The chronic alcohol consumption influences the gonadal axis in men: Results from a meta‐analysis
Open accessAbstract
BACKGROUND: Low testosterone concentrations affect 2-13% of adult males, with a direct association between reduction in testosterone (T) concentrations and cardiovascular events. Lifestyle habits have been linked to visceral fat accumulation and endocrine disorders like secondary hypogonadism. Alcohol intake has also been a topic of debate, with studies showing a detrimental effect on sperm production and underlying mechanisms. This meta-analysis aims to comprehensively evaluate the effect of alcohol consumption on T serum concentrations in adult men. METHODS: The literature search included only controlled clinical trials comparing men who drink alcohol to men who do not, or who assumed placebo or nonalcoholic beverages. The primary outcome was the comparison of total testosterone serum concentrations between the study and control groups. The publications were examined for publication bias using Egger's test. RESULTS: Twenty-one studies were included in the analysis for a total of 30 trials that examined the effects of alcohol consumption on testosterone level in 10,199 subjects. The meta-analysis showed that alcohol consumption overall is related to significant reduction in circulating concentrations of total testosterone (mean difference [MD] = -4.02; 95% CI -6.30, -1.73), free T (MD = -0.17; 95% CI -0.23, -0.12), sex hormone binding globulin (SHBG) (MD = -1.94; 95% CI -3.37, -0.48), an increase in estradiol (E2) (MD = 7.65; 95% CI 1.06, 14.23) and neutral effect on luteinizing hormone (LH) (MD = -0.15; 95% CI -0.36, 0.06), independently by age, body mass index (BMI), E2, and LH serum concentrations and alcohol intake. However, these results are evident only in healthy men exposed to chronic alcohol consumption and not in those with a recognized diagnosis of alcohol use disorder or after acute alcohol intake. CONCLUSION: This study suggests how chronic alcohol consumption may inhibit the gonadal axis in healthy men, although the exact pathophysiological mechanisms connecting alcohol exposure and steroidogenesis are still not completely clarified.
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Claims the paper makes
11 of 31 cited sources checked · 3 supported · 0 flagged · accuracy not yet measured
- Premisecitation
Several studies demonstrated that components of alcoholic beverages such as procyanidin B and phytoestrogens could bind the active site of aromatase, leading to functional dysregulations.
“several studies demonstrated that some component of alcoholic beverages, such as procyanidin B and phytoestrogens (i.e., flavones and isoflavones) could bind the active site of aromatase, leading to functional dysregulations.[133][134][135]”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites [133] 133. Eng ET, Ye J, Williams D, et al. Suppression of estrogen biosynthe- sis by procyanidin dimers in red wine and grape seeds. Cancer Res. 2003;63(23):8516-8522.
- cites [134] 134. Kijima I, Phung S, Hur G, Kwok SL, Chen S. Grape seed extract is an aromatase inhibitor and a suppressor of aromatase expression. Cancer Res. 2006;66(11):5960-5967. source
- cites [135] 135. Kao YC, Zhou C, Sherman M, Laughton CA, Chen S. Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogens: a site-directed mutagenesis study. Environ Health Perspect. 1998;106(2):85-92. source
The Results and Discussion report that flavone and isoflavone phytoestrogens bind the active site of aromatase and inhibit its activity. The paper does not establish that these compounds are components of alcoholic beverages, and it does not address procyanidin B (searched: procyanidin B, alcoholic beverages, wine, ethanol). (LLM, conf=0.88)
Experimental — accuracy not yet measured
- Findingown data
In acute alcohol intake, no significant differences in total testosterone serum concentrations were detected compared with placebo.
“No significant differences in T serum concentrations were detected when acute alcohol intake group was compared with placebo (Figure 2).”
Quote in the paperNot a substantial claim - Findingown data
Overall alcohol consumption is associated with an increase in estradiol (mean difference 7.65; 95% CI 1.06, 14.23).
“an increase in estradiol (E2) (MD = 7.65; 95% CI 1.06, 14.23)”
Quote in the paperSubstantial claim - Findingown data
In trials assessing total testosterone with chronic alcohol intake, I2 was 99% (p<0.001).
“Chronic alcohol intake I 2 calculated in trials assessing total T was 99% (p < 0.001).”
Quote in the paperNot a substantial claim - Findingown data
No differences in SHBG concentrations were detected after acute alcohol administration (p=0.910).
“In line with the latter observation, no differences were detected on SHBG concentrations after acute administration, although only two trials were analyzed (p = 0.910) (Figure 4).”
Quote in the paperNot a substantial claim
- Findingown data
The decrease in total testosterone with chronic alcohol intake was not accompanied by any LH variation (mean difference -0.03 IU/L, 95% CI -0.20, 0.13, p=0.720).
“The total T serum concentrations decrease observed in chronic alcohol intake was not accompanied by any LH variation, resulting comparable in patients compared with controls (MD -0.03 IU/L, 95%CI: -0.20, 0.13 IU/L, p = 0.720) (Supplementary Figure S2).”
Quote in the paperSubstantial claim - Findingown data
Calculated free testosterone serum concentrations were significantly higher in controls than in men exposed to chronic alcohol intake (mean difference -0.19 nmol/L, 95% CI -0.25, -0.13, p<0.001).
“Accordingly, calculated free T serum concentrations were significantly higher in controls rather than in men exposed to chronic alcohol intake (MD -0.19 nmol/L, 95%CI: -0.25, -0.13 nmol/L, p < 0.001) (Supplementary Figure S3).”
Quote in the paperSubstantial claim - Findingown data
Meta-regression showed no significant association between age and the total testosterone difference in chronic alcohol intake (S: -6.0 [-13.9, 1.8]; I: -0.9 [-4.0, 2.2], p=0.118).
“Several parameters were considered including age (S: -6.0 [-13.9, 1.8]; I: -0.9 [-4.0, 2.2], p = 0.118; see also Supplementary Figure S4)”
Quote in the paperNot a substantial claim - Findingown data
Overall alcohol consumption is associated with a reduction in sex hormone binding globulin (mean difference -1.94; 95% CI -3.37, -0.48).
“sex hormone binding globulin (SHBG) (MD = -1.94;95% CI -3.37, -0.48)”
Quote in the paperSubstantial claim - Findingown data
Total testosterone serum concentrations were significantly lower in subjects with chronic alcohol intake compared with controls (p<0.001).
“Total T serum concentrations were significantly lower in subjects with chronic alcohol intake compared with controls (without any alcohol intake) (p < 0.001) (Figure 2).”
Quote in the paperSubstantial claim - Findingown data
The overall total testosterone reduction in chronic alcohol users compared with controls is not accompanied by a compensatory increase in LH.
“Here, we demonstrated an overall total T reduction in chronic alcohol users compared with a control group not accompanied by a compensatory increase in LH.”
Quote in the paperSubstantial claim - Findingown data
Estradiol serum concentrations were significantly higher in the chronic alcohol group compared with controls (p=0.020).
“Although E2 serum concentrations were reported only in a minority of trials (n = 17), significant higher circulating estrogens were detected in alcohol group compared with controls (p = 0.020) (Figure 3).”
Quote in the paperSubstantial claim - Findingown data
The negative impact of chronic alcohol consumption on total testosterone is confirmed in a large sample of more than 16,000 subjects.
“The negative impact of chronic alcohol consumption on total T serum concentrations is here confirmed in a large sample size, accounting for more than 16,000 subjects.”
Quote in the paperSubstantial claim - Findingown data
Overall alcohol consumption is associated with a significant reduction in circulating total testosterone (mean difference -4.02; 95% CI -6.30, -1.73).
“The meta-analysis showed that alcohol consumption overall is related to significant reduction in circulating concentrations of total testosterone (mean difference [MD] = -4.02;95% CI -6.30, -1.73)”
Quote in the paperSubstantial claim - Findingown data
The funnel plot suggested no publication bias.
“The funnel plot suggested no publication bias.”
Quote in the paperNot a substantial claim - Findingown data
No difference in free testosterone serum concentrations was detected when acute alcohol administration was evaluated (mean difference -0.02 nmol/L, 95% CI -0.12, 0.07, p=0.620).
“On the contrary, no difference in terms of free T serum concentrations was detected when acute alcohol administration was evaluated (MD -0.02 nmol/L, 95%CI: -0.12, 0.07 nmol/L, p = 0.620) (Supplementary Figure S3).”
Quote in the paperNot a substantial claim - Findingown data
No differences in estradiol were detected between acute alcohol and control groups (p=0.730).
“Similarly, although only two studies evaluated the acute alcohol effect on E2, no differences were detected between alcohol and controls groups (p = 0.730) (Figure 3).”
Quote in the paperNot a substantial claim - Findingown data
Overall alcohol consumption is associated with a reduction in free testosterone (mean difference -0.17; 95% CI -0.23, -0.12).
“free T (MD = -0.17;95% CI -0.23, -0.12)”
Quote in the paperSubstantial claim - Findingown data
The association between chronic alcohol intake and lower total testosterone was confirmed only when healthy volunteers were considered (mean difference -6.5 nmol/L, 95% CI -7.5, -2.3, p<0.001).
“However, when data were further analyzed in detail, the latter association was confirmed only when healthy volunteers were considered (MD -6.5 nmol/L, 95%CI: -7.5, -2.3 nmol/L, p < 0.001) (Supplementary Figure S1).”
Quote in the paperSubstantial claim - Findingown data
Total testosterone serum concentrations were comparable before and after acute alcohol administration (mean difference 0.9 nmol/L, 95% CI -3.8, 5.6, p=0.710).
“Similarly, total T serum concentrations were comparable before and after acute alcohol administration (MD 0.9 nmol/L, 95%CI: -3.8, 5.6 nmol/L, p = 0.710).”
Quote in the paperNot a substantial claim - Findingown data
SHBG serum concentrations were significantly lower in men with chronic alcohol intake compared with controls (p=0.010).
“Moreover, SHBG serum concentrations were significantly lower in men with chronic alcohol intake compared with controls (p = 0.010).”
Quote in the paperSubstantial claim - Findingown data
Total testosterone serum concentrations did not differ between alcohol-dependent men and control subjects (mean difference -1.0 nmol/L, 95% CI -5.8, 3.7, p=0.670).
“Conversely, total T serum concentrations did not differ comparing alcohol-dependent men to control subjects (MD -1.0 nmol/L, 95%CI: -5.8, 3.7 nmol/L, p = 0.670) (Supplementary Figure S1).”
Quote in the paperSubstantial claim - Study design and conductreasoning
We cannot establish whether chronic alcohol consumers included in the study group display normal liver function.
“Thus, we cannot establish whether chronic alcohol consumers included in the study group display a normal liver function.”
Quote in the paperSubstantial claim- Rests on an assumption: Liver dysfunction could increase SHBG, thereby increasing total testosterone and reducing bioavailable testosterone.
- Study design and conductnone given
The amount of chronic alcohol intake is approximately quantified by self-filled questionnaires and not accurately determined.
“In particular, the amount of chronic alcohol intake is approximately quantified by self-filled questionnaires and not accurately determined.”
Quote in the paperSubstantial claim - Interpretationown data
The chronic alcohol intake effect on testosterone is independent of age and amount of alcohol assumed.
“Interestingly, the chronic alcohol intake on T serum concentrations here highlighted is independent from patients' age and alcohol amount assumed”
Quote in the paperSubstantial claim - Interpretationown data
Chronic alcohol consumption may inhibit the gonadal axis in healthy men.
“This study suggests how chronic alcohol consumption may inhibit the gonadal axis in healthy men”
Quote in the paperSubstantial claim- Rests on an assumption: A global view on the relationship between testosterone serum concentrations and alcohol consumption in adult men is lacking.
- Interpretationreasoning
The results could be explained by alcohol acting mainly on the hypothalamus-pituitary gonadal axis rather than on the gonad itself.
“These results could be explained by a potential action of alcohol mainly on the hypothalamus-pituitary gonadal (HPG) axis, rather than to the gonad itself.”
Quote in the paperSubstantial claim- Rests on an assumption: The alcohol effect on LH concentrations and pulsatility is still unclear in the literature.
- Rests on an assumption: Studies available have failed to clarify the primary site of alcohol action on the HPG axis.
- Study design and conductreasoning
The lack of potential confounders in all included studies prevented adjustment for several parameters.
“Nevertheless, the lack of potential confounders in all the studies included in our study preventing the analysis with an eventual adjustment for several parameters.”
Quote in the paperNot a substantial claim - Study design and conductown data
The majority of included studies did not report BMI, limiting evaluation of this potential confounder.
“However, the majority of studies included did not report BMI among variables, thus limiting the evaluation of this potential confounding factor.”
Quote in the paperNot a substantial claim- Rests on an assumption: The association between BMI and both testosterone and SHBG is well known.
- Study design and conductreasoning
The high heterogeneity among studies is the most important limitation of the meta-analysis.
“First, the high heterogeneity among studies remains the most important issue.”
Quote in the paperNot a substantial claim - Study design and conductreasoning
We cannot rule out hidden liver dysfunction in the study group when chronic alcohol consumption is considered.
“we cannot rule out a hidden liver dysfunction in the study group when chronic alcohol consumption is considered.”
Quote in the paperSubstantial claim- Rests on an assumption: Liver dysfunction could increase SHBG, thereby increasing total testosterone and reducing bioavailable testosterone.
- Premisecitation
Experimental studies in animal models demonstrated an alcohol-related testosterone decrement in male rats.
“Experimental studies in animal models demonstrated an alcohol-related T decrement in male rats, 72,101-106”
Quote in the paperNot a substantial claim0 of 7 sources checked- cites [72] 72. Ida Y, Tsujimaru S, Nakamaura K, et al. Effects of acute and repeated alcohol ingestion on hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal functioning in normal males. Drug Alcohol Depend. 1992;31(1):57-64. source
- cites [101] 101. Salonen I, Huhtaniemi I. Effects of chronic ethanol diet on pituitary- testicular function of the rat. Biol Reprod. 1990;42(1):55-62. source
- cites [102] 102. Adams ML, Little PJ, Bell B, Cicero TJ. Alcohol affects rat testicular interstitial fluid volume and testicular secretion of testosterone and beta-endorphin. J Pharmacol Exp Ther. 1991;258(3):1008-1014.
Not checked in the free run.
- cites [103] 103. Cicero TJ, Meyer ER, Bell RD. Effects of ethanol on the hypothalamic- pituitary-luteinizing hormone axis and testicular steroidogenesis. J Pharmacol Exp Ther. 1979;208(2):210-215.
Not checked in the free run.
- cites [104] 104. Rivier C, Vale W. Influence of ethanol on reproductive functions of the adult male rat as a function of body weight. Alcohol Clin Exp Res. 1983;7(2):210-212. source
- cites [105] 105. Gonzalez-Reimers E, Martinez-Riera A, Santolaria-Fernandez F, et al. Relative and combined effects of ethanol and protein deficiency on gonadal function and histology. Alcohol. 1994;11(5):355-360. source
- cites [106] 106. Cicero TJ, Bernstein D, Badger TM. Effects of acute alcohol adminis- tration on reproductive endocrinology in the male rat. Alcohol Clin Exp Res. 1978;2(3):249-254. source
- Classified as probably not a substantial claim. 16
- May combine two claims. 19
- The quote only partly states this claim. 1
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductcitationThe quality of included trials was assessed using Cochrane criteria.
“The quality of trials included was assessed using the Cochrane criteria.30”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [30] 30. Higgins JP, Altman DG, Gøtzsche PC, et al. The Cochrane Collabora- tion's tool for assessing risk of bias in randomised trials. BMJ (Clinical research ed). 2011;343:d5928. source
May combine two claims.
PremisecitationThe direct correlation between amount of alcohol consumed and liver dysfunction, fibrosis, cirrhosis and related mortality is strongly demonstrated in large observational studies.
“The direct correlation between amount of alcohol consumed and liver dysfunction, fibrosis, cirrhosis and related mortality is strongly demonstrated in large observational studies.94,95”
Quote in the paperSubstantial claim1 of 2 sources checked- cites [94] 94. Bosetti C, Levi F, Lucchini F, Zatonski WA, Negri E, La Vecchia C. Worldwide mortality from cirrhosis: an update to 2002. J Hepatol. 2007;46(5):827-839. source
- cites [95] 95. Mathurin P, Bataller R. Trends in the management and burden of alcoholic liver disease. J Hepatol. 2015;62(1):S38-S46. Suppl. source
The Burden of alcohol liver disease section (page unavailable) reports a dose–response relationship between alcohol consumed and alcoholic liver disease, gives large-cohort evidence for cirrhosis, and links population alcohol consumption with cirrhosis mortality. The Natural history section discusses fibrosis and abnormal liver tests in heavy drinkers, but does not establish the claimed direct correlation between amount consumed and fibrosis or liver dysfunction. (LLM, conf=0.86)
Experimental — accuracy not yet measured
Classified as probably not a substantial claim. May combine two claims.
PremisecitationChronic liver disease is characterized by progressive necrosis of hepatocytes and liver dysfunction, which may affect metabolism of proteins, sex hormones and lipids.
“a chronic liver disease is characterized by progressive necrosis of hepatocytes and development of liver dysfunction, which may remarkably affect the metabolism of various substances including proteins, sex hormones and lipids.96”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [96] 96. Zang G, Sun X, Sun Y, et al. Chronic liver diseases and erectile dysfunction. Front Public Health. 2022;10:1092353. source
Section 2 (Epidemiology of ED in CLDs; page unavailable) describes chronic liver disease as progressive hepatocyte necrosis leading to liver dysfunction. Section 1 (Introduction; page unavailable) says chronic liver disease commonly disrupts sex-hormone and lipid metabolism. Section 3.2 mentions protein malnutrition and low albumin in advanced disease, but does not establish the claimed effect on protein metabolism. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationCirculating estrogens are associated with increased breast cancer risk in women, and this cancer is related to alcohol intake.
“Because circulating estrogens are associated to an increased breast cancer risk in women, [123][124][125] and this cancer is related to alcohol intake, 126,127”
Quote in the paperNot a substantial claim3 of 3 sources checked- cites [123] 123. Key TJ, Appleby PN, Reeves GK, et al. Sex hormones and risk of breast cancer in premenopausal women: a collaborative reanalysis of indi- vidual participant data from seven prospective studies. Lancet Oncol. 2013;14(10):1009-1019. source
- cites [124] 124. Key TJ, Appleby PN, Reeves GK, et al. Steroid hormone measure- ments from different types of assays in relation to body mass index and breast cancer risk in postmenopausal women: reanalysis of eighteen prospective studies. Steroids. 2015;99:49-55. Pt A. source
The Discussion reports strong positive associations between estrogens and breast cancer risk, but the analysis concerns postmenopausal women rather than women generally. The alcohol-intake clause has separate citations and is not attributed to this source. (LLM, conf=0.82)
Experimental — accuracy not yet measured - cites [125] 125. Tin Tin S, Reeves GK, Key TJ. Endogenous hormones and risk of inva- sive breast cancer in pre-and post-menopausal women: findings from the UK Biobank. Br J Cancer. 2021;125(1):126-134. source
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationThe E2 serum concentration increase during chronic alcohol consumption has been studied in females, where alcohol is a risk factor for cancer development.
“The E2 serum concentrations increase during chronic alcohol consumption has been studied in females, in which alcohol consumption has been evaluated among risk factors for cancer development.122”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [122] 122. Alcohol use and burden for 195 countries and territories, 1990- 2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet (London, England). 2018;392(10152):1015-1035. source
The Results (Health risks associated with alcohol consumption; page not provided) report that cancer risk rises with alcohol consumption and include a relative-risk curve for breast cancer in females. The paper does not report that chronic drinking increases serum E2 concentrations in females; that hormonal part of the claim is unsupported. (LLM, conf=0.88)
Experimental — accuracy not yet measured
May combine two claims.
PremisecitationLess is known about the alcohol effect on estrogens in males, and E2 measurement in males has methodological pitfalls.
“However, less is known in males, in which the E2 measurement suffers of important methodological pitfalls.[129][130][131][132]”
Quote in the paperNot a substantial claim2 of 3 sources checked- cites [129] 129. Mezzullo M, Pelusi C, Fazzini A, et al. Female and male serum ref- erence intervals for challenging sex and precursor steroids by liquid chromatography-tandem mass spectrometry. J Steroid Biochem Mol Biol. 2020;197:105538. source
The Introduction (p. 5) says direct E2 immunoassays perform inadequately at low levels, and the Discussion (p. 14) reports variability between assays and a negative bias at very low levels. These passages support methodological pitfalls in E2 measurement, including measurement in men. The paper does not address alcohol’s effect on estrogens in males or whether less is known about that effect. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites [130] 130. Smy L, Straseski JA. Measuring estrogens in women, men, and children: recent advances 2012-2017. Clin Biochem. 2018;62:11-23. source
- cites [131] 131. De Vincentis S, Decaroli MC, Milic J, et al. Determinants of sexual function in men living with HIV younger than 50 years old: focus on organic, relational, and psychological issues. androl. 2022;11(6):954- 969. source
The Hormonal parameters section (p. 3) says E2 was measured using validated LC-MS/MS, and the Discussion (p. 13) calls that method a gold standard. Neither passage describes methodological pitfalls in measuring E2 in men, and the passages on alcohol use do not address its effect on estrogens. Searches for both points found no supporting passage in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measured
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationIn obese male patients treated with a very low-caloric ketogenic diet, a significant increase in total testosterone was observed, mainly due to increased SHBG.
“a significant increase of total T concentrations was observed, mainly because of a significant increase in SHBG serum concentrations.19”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [19] 19. Cignarelli A, Santi D, Genchi VA, et al. Very low-calorie ketogenic diet rapidly augments testosterone levels in non-diabetic obese subjects. androl. 2023;11(2):234-244. source
The available non-abstract passage is a repository page showing the paper’s title, not its results (section and page unavailable). It does not establish a significant increase in total testosterone or that increased SHBG was mainly responsible; searches for SHBG and the proposed explanation found no usable non-abstract passage. (LLM, conf=0.72)
Experimental — accuracy not yet measured
May combine two claims.
Findingown dataThe meta-analysis included 21 studies, 30 trials, and 10,199 subjects.
“Twenty-one studies were included in the analysis for a total of 30 trials that examined the effects of alcohol consumption on testosterone level in 10,199 subjects.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataThe difference in calculated free testosterone was confirmed only in healthy volunteers (mean difference -0.25 nmol/L, 95% CI -0.34, 0.16, p<0.001) and was lost in chronic alcohol abuse (mean difference -0.11 nmol/L, 95% CI -0.27, 0.04, p=0.150).
“However, as well observed in total T, this difference was confirmed only considering healthy volunteers (MD -0.25 nmol/L, 95%CI: -0.34, 0.16, p < 0.001), but it was lost in chronic alcohol abuse (MD -0.11 nmol/L, 95%CI: -0.27, 0.04, p = 0.150).”
Quote in the paperSubstantial claimThe quote only partly states this claim.
Findingown dataOverall alcohol consumption has a neutral effect on luteinizing hormone (mean difference -0.15; 95% CI -0.36, 0.06).
“neutral effect on luteinizing hormone (LH) (MD = -0.15;95% CI -0.36, 0.06)”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataThe effects of alcohol on testosterone are evident only in healthy men exposed to chronic alcohol consumption, not in those with a recognized diagnosis of alcohol use disorder or after acute alcohol intake.
“However, these results are evident only in healthy men exposed to chronic alcohol consumption and not in those with a recognized diagnosis of alcohol use disorder or after acute alcohol intake.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataMeta-regression showed no significant association between amount of alcohol intake and the total testosterone difference (S: 5.3 [-2.1, 12.3]; I: -0.8 [-3.7, 1.9], p=0.997), including when alcoholism and healthy volunteers were considered separately (p=0.911 and p=0.823).
“The analysis showed no significant association (S: 5.3 [-2.1, 12.3]; I: -0.8 [-3.7, 1.9], p = 0.997), even when subjects affected by alcoholism were considered separately from healthy volunteers (p = 0.911 and p = 0.823, respectively).”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataThe alcohol effect on testosterone occurs in healthy men and not in those with a recognized diagnosis of alcohol use disorder.
“In our study, we focused on T serum concentrations, showing the alcohol effect occurs in healthy men and not in those subjects with a recognized diagnosis of alcohol use disorder”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSHBG production by the liver is related to intrahepatic fat rather than fasting blood glucose, HbA1c, or circulating lipid concentrations.
“several studies in men have already suggested that SHBG production by the liver is related to intrahepatic fat 98,99 rather than fasting blood glucose, glycated hemoglobin (HbA1c), or circulating lipid concentrations.”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [98] 98. Bonnet F, Velayoudom Cephise FL, Gautier A, et al. Role of sex steroids, intrahepatic fat and liver enzymes in the associa- tion between SHBG and metabolic features. Clin Endocrinol (Oxf). 2013;79(4):517-522. source
- cites [99] 99. Tchernof A, Labrie F, Bélanger A, et al. Relationships between endogenous steroid hormone, sex hormone-binding globulin and lipoprotein levels in men: contribution of visceral obesity, insulin lev- els and other metabolic variables. Atherosclerosis. 1997;133(2):235- 244. source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe exact pathophysiological mechanisms connecting alcohol exposure and steroidogenesis are not completely clarified.
“Comprehensively, the exact pathophysiological mechanisms connecting alcohol exposure and steroidogenesis are not yet completely clarified.29”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [29] 29. Emanuele MA, Emanuele N. Alcohol and the male reproductive system. Alcohol Res Health. 2001;25(4):282-287.
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductown dataStudy identification was performed independently by two authors, with conflicts resolved by another investigator.
“The identification of relevant studies was performed independently by two of the authors (D.S., G.S.), and conflicts were resolved by another investigator (A.C.).”
Quote in the paperNot a substantial claimMay combine two claims.
PremisecitationChronic alcohol intake can promote lipid accumulation in the liver, leading to reduced protein synthesis including SHBG, with consequent decrease in total testosterone.
“In addition, chronic alcohol intake can promote the accumulation of lipids in the liver, leading to protein synthesis reduction, including SHBG, with consequent total T serum concentrations decrease.97”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [97] 97. Kley HK, Nieschlag E, Wiegelmann W, Solbach HG, Krüskemper HL. Steroid hormones and their binding in plasma of male patients with fatty liver, chronic hepatitis and liver cirrhosis. Acta Endocrinol (Copenh). 1975;79(2):275-285. source
May combine two claims.
Study design and conductown dataThe time span of chronic alcohol intake is scanty reported and not all trials evaluated it.
“Similarly, the time span of chronic alcohol intake, although used in our meta-regression analysis, is scanty reported and not all trials evaluated this important variable.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenThe meta-analysis was performed in line with PRISMA and registered in PROSPERO (ID CRD42023409978).
“This meta-analysis was performed in line with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guideline and registered in the PROSPERO database for systematic reviews (ID CRD42023409978).”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataSensitivity analyses were performed, including subgroup analyses comparing chronic and acute alcohol intake.
“Then, sensitivity analyses were performed, performing subgroup analyses and comparing studies enrolling subjects exposed to chronic alcohol intake with studies including subjects exposed to acute alcohol intake.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataPublication bias was assessed using funnel plots and the Begg adjusted rank correlation test.
“Funnel plots and the Begg adjusted rank correlation test were used to estimate possible publication or disclosure bias.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningAlcohol-exposed patients showed higher concentrations of estrogens compared with controls, so the overall feedback effect on LH from testosterone and estradiol could be neutral.
“On the other hand, alcoholexposed patients showed comprehensively higher concentrations of estrogens compared with controls; thus, the overall feedback effect on LH because of T and E2 could result neutral.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductreasoningA random-effect model was applied even when low heterogeneity was detected because heterogeneity tests can be limited with a small number of component studies.
“Even when low heterogeneity was detected, a random-effect model was applied because the validity of heterogeneity tests can be limited with a small number of component studies.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductreasoningPre-existing documented alcoholic liver dysfunction was an exclusion criterion to limit confounders.
“In addition, to limit the presence of possible confounders, pre-existing documented alcoholic liver dysfunction was considered as an exclusion criterion.”
Quote in the paperSubstantial claimMay combine two claims.
Study design and conductreasoningThe heterogeneity reflects differences in patient inclusion criteria, steroid measurement methods, and ways to evaluate alcohol consumption.
“This variability reflects a great heterogeneity for patient inclusion criteria in each study, different methodological steroids measurements and various ways to evaluate alcohol consumption.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationA reduction in intrahepatic lipid content could be responsible for a 20% increase in SHBG concentrations.
“it has been estimated that a reduction in intrahepatic lipid content could be responsible for a 20% increase in SHBG concentrations, 100”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [100] 100. Telgenkamp I, Kusters Y, Schalkwijk CG, et al. Contribution of liver fat to weight loss-induced changes in serum hepatokines: a randomized controlled trial. J Clin Endocrinol Metab. 2019;104(7):2719-2727. source
Probably not a substantial claim: may not pass S3 (load-bearing).
Interpretationown dataWe cannot rule out that the alcohol-related E2 increase detected in alcohol abuse is potentially explained by increased aromatization.
“Thus, we cannot rule out that the alcohol-related E2 increase that we detected in alcohol abuse are potentially explained by an increased aromatization.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationAlcohol could increase circulating sex hormones through increased hepatic redox state and inhibition of sulfotransferase and 2-hydroxylase, decreasing steroid degradation.
“alcohol could increase circulating sex hormones through an increased hepatic redox state and the inhibition of the activity of sulfotransferase and 2-hydroxylase, resulting in a decrease in steroid degradation.136”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [136] 136. Yao X, Xia F, Tang W, Xiao C, Yang M, Zhou B. Isobaric tags for rel- ative and absolute quantitation (iTRAQ)-based proteomics for the investigation of the effect of Hugan Qingzhi on non-alcoholic fatty liver disease in rats. J Ethnopharmacol. 2018;212:208-215. source
May combine two claims.
PremisecitationThe majority of in vivo studies showed an alcohol-related LH decrease, while others detected a gonadotropin increase or unchanged concentrations after alcohol administration.
“Whether the majority of in vivo studies on the topic showed an alcohol-related LH decrease, 27,101,103,106,108,109 confirming our hypothesis, others experiments detected a gonadotropins increase 26 or unchanged concentrations 72 after alcohol administration.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [27] 27. Little PJ, Adams ML, Cicero TJ. Effects of alcohol on the hypothalamic-pituitary-gonadal axis in the developing male rat. J Pharmacol Exp Ther. 1992;263(3):1056-1061. source
- cites [101] 101. Salonen I, Huhtaniemi I. Effects of chronic ethanol diet on pituitary- testicular function of the rat. Biol Reprod. 1990;42(1):55-62. source
- cites [103] 103. Cicero TJ, Meyer ER, Bell RD. Effects of ethanol on the hypothalamic- pituitary-luteinizing hormone axis and testicular steroidogenesis. J Pharmacol Exp Ther. 1979;208(2):210-215. source
The paper relies on this without support.
A global view on the relationship between testosterone serum concentrations and alcohol consumption in adult men is lacking.
“However, a global view on this topic in adult men is still lacking.”
The paper relies on this without support.
Liver dysfunction could increase SHBG, thereby increasing total testosterone and reducing bioavailable testosterone.
“It is well known how liver dysfunction could lead to an increase of SHBG with consequent increase in total T serum concentrations and a reduction in the amount of bioavailable T for the target tissues.”
The paper relies on this without support.
The association between BMI and both testosterone and SHBG is well known.
“Moreover, the association between BMI and both T and SHBG is well known.”
The paper relies on this without support.
The mechanism linking chronic alcohol consumption and testosterone decrease is still not completely defined.
“The mechanism linking chronic alcohol consumption and T decrease is still not completely defined, so far.”
The paper relies on this without support.
The alcohol effect on LH concentrations and pulsatility is still unclear in the literature.
“However, the alcohol effect on LH concentrations and pulsatility is still unclear in the literature.”
The paper relies on this without support.
Studies available have failed to clarify the primary site of alcohol action on the HPG axis.
“Thus, studies available failed to clarify the primary site of the actions of alcohol on HPG axis.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Low testosterone levels are associated with muscle atrophy in alcoholics.
“Vitamin D deficiency [165,166] and low testosterone levels are associated with muscle atrophy in alcoholics [167,168], which in turn leads to bone loss.”
From Emerging role of liver-bone axis in osteoporosis (2024) · cites this paper as [168]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Healthy-volunteer testosterone estimate does not match its interval
MajorThe midpoint of the reported 95% confidence interval is −4.9 nmol/L, not the stated mean difference of −6.5 nmol/L.
Reported -6.5 · recomputed -4.9
“MD -6.5 nmol/L, 95%CI: -7.5, -2.3 nmol/L, p < 0.001”
Free-testosterone interval conflicts with the estimate and significance claim
MajorThe interval's midpoint is −0.09 nmol/L rather than the reported −0.25 nmol/L. It also includes zero despite the reported p < 0.001.
Reported -0.25 · recomputed -0.09
“MD -0.25 nmol/L, 95%CI: -0.34, 0.16, p < 0.001”
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Research works printed but not linked: 1
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Cited by
Sorted by citations
Emerging role of liver-bone axis in osteoporosis
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“Vitamin D deficiency [165,166] and low testosterone levels are associated with muscle atrophy in alcoholics [167,168], which in turn leads to bone loss.”
BackgroundA Systematic Review of Proteomics in Obesity: Unpacking the Molecular Puzzle
Rodríguez-Muñoz, A., Rad, H. M., Martín-Chaves, L., Benítez‐Porres, J., Rodríguez‐Capitán, J., Gonzalez-Jimenez, A., Insenser, M. R., Tinahones, F. J., & Murri, M. (2024) · Current Obesity Reports · doi:10.1007/s13679-024-00561-4 · Cited by 34 · see citing works
Understanding the Role of Alcohol in Metabolic Dysfunction and Male Infertility
Genchi, V. A., Cignarelli, A., Sansone, A., Yannas, D., Valentina, L. D., Livraghi, D. R., Spaggiari, G., & Santi, D. (2024) · Metabolites · doi:10.3390/metabo14110626 · Cited by 20 · see citing works
“…comprehensively demonstrated that testosterone serum levels’ reduction becomes clinically relevant after chronic alcohol consumption, with around an average 4.86 nmol/L (95%CI: 7.46, 2.26 nmol/L) reduction in subjects exposed to chronic alcohol intake compared to abstaining subjects [121].”
InfluentialSelf-citationMei, Y., Chen, Y., Wang, X., Xu, R., & Feng, X. (2024) · Frontiers in Endocrinology · doi:10.3389/fendo.2024.1458193 · Cited by 13 · see citing works
To Drink or Not to Drink? Investigating Alcohol’s Impact on Prostate Cancer Risk
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“Alcohol’s influence on hormonal regulation may drive these associations, particularly its impact on testosterone levels, as well as inflammation and oxidative stress, all of which are implicated in prostate carcinogenesis [19,20].”
BackgroundSex Hormones and the Liver: Implications for Disease Progression and Hormonal Therapy
Cazzagon, N., Gambato, M., Brunetto, M. R., Villa, E., Burra, P., & Floreani, A. (2026) · Liver International · doi:10.1111/liv.70509 · Cited by 5 · see citing works
“In contrast, in men, alcohol-related hypogonadism and feminization highlight the hormonal imbalance central to disease pathogenesis [127].”
Yafi, F. A., Dewitte, M. D., Elterman, D., Hammad, M. A. M., Lotti, F., Manfredi, C., Son, H., Warner, J. N., Welliver, C., & Corona, G. (2025) · Sexual Medicine Reviews · doi:10.1093/sxmrev/qeaf071 · Cited by 1 · see citing works
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“Long-term alcohol consumption can impair the male gonadal axis and lead to a reduction in testosterone levels (33).”
Factors Affecting Human Spermatogenesis
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“Similarly, previous reviews reported that increasing body weight is associated with progressive deterioration in semen quantity and quality in a dose-dependent manner [31,32].”
Rudziński, G., Szymonek, P., Gołacki, R., Januszczak, R., Szymonek, K., Cholewa, J., Burda, B., Gołacka, K., Bąkowska, E., & Kwiatek, B. (2026) · International Journal of Innovative Technologies in Social Science · doi:10.31435/ijitss.2(50).2026.6191
Yao, H.-L., Yang, T., Tian, R., Zhao, C., Yang, F., Liu, Z., & Li, F.-P. (2026) · Asian Journal of Andrology · doi:10.4103/aja20263
Osteoporose – Plädoyer für eine konsequente Diagnostik und Therapie – auch bei Männern
Thomasius, F., & Bühring, B. (2026) · Die Innere Medizin · doi:10.1007/s00108-026-02137-x
Carpenter, B. A., & Barson, J. R. (2026) · Journal of Neuroendocrinology · doi:10.1111/jne.70186
“93 Nota-bly, alcohol consumption can lead to an increase in estradiol levels in both women and men, 94,95 so this could be a mechanism through which this upregulation occurs.”
Judith and Holofernes: alcohol's role in male sexual health in the light of the systems sexology
Yannas, D., Sansone, A., Cignarelli, A., Santi, D., Spaggiari, G., Giorgino, F., Jannini, T. B., Siracusano, A., & Jannini, E. A. (2026) · Sexual Medicine Reviews · doi:10.1093/sxmrev/qeag008
Self-citationChan, H.-B., Su, S., Lee, C., & Hsu, C.-Y. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1625498
- Authors
- Santi, D., Cignarelli, A., Baldi, M., Sansone, A., Spaggiari, G., Simoni, M., & Corona, G.
- Affiliations
- University of Modena and Reggio Emilia (IT)
- University of Bari Aldo Moro (IT)
- Azienda Ospedaliera Citta' della Salute e della Scienza di Torino (IT)
- University of Rome Tor Vergata (IT)
- Azienda Ospedaliero-Universitaria di Modena (IT)
- Azienda USL di Bologna (IT)
- Corresponding author
- Santi, Daniele
- ORCID
- Venue
- Andrology
- Publisher
- Wiley
- Published
- 2023-09-14
- Volume
- 12
- Issue
- 4
- Pages
- 768-780
- ISSN
- 2047-2919 (ISSN-L)
- 2047-2927
- OpenAlex
- W4386725926
- Cited by
- 17
- References
- 142
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 5
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Andrology (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- IRIS UNIMORE (University of Modena and Reggio Emilia) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- chronic alcohol consumption, testosterone, gonadal axis, secondary hypogonadism, sex hormone-binding globulin, estradiol, luteinizing hormone, free testosterone, steroidogenesis, male reproductive health, alcoholism
- MeSH terms
- Adult, Alcohol Drinking, Alcoholism, Estradiol, Humans, Luteinizing Hormone, Male, Semen, Sex Hormone-Binding Globulin, Testosterone
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