is given in place of pasted text.
Henry R. Kranzler and Michael Soyka, “Diagnosis and Pharmacotherapy of Alcohol Use Disorder: A Review,” JAMA 320, no. 8 (2018): 815–824.
Importance: Alcohol consumption is associated with 88,000 U.S. deaths annually. Although routine screening for heavy alcohol use can identify patients with AUD and has been recommended, only 1 in 6 U.S. adults report ever having been asked by a health professional about their drinking behavior. Alcohol use disorder (AUD), a problematic pattern of alcohol use accompanied by clinically significant impairment or distress, is present in 14% of U.S. adults, though only 7% of affected individuals are seen in an alcohol treatment facility. Observations: Four medications are approved by the Food and Drug Administration (FDA) to treat AUD: disulfiram, naltrexone–oral and long-acting injectable formulations–and acamprosate. However, patients with AUD most commonly receive counselling. Medications are prescribed to less than 9% of patients who are likely to benefit from them given evidence that they exert clinically meaningful effects and their inclusion in clinical practice guidelines as first-line treatments for moderate-to-severe AUD. Naltrexone, which can be given once daily, reduces the likelihood of a return to any drinking by 5% and binge drinking risk by 10%. Randomized clinical trials also show that some medications approved for other indications, including seizure disorder (e.g., topiramate), are efficacious in treating AUD. Currently there is not sufficient evidence to support the use of pharmacogenetics to personalize AUD treatments. Conclusions and Relevance: Alcohol consumption is associated with a high rate of morbidity and mortality and heavy alcohol use is the major risk factor for AUD. Simple, valid screening methods can be used to identify patients with heavy alcohol use, who can then be evaluated for the presence of AUD and treated with behavioral and/or pharmacological therapies, few of which are used consistently.
Sara M. Nehring, Richard J. Chen, and Andrew M. Freeman, “Alcohol Use Disorder: Screening, Evaluation, and Management,” in StatPearls [Internet] (Treasure Island, FL: StatPearls Publishing, 2026), last updated March 16, 2024.
Alcohol, the most commonly used substance in the United States, has far-reaching health consequences that impact not only individual patients but the entire healthcare system. Alcohol use in and of itself is not problematic but exists along a spectrum from low-risk use to alcohol use disorder (AUD). The diagnosis, based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, criteria, ranges from mild to severe, with withdrawal symptoms and tolerance as key indicators. Screening by primary care clinicians, supported by the United States Preventive Services Task Force, facilitates early detection. Treatment involves shared decision-making, combining pharmacotherapy and behavioral therapy with interdisciplinary collaboration essential for comprehensive care and improved outcomes.
Aqsa Zarin Khan, Jibi Varghese, Shweta Kodre, Mohini Niware, Snehal Pansare, Shreya Bhatia, Samkit Shah, and Manna Mathew, “Ayurveda and Yoga Management of Chronic Alcoholism Sequelae—A Case Report,” Journal of Ayurveda and Integrative Medicine 15, no. 1 (2024): article 100862. (Source for endnotes 5 and 19.)
Alcohol has always been a component in the dietary pattern of human civilization. It is widely used in society for celebration and socialization. Alcohol abuse is among the most serious problems in public health characterized by uncontrolled drinking which causes physical and emotional dependence on alcohol. Chronic alcoholics are at a higher risk of developing vitamin B1 deficiency due to malabsorption, poor diet, and an increased demand for nutrition. Vitamin B1 (Thiamine) is an essential nutrient required for the body’s energy metabolism and proper functioning of the nervous system. A person who excessively consumes madya (alcohol) and then abruptly discontinues drinking and takes recourse to drinking excess madya once again, suffers from Madatyaya Upadrava (chronic alcoholism) that is Vikshay. Here is a case report of an alcoholic patient who ceased drinking and then resumed alcohol in large amounts. He presented with symptoms of generalized weakness, body ache, aphasia, confusion, fever (on and off), thirst, cough, headache, and numbness. The patient underwent a two-month treatment regimen that combined Satvavajay Chikitsa, Yoga, and Shaman Chikitsa involving Rasayana medications and procedures including snehan (Oleation), swedan (fomentation), nabhi puran (filling oil with navel), nasya (nasal administration), shirodhara (continuous flow of liquid on head) and basti (medicated enema). The intervention outcome showed relief from the aforementioned symptoms and improvement in both symptoms and GCS (Glasgow coma scale) score. This treatment approach aimed to promote vitality, longevity, and an overall sense of balance and well-being. There are not many corroborating cases being reported and managed with Ayurveda. This case report highlights transforming health through the cumulative effects of Rasayana medicines, panchakarma, and yoga.
Lauren L. Jophlin, Ashwani K. Singal, Ramon Bataller, Robert J. Wong, Bryan G. Sauer, Norah A. Terrault, and Vijay H. Shah, “ACG Clinical Guideline: Alcohol-Associated Liver Disease,” American Journal of Gastroenterology 119, no. 1 (2024): 30–54.
Alcohol-associated liver disease (ALD) is the most common cause of advanced hepatic disease and frequent indication for liver transplantation worldwide. With harmful alcohol use as the primary risk factor, increasing alcohol use over the past decade has resulted in rapid growth of the ALD-related healthcare burden. The spectrum of ALD ranges from early asymptomatic liver injury to advanced disease with decompensation and portal hypertension. Compared with those with other etiologies of liver disease, patients with ALD progress faster and more often present at an advanced stage. A unique phenotype of advanced disease is alcohol-associated hepatitis (AH) presenting with rapid onset or worsening of jaundice, and acute on chronic liver failure in severe forms conveying a 1-month mortality risk of 20%–50%. The model for end stage disease score is the most accurate score to stratify AH severity (>20 defined as severe disease). Corticosteroids are currently the only available therapeutic with proven efficacy for patients with severe AH, providing survival benefit at 1 month in 50%–60% of patients. Abstinence of alcohol use, a crucial determinant of long-term outcomes, is challenging to achieve in ALD patients with concurrent alcohol use disorder (AUD). As patients with ALD are rarely treated [abstract continues in source].
Ravi Rastogi, Seema Saksena, Narendra Kumar Garg, Narinder Kumar Kapoor, Dharam Pal Agarwal, and Bhola Nath Dhawan, “Picroliv Protects Against Alcohol-Induced Chronic Hepatotoxicity in Rats,” Planta Medica 62, no. 3 (1996): 283–285.
Daily administration of ethyl alcohol (3.76 g/kg, p.o.) for 45 days resulted in significant changes in several biochemical parameters of the liver and serum of albino rats. After exposure to alcohol for 30 days when Picroliv (12 mg/kg, p.o.), an iridoid glycoside fraction of Picrorhiza kurroa, was administered for 15 days along with alcohol, the degree of change in most of the parameters was reduced.
Bhawana Sharma and Rajesh Dabur, “Protective Effects of Tinospora cordifolia on Hepatic and Gastrointestinal Toxicity Induced by Chronic and Moderate Alcoholism,” Alcohol and Alcoholism 51, no. 1 (2016): 1–10. (Paywalled beyond the abstract.)
Abstract available at: https://pubmed.ncbi.nlm.nih.gov/26589585/
K. Muniasamy, N. K. Chander, N. Gudapati, S. Pradeep, E. Raman, R. Saranya, N. S. Babu, and K. Srinidhi, “Cardiologists’ Knowledge and Implementation of Lifestyle Counselling for Cardiovascular Disease Prevention: A National Survey,” Bioinformation 20, no. 12 (2024): 1948–1953.
Cardiovascular disease remains a leading global cause of morbidity and mortality, with lifestyle modification playing a critical role in prevention. This nationwide cross-sectional survey of 100 cardiologists assessed attitudes, practices and knowledge regarding lifestyle counseling for CVD prevention. While most cardiologists recognized the importance of lifestyle counseling, gaps were evident in its consistent implementation, particularly in areas like dietary guidance and physical activity promotion. Key barriers included time and resource constraints and concerns about patient compliance. These findings highlight the need for targeted interventions and training to enhance the integration of lifestyle counseling into clinical practice, fostering a more comprehensive approach to CVD prevention.
Fernando Domínguez, Eric Adler, and Pablo García-Pavía, “Alcoholic Cardiomyopathy: An Update,” European Heart Journal 45, no. 26 (2024): 2294–2305.
Alcohol-induced cardiomyopathy (AC) is an acquired form of dilated cardiomyopathy (DCM) caused by prolonged and heavy alcohol intake in the absence of other causes. The amount of alcohol required to produce AC is generally considered as >80 g/day over 5 years, but there is still some controversy regarding this definition. This review on AC focuses on pathogenesis, which involves different mechanisms. Firstly, the direct toxic effect of ethanol promotes oxidative stress in the myocardium and activation of the renin–angiotensin system. Moreover, acetaldehyde, the best-studied metabolite of alcohol, can contribute to myocardial damage impairing actin–myosin interaction and producing mitochondrial dysfunction. Genetic factors are also involved in the pathogenesis of AC, with DCM-causing genetic variants in patients with AC, especially titin-truncating variants. These findings support a double-hit hypothesis in AC, combining genetics and environmental factors. The synergistic effect of alcohol with concomitant conditions such as hypertension or liver cirrhosis can be another contributing factor leading to AC. There are no specific cardiac signs and symptoms in AC as compared with other forms of DCM. However, natural history of AC differs from DCM and relies directly on alcohol withdrawal, as left ventricular ejection fraction recovery in abstainers is associated with an excellent prognosis. Thus, abstinence from alcohol is the most crucial step in treating AC, and specific therapies are available for this purpose. Otherwise, AC should be treated according to current guidelines of heart failure with reduced ejection fraction. Targeted therapies based on AC pathogenesis are currently being developed and could potentially improve AC treatment in the future.
Julian Mustroph, Simon Lebek, Lars S. Maier, and Stefan Neef, “Mechanisms of Cardiac Ethanol Toxicity and Novel Treatment Options,” Pharmacology & Therapeutics 197 (2019): 1–10. (Paywalled beyond the abstract.)
Abstract available at: https://pubmed.ncbi.nlm.nih.gov/30557629/
Shridhar Dwivedi, “Terminalia arjuna Wight & Arn.—A Useful Drug for Cardiovascular Disorders,” Journal of Ethnopharmacology 114, no. 2 (2007): 114–129. (Paywalled beyond the abstract.)
Abstract available at: https://pubmed.ncbi.nlm.nih.gov/17875376/
Thomas Julian, Nicholas Glascow, Roxana Syeed, and Panagiotis Zis, “Alcohol-Related Peripheral Neuropathy: A Systematic Review and Meta-Analysis,” Journal of Neurology 266, no. 12 (2019): 2907–2919.
The primary aim of this systematic review was to establish the prevalence, character, and risk factors of peripheral neuropathy amongst chronic alcohol abusers and to identify the most appropriate management strategies. In this review, possible pathogenetic mechanisms are also discussed. A systematic, computer-based search was conducted using the PubMed database. Data regarding the above parameters were extracted. 87 articles were included in this review, 29 case–control studies, 52 prospective/retrospective cohort studies and 2 randomised control trials, 1 cross sectional study, and 3 population-based studies. The prevalence of peripheral neuropathy amongst chronic alcohol abusers is 46.3% (CI 35.7–57.3%) when confirmed via nerve conduction studies. Alcohol-related peripheral neuropathy generally presents as a progressive, predominantly sensory axonal length-dependent neuropathy. The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed. At present, it is unclear what the pathogenetic mechanisms for the development of neuropathy amongst those who chronically abuse alcohol are, and therefore, it is unknown whether it is attributed to the direct toxic effects of ethanol or another currently unidentified factor. There is presently sparse data to support a particular management strategy in alcohol-related peripheral neuropathy, but the limited data available appears to support the use of vitamin supplementation, particularly of B-vitamin regimens inclusive of thiamine.
Rashmi Choudhary, S. R. Inchulkar, and Prafulla, “A Critical Review on Madatyaya (Alcoholism),” International Ayurvedic Medical Journal 6, no. 11 (2018): 2502–2508.
Madya (Alcohol) and Madatyaya (Alcoholism) is not a new problem in Ayurveda and description found since Vedic literature. But its relation with Health and Social Problem are continuously increasing day by day. In Ayurveda, the varieties of disorders caused by the excessive and improper use of alcohol are well described and documented under one heading ‘Madatyaya’ or ‘Panatyaya’. It is a Saanipataja Vyadhi (caused by vitiation of all three Doshas – Vata, Pitta and Kapha). It mainly vitiates Ojas, as Madya (alcohol) have opposite quality of Ojas. Alcohol is treated as poison (neurotoxic cerebral inebriant poison) when consume much more dose and as medicine in limited dose. In this contemporary era every disease is being understood by comparing it with modern parlance. Here is a small effort to understand the features of Madatyaya in terms of modern perspective. By understanding the features of Madatyaya we can say that Madatyaya is not just an alcohol intoxication, dependence or withdrawal state, but it is the condition where multiple systemic dysfunctions are involved from immediate and acute manifestations to chronic and severe manifestations. Neurological, gastro-hepatic and cardio-pulmonary manifestations are the commonest features seen in the patients of Madatyaya which is also similar to the descriptions of alcoholism.
Ijasul M. Haque, Akhilesh Mishra, Bhupinder Singh Kalra, and Shalini Chawla, “Role of Standardized Plant Extracts in Controlling Alcohol Withdrawal Syndrome—An Experimental Study,” Brain Sciences 11, no. 7 (2021): article 919.
Patients with alcohol use disorder experience alcohol withdrawal syndrome due to the sudden cessation of alcohol. This study was designed to evaluate the protective effect of Ashwagandha and Brahmi on alcohol withdrawal in rats. Thirty rats of either sex were taken and randomly divided into 6 groups (n = 5). Their normal diet was replaced by a modified liquid diet (MLD). Ethanol was added gradually except in the MLD group for a period of 21 days and withdrawn suddenly. Four treatment groups were administered Ashwagandha (3.75 mg of withanolide glycosides per kg body weight), Brahmi (10 mg of bacosides per kg body weight), Ashwagandha + Brahmi (3.75 mg withanolide glycosides + 10 mg bacosides per kg body weight) orally and diazepam (1 mg/kg body weight, i.p.) 45 min before alcohol withdrawal. Rats were assessed for behavioural changes (agitation score and stereotypic behaviour), anxiety and locomotor activity at 2nd and 6th hours of alcohol withdrawal. Pentylenetetrazol (PTZ) kindling seizures were assessed at 6th hour of alcohol withdrawal. Ashwagandha and Brahmi alone and in combination significantly reduced the behavioural changes in alcohol withdrawal rats at 2nd hour and their combination in 6th hour. Ashwagandha and Brahmi suppressed PTZ kindling seizures effectively and improved locomotory activity at 2nd hour and 6th hour of alcohol withdrawal. Reduction in anxiety was significant among Ashwagandha at 2nd hour and the combination group at 2nd and 6th hour. The results were comparable to diazepam. Ashwagandha and Brahmi have beneficial effects in controlling the behavioural changes, anxiety and seizures in alcohol withdrawal symptoms in rats and improved locomotory activity.
R. Padmavathi, A. P. Kumar, K. S. Dhamodhini, et al., “Role of Yoga in Stress Management and Implications in Major Depression Disorder,” Journal of Ayurveda and Integrative Medicine 14, no. 5 (2023): article 100767.
Major Depressive Disorder (MDD) is one of the leading causes of disability affecting more than 340 million people and second largest contributor to global burden of disease. Chronic stress is a common risk factor and important contributor for MDD. Stress could be defined as the “perceived inability to cope”. Stressful life events are shown to provoke a sequence of psychological and physiological adjustments including nervous, endocrine and immune mechanisms. Stress can lead to elevation of a variety of inflammatory cytokines and stress hormones, can cause autonomic dysfunction and imbalance in neurotransmitters. Yoga can reduce depressive symptoms by alleviating stress. Studies have shown that yoga can reduce inflammation, maintain autonomic balance and also has a role in maintaining the neurotransmitters. It has role on hypothalamic–pituitary–adrenal (HPA) axis, the peripheral nervous system including GABA, limbic system activity, inflammatory and endocrine responses. Yoga along with antidepressants can help in reducing the depressive symptoms in patient with MDD. Yoga is an ideal complementary and alternative therapy for mental health disorders.
Ganga N, Anusha Baburaj, and Abhishek S. L., “Achara Rasayana: A Substantial Reference That Can Determine Character Formation in Children,” Journal of Ayurveda and Integrated Medical Sciences 8, no. 3 (2023): 73–79.
Character, being an aggregate of physical & mental traits that can distinguish and individualize a person, marks its emergence right from early childhood. Since formation of character is a gradual process, influence of parents, teachers, friends, the people they talk to frequently, the food habits they follow, the circumstances they pass through, the books they read, the cinemas and videos they watch, influence of social media, the environment they live in etc. plays a very vital role in shaping a child’s personality. Ayurvedic concepts like Dinacharya, Rithucharya, Sadvritta, Achara Rasayana, remain as concepts in the texts and it is a necessity now, to inculcate these habits in daily life of children, in the early period of growth itself as it can pave a path to healthy physique & happy mental status throughout their livelihood. Achara Rasayana, a set of factors that include all these influential factors listed one by one, is till date valid yet unexplored to its fullest applicability. Aim: To evaluate the contents of Achara Rasayana and explore the ways in which it can influence character framing in children. Conclusion: The values prescribed in Achara Rasayana serves as milestones for step-by-step modification of character, if followed from early childhood. These factors are to be practiced daily, or included in the new education system as they can influence in creating quality minds and sustain it throughout the life, maintaining physical, mental, social, spiritual upgradation ending in health. Parents, educators, near surroundings of the children, should be aware of the actuality and train them with these core values to build in a healthy society.