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PubMed1978

Common alcohol-related disorders: recognition and management.

Appropriate medical treatment of alcoholics often falls between the clinical specialties of psychiatry, internal medicine, toxicology, and neurology. All physicians need to have a high index of suspicion for alcoholism, since the diagnosis of alcohol dependence is frequently overlooked. Especially when alcoholics are self-referred to nonmedical agencies, their medical complications may be inadequately treated or unrecognized. Common alcohol-related complications requiring treatment include: (1) clinicopathologic disorders, often associated with the gastroenterologic or cardiorespiratory systems, including alcoholic cirrhosis, (2) peripheral myoneural effects, (3) neuropsychiatric complications (delirium tremens, acute alcoholic hallucinosis, Korsakoff's psychosis, alcoholic dementia), and (4) psychosocial disability.

Acute Disease↗
PubMed1977

Diseases in urban and rural Black populations.

Diseases of urban and rural Blacks in South Africa are reviewed. In rural Blacks the major problems are infection and malnutrition. Other important disorders include cancer of the oesophagus, liver and cervix, and rheumatic heart disease and cardiomyopathy. The diseases in urban Blacks are those of a population in transition. Characterised by all gradations of socioeconomic development, from the relatively primitive to the completely westernised, these people exhibit a correspondingly wide and varied range of disease embracing the afflictions of rural dwellers and the new diseases of the city. Whereas the prevalence of some of the former, such as infection and malnutrition, is declining, they still constitute a considerable problem in urban Blacks. More important is the increasingly serious impact of the new disorders, which may be divided into two groups: (a) a large range and variety of alcohol-related disorders with serious effects at the social, economic, psychological and physical levels; and (b) most, if not all, of the diseases encountered in western populations. Some of these, such as obesity and hypertension, have not only attained epidemic proportions among urban Blacks, but their prevalence may actually have exceeded that among Whites. Other conditions, such as coronary heart disease, gout, gallstones and colonic cancer, which emerged later, are relatively uncommon or rare. A plea is made for much greater epidemiological research. This is necessary in order to obtain reliable knowledge of the prevalence of disease, to determine the best ways of applying present knowledge with existing and future resources, and to obtain knowledge regarding both old and new diseases of which the pathogenesis is still obscure.

Adult↗
PubMed2026

Single-nucleus profiling reveals hepatocyte identity and immune features associated with corticosteroid response in severe alcohol-related hepatitis.

BACKGROUND & AIMS: Severe alcohol-related hepatitis (sAH) is associated with high short-term mortality. However, 30-40% of patients fail to respond to corticosteroids, the only proven pharmacological treatment. The pathophysiological mechanisms underlying sAH and the marked heterogeneity in treatment response remain incompletely understood. We aimed to define cellular changes associated with corticosteroid response in sAH and to identify baseline markers predictive of treatment outcome. METHODS: Single-nucleus RNA sequencing was performed on liver biopsies from patients with biopsy-proven sAH (n = 17), including paired baseline and day 8 biopsies in a subset of patients (n = 8). Patients were classified as corticosteroid responders (sAH-R; Lille score <0.45) or non-responders (sAH-NR; Lille score &#x2265;0.45). Liver biopsies from patients with acute decompensation of alcohol-related cirrhosis (AD; n = 5) and healthy controls (n = 4) were included for comparison. Findings were validated using immunohistochemistry and spatial proteomics in a large multicenter validation cohort (n = 172). RESULTS: At baseline, sAH-R exhibited a significantly higher proportion of liver-infiltrating S100A8+ monocytes compared to sAH-NR, a difference that persisted at day 8. sAH livers showed a marked reduction in mature hepatocytes and an expansion of stressed and intermediate hepatocyte populations, indicating progressive loss of mature hepatocyte identity. This loss was more pronounced in sAH-NR, who also exhibited fewer cycling hepatocytes at day 8, consistent with impaired regenerative capacity. Expression of SULT2A1, a marker of mature hepatocyte identity, was significantly reduced in sAH-NR at baseline. Finally, liver biopsies with &#x2265;50% SULT2A1-positive hepatocytes at baseline were strongly predictive of corticosteroid response. CONCLUSIONS: This study delineates distinct immune and hepatocyte changes associated with corticosteroid response in sAH. Baseline SULT2A1 expression may facilitate stratified treatment approaches in sAH. IMPACT AND IMPLICATIONS: Severe alcohol-related hepatitis (sAH) represents one of the most devastating manifestations of alcohol-related disorders. sAH is characterized by acute hepatic inflammation and high short-term mortality. Clinical management remains challenging, as corticosteroids - the only pharmacological therapy currently applied - are ineffective in a substantial proportion of patients and are associated with significant adverse effects. These limitations highlight the need for a more detailed understanding of sAH pathophysiology and for approaches that enable improved patient stratification and therapeutic decision-making. In this study, we identify distinct pre-treatment differences between corticosteroid responders and non-responders at the level of both hepatocytes and myeloid cells, providing new insight into the cellular mechanisms underlying treatment heterogeneity in sAH. Furthermore, leveraging these findings, we developed a histology-based SULT2A1 scoring system using a commercially available antibody, which predicts corticosteroid response at baseline and may support stratified treatment approaches in clinical practice.

Humans↗
PubMed1977

Sex-related differences among 100 patients with alcoholic liver disease.

During 1975 we studied 100 patients--77 men and 23 women--who had a history of alcohol abuse and disturbed liver function test results. On presentation the women were less likely to be suspected of alcohol abuse (9; 38%) than the men (59; 77%). Although the quantity of alcohol consumed and length of history of alcohol abuse were similar for men and women, the incidence of chronic advanced liver disease was higher among women (86%) than among men (65%). Women, however, were less likely to have developed primary liver cell cancer. Overall the women had a higher incidence of other alcohol-related disorders and were less likely to stop abusing alcohol (2; 9%) than were their male counterparts (22; 29%). Women seem to be more susceptible to alcohol-related disease.

Adult↗
PubMed1977

Cross-racial foster home placement among native American psychiatric patients.

In Minnesota, about 0.5 percent of the general population are raised outside of their biologic homes. However, it has been estimated that 25 to 30 percent of all Indian children under the age of 18 years are currently living outside of their biologic homes. Clinical experience with adolescent and adult Indian psychiatric patients bears this out: about half of them have been raised in foster or adoptive homes.Seventeen American Indian patients who had been raised in non-Indian foster and adoptive homes were interviewed for five to ten hours each. Data were collected from the patients and social agencies regarding demographic characteristics, social coping, and current clinical problems. In addition, information obtained regarding their out-of-family placement included: age at placement, reason for placement, number of subsequent placements, and interracial and intraracial relationships during placement and subsequently during adulthood.This clinical sample shows a low rate of psychosis and neurosis, but a high rate of alcohol-related disorders, suicide attempts, and behavioral problems. While their education is average, their employment and marital status shows marked social disability. Most have had numerous childhood placements over a long period, all in white homes, and none have subsequently returned to their family-of-origin.These unfortunate human beings have been described by both whites and Indians in Minnesota as "apples": racially "red" or Indian on the outside, but culturally white on the inside. White groups do not accept them as whites because they are distinctively racial Indians, but they do not feel at ease in Indian communities since they were raised with white values and attitudes. While some of these people do indeed make successful adjustments in Indian or white society (or both) the results of this study show that many apparently do not.

Acculturation↗
PubMed2026

The effectiveness of protective behavioral strategies for reducing alcohol use and alcohol-related harms among adults: A systematic review and meta-analysis of randomized controlled trials.

OBJECTIVES: Excessive alcohol consumption is a major public health concern. Protective behavioral strategies (PBS) are widely incorporated into alcohol interventions, but their effectiveness and role as mechanisms of behavior change remain unclear. This systematic review and meta-analysis evaluated the effects of PBS-based interventions on alcohol consumption, alcohol-related harms, and PBS use. METHODS: PubMed, Embase, Scopus, CINAHL, and ProQuest were searched from inception to December 2025 for randomized controlled trials (RCTs) of adults (&#x2265;18 years) delivering PBS as an active intervention component. Random-effects meta-analyses using Hedges' g examined alcohol quantity, drinking frequency, alcohol-related problems, and PBS use. RESULTS: Fifteen RCTs were included, predominantly involving young adults attending U.S. universities. PBS interventions increased protective strategy use (g=0.23, p=0.005 after outlier removal), but alcohol effects were modest: no change in quantity (g=-0.05, p=0.162), small reduction in frequency (g=-0.09, p=0.014), and marginal reduction in problems (g=-0.07, p=0.052; significant in sensitivity analysis). Subgroup findings suggested greater effects at longer follow-up and when PBS was incorporated into multi-component interventions. Evidence supporting PBS as a mechanism of change was limited and inconsistent. CONCLUSIONS: PBS-based interventions produce modest, context-dependent effects on alcohol outcomes. Most evidence comes from young U.S. university students, underscoring the need for studies in more diverse adult populations and further mechanistic research.

Humans↗
PubMed1978

Family history as a diagnostic aid in two samples of adolescents.

Psychiatric diagnostic patterns were examined in two different samples of adolescents, one a group of psychiatric inpatients and the second youth apprehended by the law for alcohol-related difficulties. Affective disorder in parents was most closely correlated with a similar patient diagnosis or constellation of depressive-type symptoms in both samples of youth. Parental antisocial personalities, alcohol abuse, or drug problems correlated most closely with high levels of similar difficulties in individuals in the two studied groups. However, antisocial, alcohol, or drug problems of a mild degree were present in all subgroups of the two samples, perhaps representing a nonspecific reaction to parental illness or the occurrence of a broken home. A follow-up of future problems in both samples will be carried out to determine the importance of the family history and clinical picture in predicting the future course of problems.

Adolescent↗
PubMed1979

The relationship of family history of alcoholism to primary affective disorder.

One hundred sixty-eight patients with primary affective disorder were studied regarding history of alcohol-related problems. Alcohol-related problems were identified in 19 patients. We found that the morbid risk for alcoholism was significantly increased among relatives of male patients with drinking problems as compared to relatives of male patients without drinking problems. Our data suggest that psychiatric illness in relatives of probands with severe bipolar illness tends to be affective disorder tends to include alcoholism plus affective disorder.

Alcoholism↗
PubMed1977

Isolation of pi-alcohol dehydrogenase of human liver: is it a determinant of alcoholism?

HUMAN LIVER ALCOHOL DEHYDROGENASE (ALCOHOL: NAD(+) oxidoreductase, EC 1.1.1.1), homogeneous by physicochemical criteria, has been available in quantity only recently [Lange, L. G. & Vallee, B. L. (1976) Biochemistry 15, 4681-4686]. Until now, the biochemical basis of human alcohol metabolism had to be extrapolated from the properties and behavior of enzymes from other species, primarily horses and yeast. The biological determinants of human alcoholism have remained obscure, although recent evidence indicates a genetic predisposition, requiring delineation. A functionally distinct form of human liver alcohol dehydrogenase (ADH), which we have designated II-ADH, is provocative since, thus far, it seems to be unique to human beings. It has a high K(m) for ethanol and is remarkably insensitive (apparent K(I), 500 muM) to pyrazole and its derivatives, which are usually potent ADH inhibitors (K(I), 1 muM), a property that is the basis for the isolation of II-ADH. The affinity resin 4-[3-(N-6-aminocaproyl)aminopropyl]pyrazole-Sepharose binds all other known forms of ADH but not II-ADH, thereby separating it selectively by affinity chromatography. In turn, this has led to the establishment of its identity with that enzyme form which was previously known as the anodic band and characterized by a high K(m) for ethanol (20 mM at pH 7.5). The remarkable insensitivity of II-ADH to pyrazole inhibition has also permitted quantitation of its role in hepatic ethanol oxidation. At 5 mM ethanol, a saturating concentration for virtually all other forms of ADH, II-ADH contributes less than 15% to total ethanol oxidation. However, at intoxicating concentrations, e.g., 60 mM, it can account for as much as 40% of the total ethanol oxidation rate of liver, indicating a seemingly unique role for this enzyme form in ethanol elimination. Thus far, we have found the amount of II-ADH varies from liver to liver of individuals and is considerably more labile than the other molecular forms, phenomena whose inter- or independence requires further study. The isolation of human II-ADH advances efforts to recognize and understand biochemical mechanisms that may be biological determinants of alcoholism and alcohol-related disease states, now generally approached and managed largely as psychosocial disorders.

Alcohol Oxidoreductases↗
PubMed1975

The influence of ascorbic acid on platelet structure and function.

To determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidification levels. The effect of ascorbic acid (A.A.) was compared to that of HCl and citric acid (C.A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A.A. and C.A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultrastructure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A.A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

Adenosine Diphosphate↗
PubMed2024

Characterizing midlife-onset alcohol dependence: Implications for etiology, prevention, and healthy aging.

We evaluated the developmental epidemiology of midlife-onset alcohol dependence (AD) in the Dunedin Study (N=1,037), a population-representative cohort followed across five decades. At ages 18, 21, 26, 32, 38, and 45, past-year AD prevalence was 11.0%, 18.4%, 13.6%, 8.1%, 9.6%, and 11.3%, respectively. As expected, relative to never-diagnosed individuals, those with early-onset AD (first diagnosis: age-18 or age-21, prevalence=22.9%) were distinguished by a range of early-life and adult correlates. Individuals with midlife-onset AD (first diagnosis: age-38 or age-45, prevalence=5.6%) were distinguished by fewer early-life correlates, but exhibited a family history of AD, and adolescent dysregulation and marijuana-use. They were characterized by an array of adult correlates, including internalizing disorders, mental-health treatment-contact, criminal-behavior, perceived-stress, coping-by-drinking, lower likelihood of marriage and parenthood, and reduced preparedness for old age. They also experienced more adult alcohol-related impairment than the early-onset group. Results can guide efforts to reduce midlife alcohol-related problems and support healthy aging.

Journal Article↗
PubMed2026

Puerarin Attenuates Binge Ethanol-Induced Cortical Neurotoxicity in Association with AKT/mTOR Signaling and Autophagy-Related Responses.

Puerarin (Pue), a major isoflavone derived from Pueraria lobata, has demonstrated neuroprotective potential in multiple neurological disorders; however, its effects on ethanol (EtOH)-induced cortical injury and the associated molecular responses remain incompletely understood. In the present study, network pharmacology was combined with in vivo and in vitro experiments to investigate molecular responses associated with the effects of Pue on EtOH-induced neurotoxicity. Public databases were used to predict targets of Pue and alcohol-related brain injury, followed by protein-protein interaction analysis, Gene Ontology annotation, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment. A total of 101 overlapping targets were identified, among which TNF, AKT1, EGFR, TP53, and PPARG emerged as major hub targets, and PI3K-Akt signaling pathway was among the pathways that remained significantly enriched after FDR correction. In a 4-day binge EtOH rat model, Pue attenuated EtOH-associated increases in oxidative stress, neuronal degeneration, and apoptotic markers in cortical tissue. This was accompanied by attenuation of the EtOH-associated reductions in the p-AKT/AKT and p-mTOR/mTOR ratios, as well as an attenuation of EtOH-associated changes in LC3, ATG5, and Beclin-1 expression. In primary cortical neurons, Pue partially attenuated the EtOH-associated loss of neuronal viability and preserved neurite morphology. Bafilomycin A1 (BafA1)-based analysis of LC3-II and p62/SQSTM1 showed an overall BafA1-sensitive increase in LC3-II without a significant treatment-dependent difference in the BafA1 response. Collectively, these findings suggest that Pue attenuates binge EtOH-induced cortical neurotoxicity in association with changes in AKT/mTOR phosphorylation and autophagy-related responses.

AKT/mTOR signaling↗
PubMed1978

[Alcohol-related disturbances in haematopoiesis (author's transl)].

Alcohol-related disturbances are seen against the three blood cell systems. They appear after important alcohol consumption within few days and are independent from the existence of liver cirrhosis with splenomegaly. They are promptly and completely reversible after interruption of alcohol supply. Disturbances in erythropoiesis are manifested in bone marrow with megaloblasts, ring sideroblasts, and vacuoles in cytoplasma and nucleus of nucleated red cells. They are caused by folate deficiency and by perturbations of iron utilization, which is perhaps connected with impaired heme synthesis following pyridoxal phosphate deficiency. Serum iron generally increases during alcohol consumption and decreases in the following alcohol-free period. The anemia may be macrocytic and normochromic or dimorphic with hypochromic microcytes. Anemias of hard alcohol drinkers are observed also as consequence of bleeding or hemolysis of different causes. The lability against infections of drinkers is associated with changes in granulopoiesis. The most important findings are granulocytopenia, vacuoles in the immature marrow cells, perturbations in granulopoietic maturation, and decrease of marrow response. Frequently, alcohol drinkers demonstrate thrombocytopenia which is caused by ineffective thrombopoiesis and by shortened life span of platelets as direct effect of ethanol. Functional impairments of thrombocytes have been published, too.

Alcoholism↗
PubMed1979

Biological investigations in alcohol research.

The biological mechanisms examined in this paper cover only a small portion of those that may be involved in the pathogenesis of alcoholism. Certain areas on which a great deal of work has already been done have been entirely omitted. Among these are studies on brain acetylcholine and gamma-aminobutyric acid metabolism in alcohol-related conditions; the effect of alcohol on brain proteins and nucleotides and the relationship of changes in these to the development of tolerance and physical dependence; and a variety of other areas involving biochemical and physiological parameters. The omission of any of these areas in no way suggests that they are less significant than those that have been covered. It is just that I have attempted to present a cohesive and coherent review of some areas of biological research which thus far appear to throw light on the clinical development and phenomenology of the alcoholism syndrome. In order to present such a thesis, I have inevitably crowded the evidence to fit some of my pet hypotheses. However, in controversial areas (which are many), I have tried to present some of the evidence on both sides and, hopefully, have succeeded in offering a fair overview of the state of the science as it exists today.

Alcohol Drinking↗
PubMed2025

Global Changes in Gene Expression and Splicing in Alcoholic Liver Disease.

Alcohol use disorder is a widespread illness commonly leading to alcoholic liver disease (ALD) and cirrhosis with an increased incidence of hepatocellular carcinoma (HCC), but the mechanisms of alcohol-related oncogenesis in the liver are incompletely understood. We tested the hypothesis that ALD predisposes to HCC via dysregulation of splicing. RNA sequencing was performed on liver biopsies from patients with different stages of ALD: early alcoholic steatohepatitis (eASH), non-severe alcoholic hepatitis (nsAH), and severe alcoholic hepatitis (sAH); furthermore, explants were collected from patients who underwent liver transplantation due to sAH (exAH). We found that alcohol caused widespread changes in transcriptome in all stages of ALD: among ~ 58,000 analyzed genomic features, ~ 4,900 were altered in eASH, ~ 9,100 - in nsAH, 14,100 - in sAH, and ~ 14,300 - in exAH. We observed thousands of missplicing events in all hepatic conditions, with mutually exclusive exons (MEE) being the most common event and exon skipping (ES) - second most common event. Analysis of ~ 600,000 exons revealed that ALD is associated with a genome-wide effect on exon expression, with ~ 50,000 exons being differentially expressed in eASH, ~ 130,000 - in nsAH, ~ 150,000 - in sAH, and ~ 120,000 - in exAH. To determine whether alcohol directly perturbs splicing, we subjected rats to alcohol vapor for 7 weeks and found that the expression of multiple snRNAs was drastically decreased, while expression of splicing factors was not affected. Screening of oncogenes and tumor suppressors, commonly involved in HCC pathogenesis, revealed that ALD affected the hepatic expression and/or splicing of most of these cancer-related genes. In summary, it appears that alcohol causes profound genome-wide changes in gene expression and splicing in the liver, likely via affecting the spliceosome. This results in altered expression and missplicing of key oncogenes and tumor suppressors involved in HCC, suggesting a novel mechanism of oncogenesis in the liver of patients with ALD.

alcohol use disorder↗
PubMed1979

Alcohol-related diseases and carcinogenesis.

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.

Alcoholism↗