Alcohol and Testosterone, Adverse Health Effects
Jim is a 57 year old wine collector who consumes a bottle of wine nightly. His wine cellar contains 800 bottles of vintage wines collected over 20 years. Jim has been to many doctors for low testosterone in spite of many treatments. Alcohol consumption causes low testosterone. This is the elephant in the room ignored by his previous doctors who failed to mention it. Above left image wine glass courtesy of wikimedia commons.
Alcohols Effect on the HPA (Hypothalamic Pituitary Axis)
The harmful effects of alcohol are summarized by Dr Nadia Rachdaoui’s excellent articles, required reading for anyone thinking about drinking alcohol. Alcohol not only reduces testosterone levels, it has far reaching deleterious effects on the endocrine system, and causes “Leaky Gut”.(1)(4) Dr Nadia Rachdaoui says:
“Alcohol-induced hormonal dysregulations affect the entire body and can result in various disorders such as stress abnormalities, reproductive deficits, body growth defect, thyroid problems, immune dysfunction, cancers, bone disease and psychological and behavioral disorders.”(4)
In alcohol abusers, the HPG (Hypothalamic-Pituitary-Gonadal) dysfunction was shown to be associated with a decrease in libido, infertility and gonadal atrophy. Several studies have clearly documented that alcohol has deleterious effects on all three components of the HPG axis, the hypothalamus, pituitary, and gonads.
“Alcohol abuse disorders are often associated with chronic systemic inflammation and high circulating proinflammatory cytokine levels as well as high circulating cortisol levels. …the gut microflora-derived lipopolisacharides (LPS) were suggested as key players in alcohol-mediated inflammation…… Alcoholics have been shown to have reduced brain mass, cortical neuronal loss and impaired cognitive functions“(4)
Alcohol consumption increases aromatase activity in the liver, with increased conversion of testosterone to estrogen. There is also reduced circulating IGF-1 levels (growth hormone).(1)(4) Dr. Cicero’s experiments showed that alcohol consumption decreases LH, FSH and Testosterone levels in male rats. (7-9) He also showed alcohol directly inhibits testicular production of testosterone.(7) Left image: Alcohol courtesy of NY Times.
Alcohol and Leaky Gut
Alcohol causes increases translocation of gram negative microbes (LPS) from the gut to the blood stream.(2-3) Dr Joe Wang in 2010 World journal of gastroenterology says.(2)
“Alcohol can significantly increase the translocation of LPS from the gut. …It has been well established in humans that heavy alcohol consumption is associated with an increase in gut permeability and LPS leakage, with or without liver disease. Abstinence for 2 wk or longer is necessary for increased gut permeability to return to a baseline level. Studies of animal models show that acute alcohol feeding in mice increases LPS in plasma approximately five-fold within 30-90 min. Daily binge feeding of alcohol in rats for 4 wk increases the plasma LPS level approximately 15-fold compared to control animals.”(2)
Alcohol and the Heart -Calcium Scores
Dr da Luz showed that Calcium Scores are higher in wine drinkers compared to abstainers.(20) In addition, Zero calcium scores were more prevalent among abstainers.(20)
Alcohol Causes Thiamine Deficiency and Brain Damage
Alcohol consumption causes thiamine (vitamin B1) deficiency which, in turn, causes cerebellar degeneration and brain damage. (11-17) Alcohol consumption even in moderate amounts is a risk factor for dementia. Left Image : Alcohol causes brain atrophy. MRI Brain showing enlarged ventricles indicating atrophy (white arrows). Courtesy Washington U . Alcohol and the Brain.
Alcohol Causes Liver Disease (18)
Alcohol induced cirrhosis of the liver is a major cause of mortality globally. These patients develop portal hypertension with bleeding esophageal varices. (18)
Alcohol is an Addictive Psych Drug
Abrupt discontinuation of alcohol can cause severe withdrawal effects, “Delerium Tremors” . Slow gradual reduction is therefore recommended to avoid withdrawal effects.(19)
Conclusion: Alcohol consumption has profound effects on the endocrine system in males with reduction in testosterone, caused by inhibition at all three levels of the HPA. Alcohol also causes increased translocation of LPS from the gut (Leaky Gut), causing systemic inflammation. Alcohol causes brain and liver damage.
Jeffrey Dach MD
1) Rachdaoui, Nadia, and Dipak K. Sarkar. “Pathophysiology of the effects of alcohol abuse on the endocrine system.” Alcohol research: current reviews 38.2 (2017): 255.
Alcohol abuse disrupts all of these systems and causes hormonal disturbances that may result in various disorders, such as stress intolerance, reproductive dysfunction, thyroid problems, immune abnormalities, and psychological and behavioral disorders. Studies in both humans and animal models have helped shed light on alcohol’s effects on various components of the endocrine system and their consequences.
2) Wang, H. Joe, Samir Zakhari, and M. Katherine Jung. “Alcohol, inflammation, and gut-liver-brain interactions in tissue damage and disease development.” World journal of gastroenterology: WJG 16.11 (2010): 1304.
Chronic inflammation is often associated with alcohol-related medical conditions. The key inducer of such inflammation, and also the best understood, is gut microflora-derived lipopolysaccharide (LPS). Alcohol can significantly increase the translocation of LPS from the gut. In healthy individuals, the adverse effects of LPS are kept in check by the actions and interactions of multiple organs. The liver plays a central role in detoxifying LPS and producing a balanced cytokine milieu. The central nervous system contributes to anti-inflammatory regulation through neuroimmunoendocrine actions. Chronic alcohol use impairs not only gut and liver functions, but also multi-organ interactions, leading to persistent systemic inflammation and ultimately, to organ damage. The study of these interactions may provide potential new targets for therapeutic intervention.
Enhancement of LPS translocation by alcohol: It has been well established in humans that heavy alcohol consumption is associated with an increase in gut permeability and LPS leakage, with or without liver disease. Abstinence for 2 wk or longer is necessary for increased gut permeability to return to a baseline level. Acute heavy alcohol consumption is associated with a transient appearance of LPS in the circulation in normal human subjects. Individuals with alcoholic fatty liver but not severe liver disease also show an elevated LPS level in plasma. Studies of animal models show that acute alcohol feeding in mice increases LPS in plasma approximately five-fold within 30-90 min[41,42]. Daily binge feeding of alcohol in rats for 4 wk increases the plasma LPS level approximately 15-fold compared to control animals.
3) Lancet. 1984 Jan 28;1(8370):179-82.
The leaky gut of alcoholism: possible route of entry for toxic compounds.
Bjarnason I, Peters TJ, Wise RJ.
Intestinal permeability was investigated with a chromium-51-EDTA (edetic acid) absorption test in 36 non-intoxicated alcoholic patients without liver cirrhosis or overt clinical evidence of malabsorption or malnutrition. Patients abstaining from alcohol for less than 4 days almost invariably had higher intestinal permeability than controls, and in many the abnormality persisted for up to 2 weeks after cessation of drinking. The presence of gastritis did not correlate with the presence of increased permeability. The site of altered intestinal permeability was shown by an in-vitro permeability test to be the small bowel. The increased intestinal permeability to toxic “non-absorbable” compounds of less than 5000 molecular weight may account for some of the extraintestinal tissue damage common in alcoholic patients.
First, the Zn2+ deficiency that is common in alcoholics also adversely affects gut epithelial integrity[48,49].
full free 2013
4) Rachdaoui, Nadia, and Dipak K. Sarkar. “Effects of alcohol on the endocrine system.” Endocrinology and Metabolism Clinics 42.3 (2013): 593-615.
Chronic consumption of a large amount of alcohol disrupts the communication between nervous, endocrine and immune system and causes hormonal disturbances that lead to profound and serious consequences at physiological and behavioral levels. These alcohol-induced hormonal dysregulations affect the entire body and can result in various disorders such as stress abnormalities, reproductive deficits, body growth defect, thyroid problems, immune dysfunction, cancers, bone disease and psychological and behavioral disorders. This review summarizes the findings from human and animal studies that provide consistent evidence on the various effects of alcohol abuse on the endocrine system.
In alcohol abusers, the HPG dysfunction was shown to be associated with a decrease in libido, infertility and gonadal atrophy. Several studies have clearly documented that alcohol has deleterious effects on all three components of the HPG axis, the hypothalamus, pituitary, and gonads.
Associations between both acute and chronic alcohol consumption and lower testosterone levels have been clearly demonstrated.
Muthusami and colleagues, in a study on 66 alcoholic and 30 non-alcoholic men, found that chronic alcohol consumption significantly increased FSH, LH, and estrogen levels, whereas testosterone and progesterone were significantly decreased and prolactin (PRL) unchanged.
Ethanol increases aromatase activity, an enzyme that converts androgens to estrogens, especially in the liver70.
Alcoholic individuals often show dysregulations of the hypothalamic-pituitary-thyroid axis. A significant reduction in T4 and T3 concentrations was observed in the alcoholic groups during withdrawal and early abstinence, compared to non-alcoholic healthy groups90.
Numerous studies in both humans and experimental animals have shown that acute and chronic alcohol exposure reduces circulating GH and IGF-I levels.
Alcohol abuse disorders are often associated with chronic systemic inflammation and high circulating proinflammatory cytokine levels as well as high circulating cortisol levels. Two mechanisms through which alcohol induces inflammation have been proposed; first, the gut microflora-derived lipopolisacharides (LPS) were suggested as key players in alcohol-mediated inflammation129 and second, alcohol metabolism through production of reactive-oxygen species (ROS) and cell damage triggers the production of pro-inflammatory cytokines such as TNF-α and IL-6130. An alcohol-induced systemic inflammation that persists, in the case of alcohol abuse, has far reaching damaging actions on every organ of the body. In the brain, alcohol has neurotoxic effects that result in neuronal death and neurodegeneration131, 132. Alcoholics have been shown to have reduced brain mass, cortical neuronal loss and impaired cognitive functions133, 134.
6) Emanuele, Mary Ann, and Emanuele Nicholas. “Alcohol and the male reproductive system.” Alcohol Research 25.4 (2001): 282.
Alcohol use affects all three parts of the hypothalamic-pituitary-gonadal (HPG) axis, a system of endocrine glands and hormones involved in male reproduction. Alcohol use is associated with low testosterone and altered levels of additional reproductive hormones. Researchers are investigating several potential mechanisms for alcohol’s damage. These mechanisms are related to alcohol metabolism, alcohol-related cell damage, and other hormonal reactions associated with alcohol consumption. Chronic alcohol use in male rats also has been shown to affect their reproductive ability and the health of their offspring.
7) Cicero, THEODORE J., et al. “Ethanol and acetaldehyde directly inhibit testicular steroidogenesis.” Journal of Pharmacology and Experimental Therapeutics 213.2 (1980): 228-233.
The effects of ethanol and acetaldehyde on testicular steroidogenesis were examined. We found that ethanol markedly inhibited the gonadotropin-stimulated production of testosterone in enzymatically dispersed cell preparations of the testes of adult rats. The effects of ethanol on testicular steroidogenesis appeared to be noncompetitive since testosterone production could not be restored to nondrug-treated levels even by extremely high concentrations of gonadotropin. Acetaldehyde also inhibited testicular steroidogenesis in vitro but was between 1000 and 4000 times more effective than ethanol. As little as 50 microM acetaldehyde was effective in suppressing testicular steroidogenesis, whereas much higher (200 mM) concentrations of ethanol were required. Our results further demonstrated that cell viability was unaffected by incubation with very high concentrations of ethanol and acetaldehyde, indicating that the two drugs did not simply irreversibly impair the ability of the dispersed cells to appropriately respond to stimulation by gonadotropins. These results suggest that ethanol directly inhibits testicular steroidogenesis, but that acetaldehyde is much more potent.
8) Cicero, THEODORE J., and Thomas M. Badger. “Effects of alcohol on the hypothalamic-pituitary-gonadal axis in the male rat.” Journal of Pharmacology and experimental Therapeutics 201.2 (1977): 427-433.Effects of alcohol on the hypothalamic-pituitary-gonadal axis in the male rat Cicero 1977
9) Cicero, T. J., E. R. Meyer, and R. D. Bell. “Effects of ethanol on the hypothalamic-pituitary-luteinizing hormone axis and testicular steroidogenesis.” The Journal of pharmacology and experimental therapeutics 208.2 (1979): 210
10) Alcohol Alcohol. 1987;22(3):241-9. Vitamin A at pharmacologic doses ameliorates the membrane lipid peroxidation injury and testicular atrophy that occurs with chronic alcohol feeding in rats.
Rosenblum ER, Gavaler JS, Van Thiel DH.
The interaction of ethanol (ETOH) with testicular subcellular membranes contributes, at least in part, to alcohol-induced gonadal dysfunction. Vitamin A reaches the testes via the circulation as the retinyl ester and is converted to the free alcohol (retinol) and then to the aldehyde (retinal); retinal is the form of the vitamin which is essential for normal spermato-genesis. Because retinol can function as a free radical scavenger, testicular mitochondria were evaluated for evidence of a protective role provided by supplemental dietary vitamin A on ETOH-induced alterations in testicular structure and function in rats. Lipid peroxidation was evaluated by measurement of malonaldehyde formation and glutathione content of the testes. Compared to isocalorically matched dextrimaltose-fed controls (ISO) receiving a modified vitamin A containing diet, rats fed the corresponding ETOH diet for 50 days had a reduced testes/body ratio (ETOH: 0.0114 +/- 0.0004 vs ISO: 0.0128 +/- 0.0004). Mitochondrial enriched extracts obtained from the testes of these ETOH-fed rats showed significant increases in malonaldehyde formation; moreover, glutathione levels were reduced in the testes of the alcohol-fed animals when compared to their isocaloric controls. In contrast, no evidence for testicular atrophy was present in ETOH-fed rats receiving a standard vitamin A enriched diet; moreover, such ETOH-fed rats had a reduced rate of malonaldehyde formation as compared to their respective controls. Similarly, glutathione levels were not depleted in the testes of the ETOH-fed rats receiving the vitamin A enriched diet. Taken together, these data suggest that lipid peroxidation is a consequence of ethanol metabolism which can be attenuated, at least in part, by vitamin A.
Alcohol and thiamine deficiency
11) Martin, Peter R., Charles K. Singleton, and Susanne Hiller-Sturmhöfel. “The role of thiamine deficiency in alcoholic brain disease.” Alcohol Research 27.2 (2003): 134.
12) Mulholland, P. J., et al. “Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro.” Neuroscience 135.4 (2005): 1129-1139. Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro Mulholland Neuroscience 2005
13) Topiwala, Anya, et al. “Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study.” bmj 357 (2017): j2353.
Alcohol consumption, even at moderate levels, is associated with adverse brain outcomes including hippocampal atrophy.
14) a bottle of wine is 750ml, or 25 ounces, there are around 5 glasses of wine in a bottle
15) Schwarzinger, Michaël, et al. “Contribution of alcohol use disorders to the burden of dementia in France 2008–13: a nationwide retrospective cohort study.” The Lancet Public Health 3.3 (2018): e124-e132.
Alcohol use disorders were a major risk factor for onset of all types of dementia, and especially early-onset dementia.
16) Braillon, Alain. “Alcohol consumption and cognitive decline: the elephant in the room?.” The Lancet Public Health 3.5 (2018): e216.
17) Ladouceur, Roger. “What if alcohol were harmful, even in moderation?.” (2017): 742-742.
18) Mann, Robert E., Reginald G. Smart, and Richard Govoni. “The epidemiology of alcoholic liver disease.” Alcohol research and health 27 (2003): 209-219.The epidemiology of alcoholic liver disease Mann Robert E Alcohol research and health 2003
19) Jesse, S., et al. “Alcohol withdrawal syndrome: mechanisms, manifestations, and management.” Acta Neurologica Scandinavica 135.1 (2017): 4-16.
wine drinkers have higher calcium scores
20) da Luz, P. L., et al. “Coronary artery plaque burden and calcium scores in healthy men adhering to long-term wine drinking or alcohol abstinence.” Brazilian Journal of Medical and Biological Research 47.8 (2014): 697-705. Coronary artery plaque and calcium scores in long-term wine drinking or alcohol abstinence da Luz. Brazilian J Med Biol Res 2014
Total calcium score was significantly greater in RW drinkers compared to abstainers (144.4±362.2 vs 122.0±370.3 Agatston units, respectively; chi-square test, P,0.001).Significantly greater percentage of individuals with no calcium was observed among abstainers (in green).
Click Here for: Dr Dach’s Online Store for Pure Encapsulations Supplements
Click Here for: Dr Dach’s Online Store for Nature’s Sunshine Supplements
Web Site and Discussion Board Links:
Disclaimer click here: www.drdach.com/wst_page20.html
The reader is advised to discuss the comments on these pages with his/her personal physicians and to only act upon the advice of his/her personal physician. Also note that concerning an answer which appears as an electronically posted question, I am NOT creating a physician — patient relationship. Although identities will remain confidential as much as possible, as I can not control the media, I can not take responsibility for any breaches of confidentiality that may occur.
Link to this article: http://wp.me/p3gFbV-4yl
Copyright (c) 2017 Jeffrey Dach MD All Rights Reserved. This article may be reproduced on the internet without permission, provided there is a link to this page and proper credit is given.
FAIR USE NOTICE: This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of issues of significance. We believe this constitutes a ‘fair use’ of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. Section 107, the material on this site is distributed without profit to those who have expressed a prior interest in receiving the included information for research and educational purposes.
Serving Areas of: Hollywood, Aventura, Miami, Fort Lauderdale, Pembroke Pines, Miramar, Davie, Coral Springs, Cooper City, Sunshine Ranches, Hallandale, Surfside, Miami Beach, Sunny Isles, Normandy Isles, Coral Gables, Hialeah, Golden Beach ,Kendall,sunrise, coral springs, parkland,pompano, boca raton, palm beach, weston, dania beach, tamarac, oakland park, boynton beach, delray,lake worth,wellington,plantation