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Clinics in Dermatology 1999
Review
Topics: Anaphylaxis; Diagnosis, Differential; Ethanol; Flushing; Humans; Hypersensitivity, Immediate; Urticaria
PubMed: 10497726
DOI: 10.1016/s0738-081x(99)00027-9 -
Drug and Alcohol Dependence Jun 1983The effects of alcohol on the formation of prostaglandins (PGs) and the blockade of some actions of alcohol by PG-inhibitors suggest that PGs may be involved in the... (Review)
Review
The effects of alcohol on the formation of prostaglandins (PGs) and the blockade of some actions of alcohol by PG-inhibitors suggest that PGs may be involved in the action of ethyl alcohol. Regulation of lipid peroxidation and synthesis and release of precursor fatty acids may affect the overall formation of PGs. The effect of alcohol may be qualitative for several reasons: (i) the possible preferred formation of 1-series of PGs would mean an important qualitative change in PG-impact in some tissues; (ii) inhibition of PG-metabolism in the lung might affect mostly the plasma levels of PGE; (iii) a selective blockade of certain PG-effects and a potentiation of some others gives rise to qualitative changes in the actions of PGs. PGs may be involved in several acute or short-term reactions caused by alcohol. Chlorpropamide-alcohol flush, alcohol intolerance and hangover are effectively alleviated by a prophylactic use of PG-inhibitors. Speculatively PGs might also be involved in migraine attacks provoked by alcohol and in antabuse in reaction. The roles of PGs in the regulation of vascular tone, water and electrolyte balance as well as in certain secretory and metabolic processes may be important in the generation of alcohol related reactions.
Topics: Alcoholic Intoxication; Animals; Chlorpropamide; Disulfiram; Drug Interactions; Ethanol; Humans; Migraine Disorders; Prostaglandins
PubMed: 6352219
DOI: 10.1016/0376-8716(83)90016-9 -
Cell Feb 2024Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although...
Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.
Topics: Animals; Mice; Anti-Bacterial Agents; Butyrates; Carbohydrate Metabolism, Inborn Errors; Clostridium; Escherichia coli; Gastrointestinal Microbiome; Sorbitol
PubMed: 38366592
DOI: 10.1016/j.cell.2024.01.029 -
Alcohol and Alcoholism (Oxford,... 1999Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can... (Review)
Review
Alcohol and histamine metabolic pathways in the body have the common enzymes aldehyde dehydrogenase and aldehyde oxidase. The metabolite of ethanol, acetaldehyde, can effectively compete with the metabolites of histamine, methylimidazole acetaldehyde, and imidazole acetaldehyde. At the periphery, alcohol and acetaldehyde liberate histamine from its store in mast cells and depress histamine elimination by inhibiting diamine oxidase, resulting in elevated histamine levels in tissues. Histamine mediates alcohol-induced gastric and intestinal damage and bronchial asthma as well as flushing in Orientals. On the other hand, alcohol provokes food-induced histaminosis and histamine intolerance, which is an epidemiological problem. There are many controversial reports concerning the effect of H2 receptor antagonists on ethanol metabolism and the activity of alcohol dehydrogenase in the stomach. In addition, alcohol affects histamine levels in the brain by modulating histamine synthesis, release, and turnover. Histamine receptor antagonists can affect ethanol metabolism and change the sensitivity of animals to the hypnotic effects of alcohol. In contrast to other neurotransmitters, the involvement of the brain histamine system in the mechanisms of the central actions of alcohol and in the pathogenesis of alcoholism is poorly studied and understood.
Topics: Alcohol Deterrents; Animals; Drug Interactions; Ethanol; Ethnicity; Flushing; Histamine; Histamine Agonists; Histamine H1 Antagonists; Histamine H2 Antagonists; Humans; Receptors, Histamine
PubMed: 10344773
DOI: 10.1093/alcalc/34.2.141 -
Nature Reviews. Gastroenterology &... May 2024
Topics: Humans; Sorbitol; Food Intolerance
PubMed: 38528200
DOI: 10.1038/s41575-024-00921-4 -
British Medical Journal Aug 1966
Clinical Trial
Topics: Ethanol; Female; Hemorrhage; Hodgkin Disease; Humans; Male; Neoplasms; Pain
PubMed: 5912509
DOI: 10.1136/bmj.2.5511.437 -
Gastroenterology Jan 2014A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) often is used to manage functional gastrointestinal symptoms in... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND & AIMS
A diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) often is used to manage functional gastrointestinal symptoms in patients with irritable bowel syndrome (IBS), yet there is limited evidence of its efficacy, compared with a normal Western diet. We investigated the effects of a diet low in FODMAPs compared with an Australian diet, in a randomized, controlled, single-blind, cross-over trial of patients with IBS.
METHODS
In a study of 30 patients with IBS and 8 healthy individuals (controls, matched for demographics and diet), we collected dietary data from subjects for 1 habitual week. Participants then randomly were assigned to groups that received 21 days of either a diet low in FODMAPs or a typical Australian diet, followed by a washout period of at least 21 days, before crossing over to the alternate diet. Daily symptoms were rated using a 0- to 100-mm visual analogue scale. Almost all food was provided during the interventional diet periods, with a goal of less than 0.5 g intake of FODMAPs per meal for the low-FODMAP diet. All stools were collected from days 17-21 and assessed for frequency, weight, water content, and King's Stool Chart rating.
RESULTS
Subjects with IBS had lower overall gastrointestinal symptom scores (22.8; 95% confidence interval, 16.7-28.8 mm) while on a diet low in FODMAPs, compared with the Australian diet (44.9; 95% confidence interval, 36.6-53.1 mm; P < .001) and the subjects' habitual diet. Bloating, pain, and passage of wind also were reduced while IBS patients were on the low-FODMAP diet. Symptoms were minimal and unaltered by either diet among controls. Patients of all IBS subtypes had greater satisfaction with stool consistency while on the low-FODMAP diet, but diarrhea-predominant IBS was the only subtype with altered fecal frequency and King's Stool Chart scores.
CONCLUSIONS
In a controlled, cross-over study of patients with IBS, a diet low in FODMAPs effectively reduced functional gastrointestinal symptoms. This high-quality evidence supports its use as a first-line therapy.
CLINICAL TRIAL NUMBER
ACTRN12612001185853.
Topics: Adult; Case-Control Studies; Cross-Over Studies; Disaccharides; Female; Fermentation; Humans; Irritable Bowel Syndrome; Male; Middle Aged; Monosaccharides; Oligosaccharides; Single-Blind Method; Sugar Alcohols; Treatment Outcome; Young Adult
PubMed: 24076059
DOI: 10.1053/j.gastro.2013.09.046 -
Allergologie Select 2018Hypersensitivity reactions to alcoholic beverages (particularly red wine) are relatively frequent, affecting 10% of the general population. Hypersensitivity reactions... (Review)
Review
Hypersensitivity reactions to alcoholic beverages (particularly red wine) are relatively frequent, affecting 10% of the general population. Hypersensitivity reactions due to alcoholic drinks, mainly in the form of airway reactions (rhinitis and asthma), occur significantly more frequently in persons with pre-existing rhinitis and asthma. In terms of pathogenesis, it has to be differentiated between immunologic, mainly IgE-mediated, hypersensitivity reactions (wine allergies), and intolerance reactions in which no causative allergen-specific immune mechanisms can be detected. Allergens responsible for wine allergy could be: grape () proteins (particularly the major allergen lipid transfer protein Vit v1), proteins and ingredients used for the fining of wines such as fish gelatin or isinglass (swim bladder of the fish huso, family of sturgeons), ovalbumin, dairy (casein) products, gum arabic, enzymes (lysozyme, pectinase, glucanase, cellulase, glucosidase, urease, aromatic enzymes), molds (particularly ) responsible for the noble rot in wines, yeasts and proteins from insects that contaminated the mash. Type 1 allergic reactions (positive prick tests) have been described for inorganic components like ethanol, acetaldehyde, acetic acid and sulfites, but no specific IgE could be detected in the serum. Ethanol, acetaldehyde and acetic acid, flavonoids (anthocyanins and chatechines), sulfites, histamine and other biogenic amines are the main causative agents of intolerance reactions (pseudoallergic reactions) to wine. After a short historic review of viticulture and the importance of wine in classical antiquity, we go into the chemical processes of alcoholic fermentation and the genetically inherited "flush syndrome" caused by an acetaldehyde dehydrogenase 2 polymorphism, subsequently we focus on the different etiologic factors of allergies and intolerance reactions to wine. The most frequent intolerance reactions to sulfites occur particularly after the ingestion of white wine and in asthma patients. Intolerance reactions to histamine and other biogenic amines occur mainly after ingestion of red wine and in persons with diamine oxidase (DAO) deficiency.
PubMed: 31826033
DOI: 10.5414/ALX01420E -
CMAJ : Canadian Medical Association... May 2013
Topics: Adult; Alcohol Drinking; Chest Pain; Diagnosis, Differential; Ethanol; Hodgkin Disease; Humans; Lymph Nodes; Male; Radiography
PubMed: 23091182
DOI: 10.1503/cmaj.120974 -
PloS One 2023There is significant overlap between non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD) with regards to risk factors and disease...
BACKGROUND AND AIMS
There is significant overlap between non-alcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD) with regards to risk factors and disease progression. However, the mechanism by which fatty liver disease arises from concomitant obesity and overconsumption of alcohol (syndrome of metabolic and alcohol-associated fatty liver disease; SMAFLD), is not fully understood.
METHODS
Male C57BL6/J mice were fed chow diet (Chow) or high-fructose, high-fat, high-cholesterol diet (FFC) for 4 weeks, then administered either saline or ethanol (EtOH, 5% in drinking water) for another 12 weeks. The EtOH treatment also consisted of a weekly 2.5 g EtOH/kg body weight gavage. Markers for lipid regulation, oxidative stress, inflammation, and fibrosis were measured by RT-qPCR, RNA-seq, Western blot, and metabolomics.
RESULTS
Combined FFC-EtOH induced more body weight gain, glucose intolerance, steatosis, and hepatomegaly compared to Chow, EtOH, or FFC. Glucose intolerance by FFC-EtOH was associated with decreased hepatic protein kinase B (AKT) protein expression and increased gluconeogenic gene expression. FFC-EtOH increased hepatic triglyceride and ceramide levels, plasma leptin levels, hepatic Perilipin 2 protein expression, and decreased lipolytic gene expression. FFC and FFC-EtOH also increased AMP-activated protein kinase (AMPK) activation. Finally, FFC-EtOH enriched the hepatic transcriptome for genes involved in immune response and lipid metabolism.
CONCLUSIONS
In our model of early SMAFLD, we observed that the combination of an obesogenic diet and alcohol caused more weight gain, promoted glucose intolerance, and contributed to steatosis by dysregulating leptin/AMPK signaling. Our model demonstrates that the combination of an obesogenic diet with a chronic-binge pattern alcohol intake is worse than either insult alone.
Topics: Mice; Animals; Male; Leptin; Diet, Western; Glucose Intolerance; AMP-Activated Protein Kinases; Ethanol; Liver; Liver Diseases, Alcoholic; Non-alcoholic Fatty Liver Disease; Obesity; Lipid Metabolism; Diet, High-Fat; Mice, Inbred C57BL
PubMed: 37134024
DOI: 10.1371/journal.pone.0281954