Influence of Microelement Concentration on the Intensity of Alcohol Withdrawal Syndrome

Prior, Pedro Luis; Vaz, Marta Jezierski; Ramos, Anna Carolina; Galduróz, José Carlos Fernandes

doi:10.1093/alcalc/agu094

Cited by 10 publications

(7 citation statements)

References 27 publications

(33 reference statements)

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“…The optimal safe dose for human pregnancy needs to be clinically defined. The association of alcohol during embryonic exposure with elevated HCy levels and FA prevention (Han et al, ; Serrano et al, ) has been confirmed since then by multiple studies in the alcohol literature (Shirpoor et al, ; Kharbanda et al, ; Kruman and Fowler, ; Prior et al, ). It appears that folate deficiency is associated with the observed dyslipidemia in the fetus and placenta from a binge level of alcohol exposure.…”

Section: Discussionmentioning

confidence: 89%

Acute alcohol exposure during mouse gastrulation alters lipid metabolism in placental and heart development: Folate prevention

Linask

Han

2016

Birth Defects Research

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BackgroundEmbryonic acute exposure to ethanol (EtOH), lithium, and homocysteine (HCy) induces cardiac defects at the time of exposure; folic acid (FA) supplementation protects normal cardiogenesis (Han et al., 2009, 2012; Serrano et al., 2010). Our hypothesis is that EtOH exposure and FA protection relate to lipid and FA metabolism during mouse cardiogenesis and placentation.MethodsOn the morning of conception, pregnant C57BL/6J mice were placed on either of two FA‐containing diets: a 3.3 mg health maintenance diet or a high FA diet of 10.5 mg/kg. Mice were injected a binge level of EtOH, HCy, or saline on embryonic day (E) 6.75, targeting gastrulation. On E15.5, cardiac and umbilical blood flow were examined by ultrasound. Embryonic cardiac tissues were processed for gene expression of lipid and FA metabolism; the placenta and heart tissues for neutral lipid droplets, or for medium chain acyl‐dehydrogenase (MCAD) protein.ResultsEtOH exposure altered lipid‐related gene expression on E7.5 in comparison to control or FA‐supplemented groups and remained altered on E15.5 similarly to changes with HCy, signifying FA deficiency. In comparison to control tissues, the lipid‐related acyl CoA dehydrogenase medium length chain gene and its protein MCAD were altered with EtOH exposure, as were neutral lipid droplet localization in the heart and placenta.ConclusionEtOH altered gene expression associated with lipid and folate metabolism, as well as neutral lipids, in the E15.5 abnormally functioning heart and placenta. In comparison to controls, the high FA diet protected the embryo and placenta from these effects allowing normal development. Birth Defects Research (Part A) 106:749–760, 2016. © 2016 The Authors Birth Defects Research Part A: Clinical and Molecular Teratology Published by Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 89%

Acute alcohol exposure during mouse gastrulation alters lipid metabolism in placental and heart development: Folate prevention

Linask

Han

2016

Birth Defects Research

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“…In fact, in a study we developed, we observed a direct association between lower plasmatic levels of zinc and magnesium and greater intensity of AWS symptoms [17].…”

mentioning

confidence: 78%

Alcohol Withdrawal Syndrome: The Importance of Glutamatergic System

Galduróz¹

2015

Int Arch Addict Res Med

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“…The anorectic influence of alcohol on the satiety centers of the hypothalamus leads alcoholic abusers to refuse food. Furthermore, alcoholic patients lack adequate nutrition in their diet and attempt to meet their caloric needs from ethanol consumption leading to alcoholics being hungry many days while drinking heavily 27,28,33 .…”

Section: Discussionmentioning

confidence: 99%

Assessment of Vitamin B1 and B12 Deficiencies in Patients with Alcohol Withdrawal Syndrome

Buddorj,

Davaasuren,

Galsanjav

et al. 2019

Cent. Asian j. Med. Sci.

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Objectives: We examined the oral intake and serum concentration of vitamins B1 and B12 in patients with alcohol withdrawal syndrome to determine some risk factors leading to deficiencies of those vitamins and their impact on memory function. Methods: Data were collected from patients with alcohol withdrawal syndrome admitted to 3 addiction care clinics in Ulaanbaatar. A total of 162 subjects were selected with a ratio 1:1 in this case-control study. Nutrient intake of B1 and B12 were estimated by questioning the patients regarding their food intake during the 24 hours prior to admission. Results: Drinking while hungry resulted in inadequate oral vitamin B12 consumption (OR 9.43; 95% CI 2.42;36.64, p=.001) as did refusing food while drinking (OR 4.76; 95% CI 1.23;18.30, p=.02). Inadequate B1 intake was higher in women (OR 0.16; 95% CI 0.05;0.49, p=.001) and if the patient refused food while drinking (OR 3.38; 95% CI 1.24; 9.21, p=.01). Serum B1 and B12 deficiency were associated refusing food while drinking (OR 4.53; 95% CI 1.81; 11.31, p=.001 and OR 3.43; 95% CI 1.22; 9.61, p=.01). Short term memory impairment was associated with dietary B1 and B12 deficiency (OR 8.59; 95% CI 3.10;23.82, p=.0001 and OR 3.14; 95% CI 1.02;9.61, p=.04) and low serum B12 levels (OR 2.45; 95% CI 0.98;6.11, p=.05). Long-term memory impairment was associated with deficient B12 and B1 intake (

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Influence of Microelement Concentration on the Intensity of Alcohol Withdrawal Syndrome

Abstract: Evidence from literature and our experiment suggests that brain activity, especially the glutamatergic system, might be directly involved in micronutrient concentrations. Therefore, their supplementation to the AWS patient might improve symptom evolution.

Cited by 10 publications

References 27 publications

Acute alcohol exposure during mouse gastrulation alters lipid metabolism in placental and heart development: Folate prevention

Acute alcohol exposure during mouse gastrulation alters lipid metabolism in placental and heart development: Folate prevention

Alcohol Withdrawal Syndrome: The Importance of Glutamatergic System

Assessment of Vitamin B1 and B12 Deficiencies in Patients with Alcohol Withdrawal Syndrome

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