Case–Control Research Study of Auto-Brewery Syndrome

Abstract

Background Auto-brewery syndrome (ABS), also known as Gut Fermentation Syndrome and Endogenous Ethanol Fermentation, is afflicting people worldwide, but little is known about ABS patients’ demographics, health history, lifestyle factors, and diet. Method We conducted a broad-based case–control survey study on 52 patients known to have a diagnosis of ABS and their household members. The research compares the symptomatic group (N = 28) to the asymptomatic group (N = 18) regarding lifestyle and health, diet, and medical history. Results With a response rate of 88% and using rank-sum tests, the data demonstrate that patients with ABS have significant differences compared to people without ABS in lower quality bowel movements ( P = .048), more frequent bowel movements ( P = .038), more reports of malodorous breath ( P = .0001), and self-classify as having poorer health ( P = .009). Furthermore, participants with ABS consume more water ( P = .038), consume less tea and coffee ( P = .033), eat fewer dairy products ( P = .0185), eat less candy ( P = .032), eat out less and rely on food prepared at home ( P = .043), have more aversion to starch ( P = .008), and have more food sensitivities ( P = .043) than the group without ABS. The ABS group also reports more diarrhea ( P = .048), higher amounts of yeast in their gastrointestinal tract ( P = .015), and using acne medication for a longer time ( P = .037) than the control group. Conclusion Patients with ABS have significant differences in their lifestyle and health, diet, and medical history compared to non-ABS participants and these differences warrant further research.

Alcoholic Liver Disease: Current Mechanistic Aspects with Focus on Their Clinical Relevance

“…The human body is well prepared to get rid of the consumed alcohol in order to prevent its accumulation and more serious acute health problems. Alcohol removal proceeds preferentially through enzymatic degradation [20,23,24].…”

“…Although present also in the gastrointestinal tract [35,36,37,38,39,40,41], MEOS is predominantly found in the liver, when it was first described in 1968 [42] and 1970 [43]. Based on these early investigations and various other studies [42,43,44,45,46], and as summarized recently [20,23], MEOS can now be characterized as follows: the reaction converts ethanol to acetaldehyde, MEOS depends on reduced nicotinamide adenine dinucleotide phosphate (NADPH + H + ) or a NADPH regenerating system, and requires molecular oxygen [31,42,43,44,45,46,47,48,49]; key components of MEOS are several form of cytochrome P450 (CYP) with preference of its CYP 2E1 isoform, the NADPH-dependent cytochrome P450 reductase, and phospholipids [45,47,50,51]; MEOS is most active at a physiological pH, has a Michaelis–Menten constant of 7–11 mM and thereby active at intermediate and high alcohol concentrations, and is inducible in its activity following prolonged alcohol consumption [42,43]. Apart from ethanol, other aliphatic alcohols and various chemicals are known substrates of this special enzyme system [20,23].…”

“…It has also been suggested that when corrected for microsomal losses during preparation, half to two thirds of the increase in the rate of ethanol oxidation after chronic alcohol use can be accounted for by MEOS [33]. Conservatively speaking and considering variable results, MEOS may contribute >25% of overall hepatic alcohol metabolism at high alcohol concentrations and after prolonged alcohol abuse considering mostly kinetic characteristics and also, rarely, inhibitory studies [55], with details outlined recently [23].…”

“…This has a major impact on hepatic intermediary pathways, which require NAD + or are inhibited by excess NAD + H + [34]. Certainly, part of the redox changes can be attenuated by reducing equivalents in the form of NADPH + H + required for ethanol oxidation via MEOS [23].…”

“…For understanding the pathogenesis of ALD the occurrence and action of ROS is of pivotal importance [7,23,58,59,60,61]. Along the NADPH dependent MEOS reaction also involving CYP 2E1, acetaldehyde and a variety of ROS are generated from incomplete split of molecular oxygen [7,23]: ethoxy radical CH 3 CH 2 O • , hydroxyethyl radical CH 3 C( • )HOH, acetyl radical CH 3 CHO • , singlet radical 1 O 2, superoxide radical HO • 2 , hydrogen peroxide H 2 O 2 , hydroxyl radical HO • , alkoxyl radical RO • , and peroxyl radical ROO • . ROS undergoes covalent bonding to macromolecules within the liver cells including those present in membranes of subcellular organelles like mitochondria with their structural proteins and phospholipids.…”