Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Cristian Sandoval
 + 1564 word(s) 1564 2022-03-23 04:11:40 |
2 update layout and references
Amina Yu
 -7 word(s) 1557 2022-03-24 04:16:58 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Sandoval, C. Vitamin Supplements and Chronic Alcohol Consumption. Encyclopedia. Available online: https://encyclopedia.pub/entry/20951 (accessed on 15 November 2024).
Sandoval C. Vitamin Supplements and Chronic Alcohol Consumption. Encyclopedia. Available at: https://encyclopedia.pub/entry/20951. Accessed November 15, 2024.
Sandoval, Cristian. "Vitamin Supplements and Chronic Alcohol Consumption" Encyclopedia, https://encyclopedia.pub/entry/20951 (accessed November 15, 2024).
Sandoval, C. (2022, March 23). Vitamin Supplements and Chronic Alcohol Consumption. In Encyclopedia. https://encyclopedia.pub/entry/20951
Sandoval, Cristian. "Vitamin Supplements and Chronic Alcohol Consumption." Encyclopedia. Web. 23 March, 2022.
Vitamin Supplements and Chronic Alcohol Consumption
Edit
This entry is adapted from the peer-reviewed paper 10.3390/antiox11030564

Alcoholic drinks are extensively consumed worldwide. Drinking alcohol has negative and positive consequences. The health consequences of alcohol intake vary depending on the amount and pattern of consumption.

alcoholic liver disease vitamin B1 vitamin C vitamin D vitamin E

1. The Pathophysiology of Alcohol Drinking

Ethanol is harmful to the human body and can cause toxicity and death when ingested in excessive amounts. Ethanol metabolism produces an alcoholic fatty liver, alcoholic hepatitis, or cirrhosis [1][2]. The major pathway of ethanol metabolism is the oxidative pathway that involves alcohol dehydrogenase (ADH) present in the cytosol of hepatocytes [3]. This ADH produces acetaldehyde, which is toxic due to its high reactivity and may form DNA or protein adducts [4][5]. Some of the alcohol that is ingested orally does not enter the systemic circulation but may be oxidized in the stomach by ADH and their isoforms. Since the Km of most ADH isozymes for ethanol is low (about 1 mM), ADH is saturated at low concentrations of alcohol, and the MEOS system is activated [6].
Another quantity of ethanol is metabolized by the cytochrome P450 2E1 (CYP2E1) in the microsomal ethanol oxidizing system (MEOS) located within the smooth endoplasmic reticulum of hepatocytes, which leads to lipid peroxidation and to the mitochondrial glutathione and S-adenosylmethionine depletion, producing increased oxidative stress and liver injury [7][8][9]. In addition, fatty acid ethyl esters (FAEE) synthase produces FAEEs via nonoxidative metabolism [10].
Through alcohol intoxication, the CYP2E1-dependent system and the microsomal respiratory chain are the principal sources of reactive oxygen species (ROS) within the hepatocytes. Because of its propensity to metabolize and activate a variety of hepatotoxic substrates in the liver, CYP2E1 is of particular interest. Ethanol, carbon tetrachloride, acetaminophen, and N-nitrosodimethylamine, as well as several hazardous compounds, are among these substrates. [11][12]. The ethanol-induced activation of cytochrome CYP2E1 appears to be one of the main mechanisms by which ethanol causes oxidative stress. Furthermore, when ethanol is oxidized by CYP2E1, it creates acetaldehyde, a highly reactive molecule that may contribute to ethanol’s toxicity [13].

2. Vitamin B

It has been described that vitamin B (vitamin B1, vitamin B2 and vitamin B6) deficiency in ALD is caused by different factors, such as inadequate dietary intake, increased use of vitamin B, decreased hepatic storage, impairment of intestinal absorption by ethanol, or abnormal metabolism of the vitamins [14][15].
Due to decreased hepatic storage, vitamin B9 and vitamin B12 deficiencies can develop quickly in chronic liver illness. However, alcohol consumption affects the metabolism of homocysteine (tHcy) because the enzyme cofactor for the conversion of tHcy to methionine is vitamin B12. Decreased levels of vitamin B12 levels were shown to be adversely connected with tHcy and significantly linked with indicators of alcohol-related liver impairment in recent research [16]. Another research found that individuals with severe chronic liver disease had high vitamin B12 plasma levels but decreased vitamin B9 plasma levels [17]. Conversely, Gibson et al. [18] has shown that two weeks of moderate consumption of alcohol (i.e., red wine, or vodka) increased tHcy and reduced the statuses of both vitamin B9 and B12. In addition, other studies have studied vitamin B status as well [19][20][21]. For example, Van der Gaag et al. [19] showed that type-dependent alcohol had no effect on vitamin B12, but a fall in folate with spirits consumption and an increase in vitamin B6 with all alcohol types were observed. In contrast, Laufer et al. [20] only showed an effect of ethanol on vitamin B12, with no effect on vitamin B9. However, in another study, Beulens et al. [21] showed that beer drinking raised vitamin B6 and appeared to reduce vitamin B12 levels while having no effect on vitamin B9 levels. In this regard, Laufer et al. [20] noted that a lack of vitamins and alcohol use may interact to deplete vitamin B9 and vitamin B12 status and that if nutritional intake matches recommended levels, a decreasing impact of alcohol on vitamin B9 may not be detected. However, further studies are required to clarify the relationship between alcohol consumption and the intake of vitamin B to be able to provide nutritional management strategies for chronic liver disease.

3. Vitamin C

One of the many risk factors for vitamin C (including the three forms of vitamin C) and E insufficiency is excessive alcohol intake [22][23]. Vitamin C and E levels are decreased in alcoholics [24]. When compared to those who do not consume alcohol, urine ascorbic acid excretion increased by 47% after acute alcohol consumption of up to 0.58 g ethanol/kg body weight [25]. In effect, pretreatment with vitamin C (doses of 5 g, 1000 mg five times daily for two weeks) significantly improved blood ethanol elimination [26] whereas pretreatment with vitamin C (doses of 2 g, 500 mg four times daily for two weeks) significantly improved alcohol elimination in plasma in the short and long term, implying that vitamin C plays a role in ethanol oxidation [27]. Furthermore, short-term intravenous vitamin C therapy (500 mg/day for five days) significantly improved serum vitamin C levels in chronic alcoholics with hypovitaminosis C [28]. Despite these findings, a previous study indicated that chronic drinkers’ blood levels can take up to three months to restore to normal after taking oral vitamin C supplements [29][30].
Hepatocytes metabolize around 90% of ethanol, which is transformed to acetaldehyde by the enzyme ADH. Once the ADH has exhausted its ability to metabolize alcohol, cytochrome P450 isoenzymes take over and convert the molecule to acetaldehyde [31]. This has been found in tissues, including the liver and brain, that have poor ADH activity. By acting as an electron donor and, thereby, unleashing the NAD/NADH pathway, vitamin C is theorized to speed up alcohol metabolism [32]. A positive relationship between ADH activity and leukocyte ascorbic acid concentration has been discovered in people with liver disease [33]. Furthermore, the acetaldehyde produced has been associated with ethanol-induced hepatotoxicity [34][35], and when paired with hepatic CYP2E1 activation, these factors enhance oxidative stress in hepatocytes [36][37][38][39]. On the other hand, vitamin C has been demonstrated to protect against the detrimental effects of acetaldehyde in animal experiments [40]. Given the function of acetaldehyde in the brain’s dopaminergic stimulation of opiate receptors, this could reduce hepatotoxicity and possibly the biochemical basis of addiction [28].

4. Vitamin D

Calcium homeostasis and bone metabolism require vitamin D to function properly [41]. It is well known for its role in immune response control as well as its anticancer activities [42][43]. Vitamin D deficiency, less than 50 nmol/L of 25-hydroxy vitamin D (25(OH)D) is increasingly being recognized as a global public health issue [44]. According to published studies, the activities and functions of important vitamins and minerals including vitamin B9 and vitamins D, C and E are impaired by chronic ethanol consumption [15][45]. In effect, chronic alcohol consumption has been demonstrated to lower vitamin D levels (inactive vitamin D (25(OH)D3) and active vitamin D (1,25(OH)2D3) as well as cathelicidin/LL-37 expression [46].
Immune system deficiency, muscle weakness, osteopenia, osteoporosis, severe upper respiratory tract infections, community-acquired pneumonia, and acute respiratory distress syndrome have all been associated with vitamin D deficiency [47][48][49][50][51]. Furthermore, epidemiologic data linking vitamin D insufficiency to autoimmune disorders, such as multiple sclerosis (MS), rheumatoid arthritis (RA), diabetes mellitus (DM), inflammatory bowel disease, and systemic lupus erythematosus (SLE), have been raised [52]. Vitamin D deficiency, in effect, has been found to hasten the course of existing autoimmune disorders [53]. Reduced immunological function and responsiveness can be caused by lower amounts of inactive vitamin D and active vitamin D. As a result, the frequency of community-acquired and bacterial pneumonia has increased among susceptible populations, such as those with alcoholism [54][55]. Furthermore, in a mouse model of alcoholic myopathy, low vitamin D levels were associated with muscle fiber atrophy [56] where changes in muscular antioxidant enzyme levels may play a key role in the alcoholic etiology.

5. Vitamin E

Antioxidants are necessary for avoiding free radical-induced cellular damage. Vitamin E is a lipid-soluble vitamin that is carried as a component of lipoprotein, and efficiently reduces peroxidation susceptibility both in in vivo and in vitro assays [57][58].
Vitamin E insufficiency has long been linked to ALD [59]. Vitamin E levels in the liver of alcoholics with cirrhosis are frequently low [60]. Vitamin E deficiency, according to earlier research, makes the liver more sensitive to alcohol [61]. Vitamin E has been demonstrated to have hepatoprotective characteristics in rat models, including membrane stability, reduced nuclear factor-kappa B activation, decreased TNF-α generation, and suppressed hepatic stellate cell activation [36][37][39][59].
There are three histological stages for ALD, and they could be classified into the following: (1) simple steatosis or fatty liver, (2) alcoholic hepatitis (AH), and (3) chronic hepatitis with hepatic fibrosis or cirrhosis [62]. The first-line treatment for severe AH is the administration of corticosteroids [63]. However, some patients with severe AH are refractory to corticosteroids. Nonetheless, Miyashima et al. [64] have reported that vitamin E, as a supplement to corticosteroids therapy, may be a new therapeutic option for these patients.
By raising ROS and lowering endogenous antioxidant levels, alcohol promotes oxidative stress [65]. In this sense, Prakash et al. [66] have demonstrated that prognostic factors, including the Child−Pugh score and the Model for End-Stage Liver Disease (MELD) score, increased significantly, demonstrating that vitamin E treatment improves short-term mortality more than long-term mortality. In addition, Kaur et al. [67] examined vitamin E supplementation in ethanol-treated mice and found that it restored redox state, decreased apoptosis, and lowered oxidative stress markers. However, as compared to the placebo, 1000 IU of vitamin E per day improved serum hyaluronic acid but had no favorable impact on liver function tests or mortality in individuals with mild to severe alcoholic hepatitis [68].

References

  1. García Gutiérrez, E.; Lima Mompó, G.; Aldana Vilas, L.; Casanova Carrillo, P.; Feliciano Álvarez, V. Alcoholismo y sociedad, tendencias actuales. Rev. Cuba. Med. Mil. 2004, 33, 1–10.
  2. Arias, D.R. Reacciones fisiológicas y neuroquímicas del alcoholismo. Diversitas 2005, 1, 138–147.
  3. Lakshman, R.; Cederbaum, A.I.; Hoek, J.B.; Konishi, M.; Koop, D.; Donohue, T.M. Use of CYP2E1-transfected human liver cell lines in elucidating the actions of ethanol. Alcohol Clin. Exp. Res. 2006, 29, 1726–1734.
  4. Setshedi, M.; Wands, J.R.; Monte, S.M. Acetaldehyde adducts in alcoholic liver disease. Oxid. Med. Cell Longev. 2010, 3, 178–185.
  5. Robinson, K.E.; Shah, V.H. Pathogenesis and pathways: Nonalcoholic fatty liver disease & alcoholic liver disease. Transl. Gastroenterol. Hepatol. 2020, 5, 49.
  6. Cederbaum, A.I. Alcohol metabolism. Clin. Liver Dis. 2012, 16, 667–685.
  7. Zima, T.; Kalousová, M. Oxidative stress and signal transduction pathways in alcoholic liver disease. Alcohol Clin. Exp. Res. 2005, 29, 110S–115S.
  8. Dunn, W.; Shah, V.H. Pathogenesis of Alcoholic Liver Disease. Clin. Liver Dis. 2016, 20, 445–456.
  9. Peeraphatdit, T.B.; Kamath, P.S.; Karpyak, V.M.; Davis, B.; Desai, V.; Liangpunsakul, S.; Sanyal, A.; Chalasani, N.; Shah, V.H.; Simonetto, D.A. Alcohol Rehabilitation Within 30 Days of Hospital Discharge is Associated with Reduced Readmission, Relapse, and Death in Patients with Alcoholic Hepatitis. Clin. Gastroenterol Hepatol. 2019, 18, 477–485.
  10. Wu, H.; Cai, P.; Clemens, D.L.; Jerrells, T.R.; Shakeel Ansari, G.A.; Kaphalia, B.S. Metabolic basis of ethanol-induced cytotoxicity in recombinant HepG2 Cells: Role of nonoxidative metabolism. Toxicol. Appl. Pharmacol. 2006, 216, 238–247.
  11. Lu, Y.; Cederbaum, A.I. CYP2E1 and oxidative liver injury by alcohol. Free Rad. Biol. Med. 2008, 44, 723–738.
  12. Carrasco, C.; Carrasco, C.; Souza-Mello, V.; Sandoval, C. Effectiveness of antioxidant treatments on cytochrome P450 2E1 (CYP2E1) activity after alcohol exposure in humans and in vitro models: A systematic review. Int. J. Food Prop. 2021, 24, 1300–1317.
  13. Yang, Z.; Klionsky, D.J. Eaten alive: A history of macroautophagy. Nat. Cell Biol. 2010, 12, 814–822.
  14. Roongpisuthipong, C.; Sobhonslidsuk, A.; Nantiruj, K.; Songchitsomboon, S. Nutritional assessment in various stages of liver cirrhosis. Nutrition 2001, 17, 761–765.
  15. Leevy, C.M.; Moroianu, S.A. Nutritional aspects of alcoholic liver disease. Clin. Liver Dis. 2005, 9, 67–81.
  16. Cylwik, B.; Czygier, M.; Daniluk, M.; Chrostek, L.; Szmitkowski, M. Vitamin B12 concentration in the blood of alcoholics. Pol. Merkur. Lek. 2010, 28, 122–125.
  17. Muro, N.; Bujanda, L.; Sarasqueta, C. Plasma levels of folate and vitamin B(12) in patients with chronic liver disease. Gastroenterol. Hepatol. 2010, 33, 280–287.
  18. Gibson, A.; Woodside, J.V.; Young, I.S.; Sharpe, P.C.; Mercer, C.; Patterson, C.C.; Mckinley, M.C.; Kluijtmans, L.A.J.; Whitehead, A.S.; Evans, A. Alcohol increases homocysteine and reduces B vitamin concentration in healthy male volunteers-a randomized, crossover intervention study. QJM 2008, 101, 881–887.
  19. Van der Gaag, M.S.; Ubbink, J.B.; Sillanaukee, P.; Nikkari, S.; Hendriks, H.F. Effect of consumption of red wine, spirits, and beer on serum homocysteine. Lancet 2000, 355, 1522.
  20. Laufer, E.M.; Hartman, T.J.; Baer, D.J.; Gunter, E.W.; Dorgan, J.F.; Campbell, W.S.; Clevidence, B.A.; Brown, E.D.; Albanes, D.; Judd, J.T.; et al. Effects of moderate alcohol consumption on folate and vitamin B(12) status in postmenopausal women. Eur. J. Clin. Nutr. 2004, 58, 1518–1524.
  21. Beulens, J.W.; Sierksma, A.; Schaafsma, G.; Kok, F.J.; Struys, E.A.; Jakobs, C.; Hendriks, H.F. Kinetics of homocysteine metabolism after moderate alcohol consumption. Alcohol Clin. Exp. Res. 2005, 29, 739–745.
  22. Navasumrit, P.; Ward, T.H.; Dodd, N.C.F.; O’Connor, P.J. Ethanol-induced free radicals and hepatic DNA strand breaks are prevented in vivo by antioxidants: Effects of acute and chronic ethanol exposure. Carcinogenesis 2000, 21, 93–99.
  23. Hercberg, S.; Galan, P.; Preziosi, P.; Bertrais, S.; Mennen, L.; Malvy, D.; Roussel, A.M.; Favier, A.; Briançon, S. The SU.VI.MAX Study: A randomized, placebo-controlled trial of the health effects of antioxidant vitamins and minerals. Arch. Intern. Med. 2004, 164, 2335–2342.
  24. Suresh, M.V.; Sreeranjit Kumar, C.V.; Lal, J.J.; Indira, M. Impact of massive ascorbic acid supplementation on alcohol induced oxidative stress in guinea pigs. Toxicol. Lett. 1999, 104, 221–229.
  25. Faizallah, R.; Morris, A.I.; Krasner, N.; Walker, R.J. Alcohol enhances vitamin C excretion in the urine. Alcohol Alcohol. 1986, 21, 81–84.
  26. Susick, R.L.; Zannoni, V.G. Effect of ascorbic acid on the consequences of acute alcohol consumption in humans. Clin. Pharmacol. Ther. 1987, 41, 502–509.
  27. Chen, M.F.; Boyce, H.W.; Hsu, J.M. Effect of ascorbic acid on plasma alcohol clearance. J. Am. Coll. Nutr. 1990, 9, 185–189.
  28. Majumdar, S.K.; Patel, S.; Shaw, G.K.; O’Gorman, P.; Thomson, A.D. Vitamin C utilization status in chronic alcoholic patients after short-term intravenous therapy. Int. J. Vitam. Nutr. Res. 1981, 51, 274–278.
  29. Sviripa, E.V. Vitamin C metabolism in alcoholism and alcoholic psychoses. Zh. Nevrol. Psikhiatr. im. S.S. Korsakova 1971, 71, 422–425.
  30. Lim, D.J.; Sharma, Y.; Thompson, C.H. Vitamin C and alcohol: A call to action. BMJ Nutr. Prev. Health 2018, 1, 17–22.
  31. Hansson, T.; Tindberg, N.; Ingelman-Sundberg, M.; Köhler, C. Regional distribution of ethanol-inducible cytochrome P450 IIE1 in the rat central nervous system. Neuroscience 1990, 34, 451–463.
  32. Dow, J.; Goldberg, A. Ethanol metabolism in the vitamin C deficient guinea-pig. Biochem. Pharmacol. 1975, 24, 863–866.
  33. Dow, J.; Krasner, N.; Goldberg, A. Relationship between hepatic alcohol dehydrogenase activity and the ascorbic acid in leucocytes of patients with liver disease. Clin. Sci. Mol. Med. 1975, 49, 603–608.
  34. Ghorbani, Z.; Hajizadeh, M.; Hekmatdoost, A. Dietary supplementation in patients with alcoholic liver disease: A review on current evidence. Hepatobiliary Pancreat. Dis. Int. 2016, 15, 348–360.
  35. Fuster, D.; Samet, J.H. Alcohol use in patients with chronic liver disease. N. Engl. J. Med. 2018, 379, 1251–1261.
  36. Sandoval, C.; Vásquez, B.; Mandarim-de-Lacerda, C.; del Sol, M. Ethanol intake and toxicity: In search of new treatments. Int. J. Morphol. 2017, 35, 942–949.
  37. Sandoval, C.; Vásquez, B.; Souza-Mello, V.; Adeli, K.; Mandarim-de-Lacerda, C.; del Sol, M. Morphoquantitative effects of oral b-carotene supplementation on liver of C57BL/6 mice exposed to ethanol consumption. Int. J. Clin. Exp. Pathol. 2019, 12, 1713–1722.
  38. Abhilash, P.A.; Harikrishnan, R.; Indira, M. Ascorbic acid supplementation down- regulates the alcohol induced oxidative stress, hepatic stellate cell activation, cytotoxicity and mRNA levels of selected fibrotic genes in guinea pigs. Free Radic. Res. 2012, 46, 204–213.
  39. Sandoval, C.; Vásquez, B.; Souza-Mello, V.; Mandarim-de-Lacerda, C.A.; del Sol, M. Rol del consumo de alcohol y antioxidantes sobre la metilación global del ADN y cáncer. Int. J. Morphol. 2018, 36, 367–372.
  40. Sprince, H.; Parker, C.M.; Smith, G.G. L-Ascorbic Acid in Alcoholism and Smoking: Protection against Acetaldehyde Toxicity as an Experimental model. Int. J. Vitam. Nutr. Res. 1977, 47, 185–217.
  41. Veldurthy, V.; Wei, R.; Oz, L.; Dhawan, P.; Jeon, Y.H.; Christakos, S. Vitamin D, calcium homeostasis and aging. Bone Res. 2016, 4, 16041.
  42. Li, Y.C.; Chen, Y.; Liu, W.; Thadhani, R. MicroRNA-mediated mechanism of vitamin D regulation of innate immune response. J. Steroid. Biochem. Mol. Biol. 2014, 144 Pt A, 81–86.
  43. Jiménez-Sousa, M.A.; Martínez, I.; Medrano, L.M.; Fernández-Rodríguez, A.; Resino, S. Vitamin D in Human Immunodeficiency Virus Infection: Influence on Immunity and Disease. Front. Immunol. 2018, 12, 458.
  44. Holick, M.F.; Binkley, N.C.; Bischoff-Ferrari, H.A.; Gordon, C.M.; Hanley, D.A.; Heaney, R.P.; Hassan Murad, M.; Weaver, C.M. Evaluation, treatment, and prevention of vitamin D deficiency: An Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab. 2011, 96, 1911–1930.
  45. Kent, J.C.; Devlin, R.D.; Gutteridge, D.H.; Retallack, R.W. Effect of alcohol on renal vitamin D metabolism in chickens. Biochem. Biophys. Res. Commun. 1979, 89, 155–161.
  46. Ogunsakin, O.; Hottor, T.; Mehta, A.; Lichtveld, M.; McCaskill, M. Chronic Ethanol Exposure Effects on Vitamin D Levels Among Subjects with Alcohol Use Disorder. Environ. Health Insights 2016, 10, 191–199.
  47. Engs, R.C.; Aldo-Benson, M. The association of alcohol consumption with selfreported illness in university students. Psychol. Rep. 1995, 76, 727–736.
  48. Fernandez-Sola, J.; Junque, A.; Estruch, R.; Monforte, R.; Torres, A.; Urbano-Marquez, A. High alcohol intake as a risk and prognostic factor for community-acquired pneumonia. Arch. Intern. Med. 1995, 155, 1649–1654.
  49. McCaskill, M.L.; Hottor, H.T.; Sapkota, M.; Wyatt, T.A. Dietary diallyl disulfide supplementation attenuates ethanol-mediated pulmonary vitamin D speciate depletion in C57Bl/6 mice. BMC Nutr. 2015, 1, 18.
  50. Wijnia, J.W.; Wielders, J.P.M.; Lips, P.; van de Wiel, A.; Mulder, C.L.; Nieuwenhuis, K.G.A. Is Vitamin D Deficiency a Confounder in Alcoholic Skeletal Muscle Myopathy? Alcohol Clin Exp Res. 2013, 37 (Suppl. 1), E209–E215.
  51. Tardelli, V.S.; Lago, M.P.P.D.; Silveira, D.X.D.; Fidalgo, T.M. Vitamin D and alcohol: A review of the current literature. Psychiatry Res. 2017, 248, 83–86.
  52. Adorini, L. Intervention in autoimmunity: The potential of vitamin D receptor agonists. Cell Immunol. 2005, 233, 115–124.
  53. Zold, E.; Szodoray, P.; Gaal, J.; Kappelmayer, J.; Csathy, L.; Gyimesi, E.; Zeher, M.; Szegedi, G.; Bodolay, E. Vitamin D deficiency in undifferentiated connective tissue disease. Arthritis Res. Ther. 2008, 10, R123.
  54. White, M.; Mankan, A.; Lawless, M.W.; O’Dwyer, M.J.; McManus, R.; Ryan, T. Mortality in humans with pneumonia and sepsis is related to an uncompensated anti-inflammatory response to infection. Arch Intern Med. 2008, 168, 1468–1469.
  55. Gombart, A.F. The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Future Microbiol. 2009, 4, 1151–1165.
  56. González-Reimers, E.; Durán-Castellón, M.C.; López-Lirola, A.; Santolaria Fernández, F.; Abreu-González, P.; Alvisa-Negrón, J.; Sánchez-Pérez, M.J. Alcoholic myopathy: Vitamin D deficiency is related to muscle fibre atrophy in a murine model. Alcohol Alcohol. 2010, 45, 223–230.
  57. Pirozhkov, S.V.; Eskelson, C.D.; Watson, R.R.; Hunter, G.C.; Piotrowski, J.J.; Bernhard, V. Effect of chronic consumption of ethanol and vitamin E on fatty acid composition and lipid peroxidation in rat heart tissue. Alcohol 1992, 9, 329–334.
  58. Brockes, C.; Buchli, C.; Locher, R.; Koch, J.; Vetter, W. Vitamin E prevents extensive lipid peroxidation in patients with hypertension. Br. J. Biomed. Sci. 2003, 60, 5–8.
  59. Arteel, G.; Marsano, L.; Mendez, C.; Bentley, F.; McClain, C.J. Advances in alcoholic liver disease. Best Pract. Res. Clin. Gastroenterol. 2003, 17, 625–647.
  60. Leo, M.A.; Rosman, A.S.; Lieber, C.S. Differential depletion of carotenoids and tocopherol in liver disease. Hepatology 1993, 17, 977–986.
  61. Lieber, C.S. Relationships between nutrition, alcohol use, and liver disease. Alcohol Res. Health 2003, 7, 220–231.
  62. O’Shea, R.S.; Dasarathy, S.; McCullough, A.J. Alcoholic liver disease. Hepatology 2010, 51, 307–328.
  63. Lucey, M.R.; Mathurin, P.; Morgan, T.R. Alcoholic hepatitis. N. Engl. J. Med. 2009, 360, 2758–2769.
  64. Miyashima, Y.; Shibata, M.; Honma, Y.; Matsuoka, H.; Hiura, M.; Abe, S.; Harada, M. Severe Alcoholic Hepatitis Effectively Treated with Vitamin E as an Add-on to Corticosteroids. Intern Med. 2017, 56, 3293–3297.
  65. Dey, A.; Cederbaum, A.I. Alcohol and oxidative liver injury. Hepatology 2006, 43, S63–S74.
  66. Prakash, K.B.; Prasanand, S.; Adithiya, K. Efficacy of Vitamin E supplementation in patients with alcoholic liver disease: An open-label, prospective, randomized comparative study. Int. J. Nutr. Pharmacol. Neurol. Dis. 2016, 6, 101–110.
  67. Kaur, J.; Shalini, S.; Bansal, M.P. Influence of vitamin E on alcohol-induced changes in antioxidant defenses in mice liver. Toxicol. Mech. Methods 2010, 20, 82–89.
  68. Mezey, E.; Potter, J.J.; Rennie-Tankersley, L.; Caballeria, J.; Pares, A. A randomized placebo-controlled trial of vitamin E for alcoholic hepatitis. J. Hepatol. 2004, 40, 40–46.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Substance Abuse; Food Science & Technology
Contributor MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Cristian Sandoval
View Times: 2.8K
Revisions: 2 times (View History)
Update Date: 24 Mar 2022
Table of Contents
    1000/1000
    Hot Most Recent
    ScholarVision Creations
    Feedback