| Adler (1997) [12] | Cohort Study | US | With Ne: 58; Without Ne: 230 | With Ne: 1:57; Without Ne: 11:219 | With Ne: 64.0; Without Ne: 61.5 | DM ± Incident Ne | Alcohol: CAGE rating, historical past of remedy, present use | High (4) CAGE alcohol rating considerably related to incident Ne (41.7% vs. 58.3%, p = 0.049; β = 1.94, SE = 0.7281, 6.96 [1.67–28.99], p = 0.008). |
| Braffett (2020) [13] | Cohort Study | US | With DPN: 455; Without DPN: 931 | With DPN: 182:273; Without DPN: 475:456 | ^ With DPN: 29 (24, 34); Without DPN 26 (21, 32) | T1DM ± DPN | Occasional or common alcohol use | Alcohol consumption not considerably related to DPN (1.14 [0.93–1.41], p > 0.05). |
| Christensen (2020) [14] | Cohort Study | Denmark | Overall: 5249; With DPoN: 938; With DPoN + Pain: 386 | Overall: 2205:3144 | ^ 65 (57, 72) | T2DM ± DPoN ± Pain | Alcohol: ≤14 (F)/21 (M) models, >14 (F)/21 (M) models | Alcohol consumption above really helpful restrict considerably related to elevated ache prevalence (aPR: 1.31 [1.01–1.69]. |
| Elgendy (2019) [15] | Cohort Study | Canada | 1413 | 705:708 | 60 ± 8.4 | T2DM ± PN | Alcohol frequency: Never, ≤1/mo, 2–4/mo, 2–3/wk, ≥4/wk; Number of drinks/d | High alcohol frequency + depressive signs considerably related to prevalent Ne (1.02 [1.00–1.04], p = 0.04). |
| Ellis (2020) [16] | Cohort Study | US | 254 | 54:200 | 43.5 ± 8.01 | HIV ± DSPoN | Lifetime Alcohol Abuse: Yes, No | Lifetime alcohol abuse not considerably related to DSPoN (statistics NR). |
| Hawley (1982) [17] | Cohort Study | US | 63 | 0:63 | 53.3 (29–69) | PN on account of Alcohol | History of alcoholism | Alcohol abstinence related to important electrophysiology enchancment in PN (+0.12 m/s/abstinent mo, p < 0.05). |
| Hillbom (1984) [18] | Cohort Study | Sweden | 10 | 0:10 | 53.1 (38–72) | Chronic alcoholism ± PN | History of alcoholism and in search of rehabilitation | Alcohol abstinence related to enchancment in medical/electrophysiological PN. |
| Iturralde (2024) [19] | Cohort Study | US | Overall: 222,334; AUD+: 1998; AUD−: 220,336 | Overall: 106,353:115,978; AUD+: 477:1521; AUD−: 105,876:114,457 | AUD+: 57 ± 11.3; AUD−: 64.3 ± 12.7 | T2DM ± AUD ± Ne | AUD (sure, no) | AUD considerably related to the next danger of Ne in unadjusted (p < 0.001) and adjusted (p < 0.001) fashions. |
| Kerns (2025) [20] | Cohort Study | US | 1 drink/d: 539; >1 drink/d: 76 | 0:615 | 45 (22–79) | Testicular most cancers survivors ± worsening PSN, or NP | History of alcohol consumption (1 drink/d, >1 drink/d) | Alcohol consumption (>1 drink/d) not considerably related to PSN (0.75 [0.40–1.44], p = 0.392), or NP (0.76 [0.29–1.98], p = 0.570). |
| Khan (2023) [21] | Cohort Study | US | TUD: 8009; TAUD: 1672; PSUD: 642; TUD Co: 8009; TAUD Co: 1672; PSUD Co: 642 | TUD: 4660:3349; TAUD: 582:1090; PSUD: 233:409; TUD Co: 4665:3344; TAUD Co: 584:1088; PSUD Co: 234:408 | TUD: 61.6 ± 12.1; TAUD: 61.52 ± 10.3; PSUD: 57.84 ± 8.3; TUD Co: 61.6 ± 12.1; TAUD Co: 61.42 ± 10; PSUD Co: 57.88 ± 8.1 | T2DM + Hypertension ± Ne | TUD: Yes, No; TAUD: Yes, No; PSUD: Yes, No | PSUD related to considerably increased danger of DN (1.76 [1.33–2.32], p < 0.05) in comparison with TUD. |
Kindl (2021)
[22] | Cohort Study | Germany | With MSK: 255; With CRPS: 223 | With MSK: 160:95; With CRPS: 173:50 | With MSK: 54.6 (20–80); With CRPS: 50.9 (18–77) | CRPS or MSK, on account of trauma | Alcohol Consumption: Yes, No, Daily, Weekly, Monthly | Prevalence of alcohol consumption important with MSK (58%, p < 0.001), and CRPS (43%, p < 0.001). |
| Kuguyo (2024) [23] | Cohort Study | Zimbabwe | 252 | 252:0 | (26–90); ^ 50 (43–61) | Breast most cancers survivors ± sensory loss (cisplatin) | History of alcohol consumption | Alcohol consumption not considerably related to diminished electrophysiology (p > 0.05). |
| Lehtinen (1993) [24] | Cohort Study | Finland | With ND: 12; Without ND: 101 | With ND: 9:3; Without ND: 46:55 | With ND: 57.2 ± 4.7; Without ND: 55.4 ± 10.4 | DM ± ND | Alcohol use (>30 g/wk) | Alcohol use not considerably completely different between ND teams (17% vs. 30%, p > 0.05). |
| Sreeram (2023) [25] | Cohort Study | US | Overall: 1034; With CIPN: 704; Without CIPN: 330 | Overall: 797:237; With CIPN: 570:134; Without CIPN: 227:103 | Overall: 57.1 ± 10.9 (27–79); With CIPN: 55.8 ± 10.8 (27–79); Without CIPN: 59.9 ± 10.4 (27–79) | Cancer survivors ± CIPN | Alcohol use (Past 4 wks): Yes, No | Alcohol use not considerably completely different between CIPN teams, or related to CIPN prevalence (51.2% vs. 46.4%, 1.10 [0.81–1.49], p > 0.05). |
| Xu (2025) [26] | Cohort Study | China | Low-Risk Stable CIPN: 148; Mod-Risk Progressive CIPN: 145; High-Risk Progressive CIPN: 57 | 350:0 | 18–44: n = 89; 45–59: n = 179; >60: n = 82 | Breast most cancers survivors ± CIPN | History of dangerous alcohol consumption (sure, no) | History of dangerous alcohol consumption not considerably completely different between CIPN teams (1.4% vs. 2.1% vs. 1.8%, x2 = 0.225, p = 0.894). |
| Agelink (1998) [27] | Case–Control Study | Germany | Ca: 35; Co: 80 | Ca: 15:20; Co: 33:47 | Ca: 42.9 ± 10 (28–74); Co: 41.8 ± 14.7 (27–77) | Alcoholism ± PN & CAN vs. wholesome co | Duration of alcohol dependence (yrs), imply TLDA | Duration of alcohol dependence was considerably longer (6.1 ± 3.8 vs. 16.2 ± 7.1, p < 0.0005) and imply TLDA was considerably bigger (438 ± 342 vs. 1930 ± 1173, p < 0.001) with AUD PN vs. with out. |
| Doneddu (2020) [28] | Case–Control Study | Italy | Ca: 195; Co: 195 | Ca: 109:86; Co: 109:86 | NR | CIDP on account of any etiology and their companions | Alcohol Consumption: Yes, No | Alcohol consumption not considerably related to CIDP (0.79 [0.50–1.24], p > 0.05). |
| Fouchard (2023) [29] | Case–Control Study | France | Overall: 323; Ca: 162; Co: 161 | Overall: 192:131; Ca: 88:74; Co: 104:57 | Ca: 56 ± 16; Co: 69 ± 13 | Cutaneous paresthesia ± SFN by way of IENFD on account of any etiology | Alcoholism: Yes, No | Alcohol consumption not considerably completely different between SFN teams (3.7% vs. 1.2%, p > 0.05). |
| Franklin (1994) [30] | Case–Control Study | US | Ca: 77; Co: 200 | Ca: 29:48; Co: 118:82 | Ca: 61.7; Co: 58.6 | NIDDM ± DSN | Alcohol use: by no means, g/wk (<20, >20) | Alcohol (g/wk: <20, >20) not considerably related to DSN (0.71 [0.29–1.72] p = 0.69, 1.03 [0.40–2.62]). |
| Frost (2013) [31] | Case–Control Study | Denmark | Ca: 324; Co: 832 | Ca: 121:203; Co 317:515 | Ca Smokers: 49 ± 9.7; Ca Non-Smokers: 44 ± 11.5; Co Smokers: 50 ± 9; Co Non-Smokers: 48 ± 9.9 | Ca: Electroneurographically confirmed UN; Co: Without UN | Alcohol: u/wk | Alcohol consumption not considerably related to UN (0.81 [0.44–1.48]). |
| Gebabo (2021) [32] | Case–Control Study | Ethiopia | Overall: 528; Ca: 264; Co: 264 | Ca: 101:163; Co: 105:159 | Ca: <40: 43; 40–65: 178; 65+: 43; Co: <40: 64; 40–65: 178; 65+: 17 | T1DM or T2DM ± PN | Alcohol Consumption (Ever): Yes, No | Alcohol consumption considerably increased with PN vs. with out (5.3% vs. 1.5%, p = 0.024). |
| Koike (2001) [33] | Case–Control Study | Japan | 18 | 0:18 | 47.7 ± 10.5 (31–70) | Alcoholism PoN vs. wholesome co | History of heavy alcohol consumption (100 g eth/d for >10 yrs) | History of heavy alcohol consumption considerably related to diminished electrophysiology (p < 0.005). |
| Mitchell (1990) [34] | Case–Control Study | US | IDDM: Ca: 54, Co: 56; NIDDM: Ca: 39, Co: 65 | IDDM: Ca: 31:23, Co: 35:21; NIDDM: Ca: 25:14, Co: 44:21 | IDDM: Ca: 36.1, Co: 32.7; NIDDM: 59.4: 39, Co: 57.7 | DM ± Ne | Alcohol: median drink-yrs | Median alcohol consumption not considerably related to Ne in IDDM (996 vs. 485). or NIDDM (0 vs. 14). |
| Mondelli (2020) [35] | Case–Control Study | Italy | Ca: 220; Co: 460 | Ca: 84:136; Co: 242:218 | Ca: 51.7 ± 11.8; Co: 47.8 ± 12.4 | Ca: UNE; Co: Upper limb complaints | Alcohol: u/wk or d | Alcohol consumption not considerably completely different between UNE teams (p = 0.463). |
| Pessione (1995) [36] | Case–Control Study | France | Ca: 32; Co: 58 | Ca: 6:26; Co: 22:36 | Ca: 49 ± 10.1; Co: 46.8 ± 9.6 | Alcoholism ± PN | Alcohol: parental historical past of alcoholism, alcohol dependence, weekly alcohol consumption (drinks) | Alcohol-related danger components all considerably increased in these with PN vs. with out in univariate (p < 0.01); and multivariate p < 0.05) analyses. |
| Richardson (2016) [37] | Case–Control Study | US | Ca: 50; Co: 50 | Ca: 18:32; Co: 34:16 | Ca: 48.4 ± 12.8; Co: 39.2 ± 12 | Ca: UNE+; Co: UNE- | Alcohol: Eth/wk (ounces) | Eth/wk didn’t considerably differ between UNE teams (1.2 ± 1.9 vs. 1.2 ± 2.2, p = 0.993). |
| Walsh (1970) [38] | Case–Control Study | Australia | Ca: 11; Co: 20 | 1:10 | Ca: 58 (41–73); Co: 54 (38–73) | PN on account of alcoholism | History of PN on account of alcoholism: Yes, No | History of heavy alcohol consumption related to diminished electrophysiology (p < 0.01), and fiber densities (3.39 ± 0.86 vs. 5.78 ± 0.90, p < 0.001). |
| Alessi (2020) [39] | Cross-Sectional Study | US | Overall: 934; Never Drinker: 103; Former Drinker: 89; Nonbinge Drinker: 567; Binge Drinker: 174 | Overall: 569:365; Never Drinker: 61:42; Former Drinker: 51:38; Nonbinge Drinker: 373:194; Binge Drinker: 84:90 | Overall: 38.3 ± 15.8; Never Drinker: 31.8 ± 16.8; Former Drinker: 44.1 ± 16.1; Nonbinge Drinker: 39.8 ± 15.8; Binge Drinker: 34 ± 13 | T1DM ± PN | Alcohol Consumption: Never, Former, Current (Nonbinge), Current (Binge) | Ne considerably decrease in by no means vs. former alcohol consumption (11% vs. 35%, p = 0.006). |
| Ammendola (2000) [40] | Cross-Sectional with Nested Case–Control | Italy | 62 | 18:44 | 43.3 (28–69) | Chronic alcoholism (>100 g/d for >2 yrs) ± PN | Mean alcohol-related illness length; Mean TLDE | Diminished electrophysiology considerably related to AUD (p < 0.01), longer illness length (p < 0.01), and better TLDE (p < 0.05). |
| Ammendola (2001) [41] | Cross-Sectional Study | Italy | Overall: 76; With Ne: 51; Without Ne: 25 | Overall: 21:55; With Ne: 14:37; Without Ne: 7:18 | Overall: 24–69; With Ne: 45.3 ± 9.4; Without Ne: 39.1 ± 7.7 | Chronic alcoholism ± PN | Family historical past of alcoholism (Yes, No); length of alcoholism; TLDE | Prolonged alcohol-related illness length (16.2 ± 9.4 vs. 11.1 ± 8.2, p < 0.05), excessive TLDE (27.9 vs. 14.8 ± 15.9, p < 0.05), and diminished electrophysiology (p < 0.01) considerably related to Ne. |
| Asai (2022) [42] | Cross-Sectional Study | Japan | Overall: 817; With CP: 35; Without CP: 782 | Overall: 431:386; With CP: 24:11; Without CP: 407:375 | With CP: 63.91 [60.11–67.72]; Without CP: 63.75 [63.02–67.72] | Chronic neck/shoulder/higher limb ache on account of any etiology | Current drinker: Yes, No | Alcohol consumption not considerably completely different between CP teams (42.86% vs. 47.19%, p > 0.05). |
| Beulens (2008) [43] | Cross-Sectional Study | Europe | 1857 | 893:964 | (15–60) | T1DM ± Ne | Alcohol consumption (g/wk) | Moderate alcohol consumption (30–70 g/wk)/frequency (5–7 d/wk) related to considerably decrease danger of Ne (0.61 [0.41–0.91], p < 0.01; 0.49 [0.34–0.71], p < 0.001). |
| Blackstock (1972) [44] | Cross-Sectional Study | United Kingdom | Chronic Alcoholism: 30; Hospital Personnel: 14 | Chronic Alcoholism: 7:23; Hospital Personnel: NR | Chronic Alcoholism: 44.8 (21–65); Hospital Personnel: 36.6 ± 6.9 | Chronic alcoholism ± PoN vs. hospital personnel | Chronic alcohol consumption/dependency | Greater electrophysiological perturbation in these with AUD vs. hospital personnel (p < 0.001). |
| Callaghan (2020) [45] | Cross-Sectional Study | US | BMI < 35 kg—Ne: 45; BMI > 35 kg—Ne: 110; BMI > 35 kg + Ne: 28 | BMI < 35 kg—Ne: 37:8; BMI > 35 kg—Ne: 87:23; BMI > 35 kg + Ne: 18:10 | BMI < 35 kg—Ne: 43.8 ± 12.1; BMI > 35 kg—Ne: 43.5 ± 11.2; BMI > 35 kg + Ne: 51.4 ± 9.6 | Ca: BMI > 35 kg ± Ne; Co: BMI < 25 kg
BMI < 35 kg—Ne; BMI > 35 kg—Ne; BMI > 35 kg + Ne | Alcohol: drinks/wk (previous yr) | Alcohol consumption not considerably completely different between Ne teams (p > 0.05). |
| Chang (2025) [46] | Cross-Sectional Study | China | DPN+: 163; DPN−: 107 | DPN+: 69:94; DPN-: 49:58 | DPN+: 67 (63–70); DPN−: 65 (62–69) | Elderly T2DM ± DPN | History of alcohol consumption (sure, no) | Alcohol consumption not considerably correlated with DPN (p = 0.310). |
| Chaware (2022) [47] | Cross-Sectional Study | India | 100 | 0:100 | 39.91 | Chronic alcoholism ± PN | Chronic alcoholism (>60 g eth/d or >15 drinks/wk): <5 yrs, 5–15 yrs, >15 yrs | Greater severity of DPN considerably related to longer consumption (<5 yrs: 21.8 ± 3.4; 5–15 yrs: 28.1 ± 3.7; >15 yrs: 33.7 ± 3.9; p = 0.001). |
| Ching (2024) [48] | Cross-Sectional Study | Malaysia | Overall: 1283; PN−: 943; PN+: 340 | Overall: 635:648; PN−: 495:448; PN+: 140:200 | 40.6 ± 12.9 (18–80) | Any etiology ± PN | Alcohol consumption (sure, no) | Alcohol consumption not considerably completely different between PN teams (18.53% vs. 19.72%, p > 0.05). |
| Chukwubuzo (2022) [49] | Cross-Sectional Study | Nigeria | 422 | 289:133 | 57.6 ± 10.1 | T1DM or T2DM ± PN | Alcohol Consumption: Yes, No | Alcohol consumption not considerably related to painful DPN (1.48 [0.74–2.98], p < 0.05). |
| Claus (1985) [50] | Cross-Sectional Study | Germany | Chronic Alcoholism: 30; Healthy Volunteers: 30 | Chronic Alcoholism: 0:30; Healthy Volunteers: 2:28 | Chronic Alcoholism: 38.2 ± 6.4 (26–48); Healthy Volunteers: 34.9 ± 6 | Chronic alcohol use ± PoN | History of alcohol consumption (as much as >400 mL/d for five–12 yrs) | Alcohol consumption (>12 yrs) considerably correlated with increased PoN frequency (p = 0.007). Electrophysiology considerably impaired vs. management (p < 0.01 for all). |
| Correa (2023) [51] | Cross-Sectional Study | Brazil | Overall: 444; LLBP: 313; PNBP: 33; WP: 98 | Overall: 289:155; LLBP: 188:125; PNBP: 26:7; WP: 75:23 | Overall: 39.72 ± 14.68; LLBP: 37.02 ± 13.39; PNBP: 8.45 ± 14.30; WP: 48.78 ± 15.59 | Chronic BP on account of any etiology | Alcohol Abuse: Yes, No | Reported alcohol consumption: LLBP: 12.1%, PNBP: 9.1%, WP: 12.2% (statistics NR). |
| D’Amour (1991) [52] | Cross-Sectional Study | Canada | Chronic Alcoholism: 20; Hospital Personnel: 20 | NR | Chronic Alcoholism: 46 (31–67); Hospital Personnel: 38 (21–50) | Chronic alcoholism ± PN vs. hospital personnel | History of alcohol consumption (>10 yrs or >100 g/d) | PN in 75% of AUD. Electrophysiology considerably diminished in sufferers with alcoholism vs. wholesome hospital personnel (p < 0.05). |
| Estruch (1993) [53] | Cross-Sectional Study | Spain | Chronic Alcoholism: 250; Healthy Volunteers: 100 | Chronic Alcoholism: 0:250; Healthy Volunteers: 0:100 | Chronic Alcoholism: 41 ± 11 (20–65); Healthy Volunteers: 40 ± 10 (20–65) | Chronic alcoholism ± PN vs. wholesome volunteers | Daily ethanol consumption (>100 g) over final 2 yrs | PN current in 16% (41) of AUD. AUD + PN had increased ethanol consumption vs. these with out PN (34.7 vs. 22.4, p < 0.001); TLDE was an impartial danger issue for PN in multivariate evaluation (p < 0.001). |
| Fernandez-Sola (1995) [54] | Cross-Sectional Study | Spain | 100 | 0:100 | 41 ± 9 (25–60) | Chronic alcoholism ± PN | Daily eth consumption (g/d); length of eth consumption; TLDE | PN (39% vs. 15%, p = 0.014) and TLDE (31.7 ± 17 vs. 23.3 ± 14, p = 0.01) considerably increased in these with power alcoholism + sort II fiber atrophy vs. with out. |
| Gierthmühlen (2024) [55] | Cross-Sectional Study | Denmark, France, Germany, Israel, Spain, UK | Overall: 1181; Ne + Pain: 843; Ne − Pain: 338 | Overall: 405:776; Ne + Pain: 285:558; Ne − Pain: 120:218 | Overall: 65.8 ± 12 (19–92); Ne + Pain: 64.9 ± 12.4 (19–92); Ne − Pain: 68.1 ± 10.6 (19–87) | Any etiology Ne ± ache | Current or earlier alcohol misuse (sure, no) | Prevalence of present or earlier alcohol misuse considerably decrease amongst these with ache vs. with out (6.6% vs. 11.5%, p = 0.0022). |
| Gylfadottir (2020) [56] | Cross-Sectional Study | Denmark | 5514 | 2355:3159 | 64.1 ± 10.9 | T2DM ± DPoN | Alcohol: >7 (F)/14 (M) models | Alcohol consumption above really helpful restrict not considerably related to DPoN (0.94 [0.74–1.18], p > 0.05), or painful DPoN (1.09 [0.81–1.46], p > 0.05), in multivariable logistic regression. |
| Hicks (2022) [57] | Cross-Sectional Study | US | Overall: 6902; With PN: 1181; Without PN: 5721 | Overall: 3589:3313; With PN: 443:738; Without PN: 3101:2620 | % (!) 40–49: 36 (0.9); 50–59: 27.8 (0.8); 60–69: 18.2 (0.6); 70–79: 12.8 (0.4); ≥80: 5.2 (0.3) | DM ± PN | Alcohol: Never, Former, Current | Alcohol consumption reported between PN teams: Never: 16.4%, Former: 27.2%, Current: 56.5% vs. 11.8%, 20.9%, 67.3% (statistics NR). |
| Ireri (2024) [58] | Cross-Sectional Study | Kenya | 314 | 182:132 | 58.49 ± 17.43 | DM ± Ne | History of alcohol consumption | Alcohol consumption not considerably related to Ne (p = 0.481). |
| Jeyam (2020) [59] | Cross-Sectional Study | Scotland | Overall: 5558; With DPN 715; Without DPN 4842 | Overall: 2449:3109; With DPN: 320:395; Without DPN 2129:2713 | ^ Overall: 44.7 (33, 55.2); With DPN: 50.6 (41, 59.3); Without DPN: 43.7 (32, 54.4) | T1DM ± DPN | Alcohol (u/wk): 2–6, 6–14, 14–21, 21–32, >32 | Alcohol consumption beneath 32 u/wk related to decrease odds of DPN (0.47 [0.29–0.75], p < 0.05), whereas above 32 u/wk was not (0.88 [0.56–1.38], p > 0.05). Authors counsel reverse causation–protopathic bias. |
| Li (2023) [60] | Cross-Sectional Study | China | Overall: 25,710; With PDPN: 14,699; Without PDPN: 11,011 | Overall: 10,785:14,925; With PDPN: 6240:8459; Without PDPN: 4545:6466 | ^ Overall: 63 (55, 71); With PDPN: 65 (56, 73); Without PDPN: 61 (53, 69) | T2DM ± PDPN | Alcohol Abuse: Yes, No | PDPN considerably decrease with alcohol abuse vs. with out (54.1% vs. 57.1%, p = 0.002). Authors counsel reverse causation–protopathic bias. |
| Mawdsley & Mayer (1965) [61] | Cross-Sectional Study | US | Chronic Alcoholism: 76; Healthy Personnel: 105 | Chronic Alcoholism: 12:64; Healthy Personnel: NR | Chronic Alcoholism: 25–69; Healthy Personnel: 20–70 | Chronic alcohol use ± PN | History of alcohol consumption (1 pint whisky to 1 gallon wine/d) | Electrophysiology considerably diminished vs. management (p < 0.001 for all). |
| McCulloch (1980) [62] | Cross-Sectional | Scotland | 541 | 0:541 | 44 ± 11.6 (20–59) | DM ± PN | Alcohol Intake: Moderate (6 drinks/yr to 10 drinks/wk) vs. Excessive (3–4 drinks/d to recognized alcoholism) | PN considerably increased in DM males with extreme alcohol consumption vs. these with reasonable (36% vs. 14%, p < 0.001) and most evident with shorter durations of DM (<5 yrs: 32% vs. 8%, p < 0.001). |
| Melgaard (1986) [63] | Cross-Sectional Study | Denmark | 468 | 0:468 | 45 | “Normal” inhabitants ± PoN | Alcohol questionnaire together with length and frequency of use | Dependence-related behaviors have been considerably correlated with disturbed electrophysiology (p < 0.05). |
| Mellion (2014) [64] | Cross-Sectional Study | US | Overall: 18; Heavy Drinkers: 9; Healthy Co: 9 | 9:9 | Heavy Drinkers: 35.4; Healthy Co: 43.3 | Heavy alcohol ingesting (>5 drinks/d (M), >4 drinks/d (F)) + PN vs. wholesome co | Eth consumed day by day (g); Average length heavy ingesting | Individuals with a historical past of heavy alcohol consumption exhibited diminished electrophysiology, in comparison with these with out (p < 0.05). |
| Mick (2020) [65] | Cross-Sectional Study | France, Italy, Spain, UK | 1030 | 651:379 | 60.2 ± 15.32; ^ 61 (49–72) | Localized NP on account of any etiology | Alcohol Abuse/Dependence: Current, Past, Never | Current or previous alcohol dependence/abuse was reported in 6.36% of sufferers with NP (additional statistics NR). |
| Mills (1986) [66] | Cross-Sectional Study | UK | 19 | 4:15 | (30–71) | Chronic alcoholism ± PN | History of alcoholism (120 g eth/d for 4+ yrs) | Chronic alcohol consumption (>100 g/d) considerably related to electrophysiological PN in 12/19 (statistics NR). |
| Monforte (1995) [67] | Cross-Sectional Study | Spain | Alcohol-Dependent: 107; Healthy Reference: 61 | Alcohol-Dependent: 18:89; Healthy Reference: 10:51 | Alcohol-Dependent: 43 ± 11; Healthy Reference: 41 ± 14 | Chronic alcohol use ± PN | History of alcohol consumption (>100 g/d (M) or >80 g/d (F) for >2 yrs) | Electrophysiological PN recognized in 36.8% of alcohol-dependent people vs. 1 management (1.64%), p < 0.001). Diminished electrophysiology correlated with better TLDE (r = −0.43, p < 0.001). |
| Nagakura (2023) [68] | Ecological Cross-Sectional Study | Japan | Pregabalin Reimbursement Claims per 1000 inhabitants; as much as 126 million | NR | (40–74) | NP on account of any etiology handled with pregabalin | Alcohol: Daily, Sometimes, Rarely/Never | Excessive alcohol consumption considerably related to prevalent NP (β = 0.2683, p < 0.01); low-to-moderate consumption diminished prevalence (r = −0.4713, p < 0.01); day by day consumption elevated prevalence (r = 0.6253, p < 0.01). |
| Nicolosi (2005) [69] | Cross-Sectional Study | Italy | 40 | 4:36 | 49.2 ± 10.3 (33–76) | Chronic alcohol use ± SoN | History of alcohol consumption (100–400 g/d for five–25 yrs) | SoN in 62.5% (25). Electromyography scores have been statistically considerably positively correlated with TLDE (r = 0.35, p < 0.03). |
| Nielsen (2022) [70] | Cross-Sectional Study | Denmark | 2839 | High CIPN Score: 274:146; Low CIPN Score: 1193:870 | ^^ High CIPN Score: 69; Low CIPN Score: 67; (18–99) | Cancer prognosis at any stage of remedy ± CIPN | Alcohol: sure/no + u/wk | Alcohol consumption considerably completely different between CIPN teams (60.2% vs. 73.5%, p < 0.001); excessive consumption (>14 u/wk) considerably related to excessive CIPN20 scores in males (22% vs. 11%, p = 0.002). |
| Papantoniou (2024) [71] | Cross-Sectional Study | Greece | 90 | 34:56 | 51.98 ± 8.86 (27–74) | AUD ± PN | Duration of Abuse; Total Alcohol Units (kg alcohol/lifetime) | Alcohol abuse considerably longer in these with Ne vs. with out (8.08 ± 7.25 vs. 6.92 ± 4.38, p = 0.024), and in these with impaired electrophysiology (p = 0.02). |
| Revesz (2022) [72] | Cross-Sectional Study | The Netherlands | Overall: 1516; With PN: 980; Without PN: 536 | Overall: 634:882; With PN: 445:535; Without PN: 189:347 | Overall: 69.1 ± 9.4; With PN: 70.1 ± 9.4; Without PN: 67.2 ± 9.2 | Colorectal most cancers survivors ± PN | Alcohol Consumption: Drinks/wk | Alcohol consumption considerably decrease in people with PN vs. with out (median 4 vs. 5 drinks/wk, vary 0–100 vs. 0–50, p = 0.006) in univariate evaluation solely. |
| Sahito (2022) [73] | Cross-Sectional Study | Pakistan | Overall: 1057; With PN: 607; Without PN: 450 | Overall: 414:643; With PN: 230:377; Without PN: 184:266 | 30–40: 119; 41–50: 316; 51–60: 324; 61–70: 165; >70 yrs: 133 | T2DM ± PN | History of alcohol consumption: Yes, No | Alcohol consumption reported between PN teams: 4.7% vs. 1.4% (statistics NR). |
| Shetty (2025) [74] | Cross-Sectional Study | India | 110 | 9:101 | 41.5 ± 11.9 (22–84) | Chronic liver illness ± PN | History of alcohol consumption (≥5 yrs) | Duration (13.9 ± 6.1 yrs vs. 9.6 ± 4.6 yrs, p < 0.05), and amount of alcohol consumption considerably increased in these with PN vs. with out. |
| Srivastava (2022) [75] | Cross-Sectional Study | India | 98 | 79:19 | 51.63 ± 10.68 | Cancer survivors ± CIPN | History of alcohol consumption: Yes (present, former), No | History of alcohol consumption not considerably related to CIPN sensory/motor severity (18.37% vs. 81.63%, p > 0.05). |
| Trendowski (2021) [76] | Cross-Sectional Study | US | With CIPN: 550; Without CIPN: 495 | With CIPN: 440:110; Without CIPN: 355:140 | ^^ With CIPN: 56 (23–79); Without CIPN: 58 (21–79) | African American most cancers survivors ± CIPN | Alcohol: sure (earlier 4 wks)/no; Alcohol Consumed (drinks/wk): 0–4, ≥5 | Alcohol consumption, drinks/d, not considerably related to CIPN (aPR: 0.88 [0.68–1.14], p = 0.32; aPR: 0.99 [0.91–1.07], p = 0.73). |
| Van der Velde (2020) [77] | Cross-Sectional Study | The Netherlands | Overall: 2401; High Sural SNAPA: 793; Med Sural SNAPA: 796; Low Sural SNAPA: 812 | Overall: 1174:1227; High Sural SNAPA: 464:329; Med Sural SNAPA: 377:419; Low Sural SNAPA: 334:478 | Overall: 59.3 ± 8.2; High Sural SNAPA: 56.4 ± 8.2; Med Sural SNAPA: 59.4 ± 7.9; Low Sural SNAPA: 62 ± 7.5 | T2DM ± PN | Alcohol: >7 (F)/14 (M) models | Alcohol consumption reported between PN teams: High: 26.7%, Medium: 25.8%, Low: 27.6% (statistics NR). |
| Villalta (1989) [78] | Cross-Sectional Study | Spain | Chronic Alcoholism: 70; Hospital Personnel: 70 | Chronic Alcoholism: 0:70; Hospital Personnel: NR | Chronic Alcoholism: 39.7 ± 9.6 (20–60); Hospital Personnel: 39.2 ± 11 (20–59) | Chronic alcoholism + PN vs. hospital personnel | History of alcohol consumption (>100 g/d for >2 yrs) | Prevalence of PN in 37% (21/56). Motor CV considerably negatively correlated with TLDE (r = −0.28, p < 0.05). |
| Vittadini (2001) [79] | Cross-Sectional Study | Italy | 296 | 87:209 | 45.2 ± 11.2 (20–77) | Chronic alcohol use ± PoN | History of alcohol consumption (>100 g/d) | Prevalence of electrophysiological PoN in 48.6% (144/296). PoN severity elevated as length of alcohol misuse lengthened (19.8% at 5 yrs to 40.4% at 10 yrs, p < 0.05). |
| Wang (2023) [80] | Cross-Sectional Study | China | Overall: 14,908; With DPN: 10,084; Without DPN: 4824 | Overall: 6322:8586; With DPN: 4365:5719; Without DPN: 1957:2867 | Overall: 61.3 ± 13, ^ 62 (53, 70); With DPN: 62.6 ± 12.5, ^ 63 (55, 71); Without DPN: 58.5 ± 13.5, ^ 59 (50, 67) | T2DM ± DPN | Alcohol Abuse (Pure Consumption in g/d): >40 (F)/60 (M); Never, Former, Current | Alcohol abuse considerably decrease amongst these with DPN vs. with out (8.2% vs. 11%, p < 0.001). |
| Wetterling (1999) [81] | Cross-Sectional Study | Germany | 241 | 64:177 | F: 43.8 ± 8.8; M: 41 ± 9.9 | Chronic alcohol use ± PoN | History of alcohol consumption: episodic (<1 d/wk), frequent (>3 d/wk), steady (day by day) | Prevalence of PoN elevated with growing alcohol consumption (11.3%, 29.6%, 29.9%, p = 0.025), and TLDE (p = 0.0104). |
| Wilson & Thompson (2021) [82] | Cross-Sectional Study | UK | Detoxification+: 17; Detoxification−: 13 | Detoxification+: 6:11; Detoxification−: 6:7 | Detoxification+: 46.8 ± 9 (37–64); Detoxification−: 54.5 ± 10.5 (30–70) | High-risk alcohol use ± historical past of cleansing ± NP | High-risk alcohol use by way of FAST rating ≥ 3 | Prevalence of NP (IDPQ ≥ 3) considerably better in these with historical past of cleansing (8/9) vs. these with out (1/12), p = 0.04. |
| Wu (2025) [83] | Cross-Sectional Study | US | Overall: 1068; MNSI+: 666; MNSI−: 402 | 641:427 | 84.1 (78–100) | Very outdated adults ± PN | Alcohol: Never, Former, Current | Current, former alcohol use not related to MNSI-defined neuropathy (0.90 [0.59–1.37], 1.02 [0.67–1.54], respectively). Former use not related to monofilament insensitivity (0.78 [0.52–1.16]), whereas present use was (0.65 [0.43–0.98]). |
| Yokoyama (2020) [84] | Cross-Sectional Study | Japan | Overall: 9914; Without DPoN: 6180; With DPoN: 2745 (with DPoNS: 1689; with UDoPN: 989) | Overall: 3715:6139; Without DPoN: 2273:3904; With DPoN: 1041:1705 (with DPoNS: 664:1025, with UDPoN: 397:530) | ^^ Overall: 66 (69–73); Without DPoN: 65 (57–71); With DPoN: 70 (63–77) (with DPoNS: 69 (63–76), with UDPoN: 67 (59–75)) | T2DM ± DPoN | Alcohol: Current, Former, Never | Former alcohol consumption related to increased odds of DPN (2.02 [1.25–3.27], p = 0.004), whereas present was not. Authors counsel reverse causation–protopathic bias. |
| Zahr (2019) [85] | Cross-Sectional Study | US | Ca: 154; Co: 99 | Ca: 43:111; Co: 41:58 | Ca: 49.8 ± 10.5 (21–77); Co: 50.9 ± 13.3 (21–74) | Ca: AUD ± PN; Co: wholesome ± PN | History of AUD | Prevalence of PN (Ca: 20 vs. 134; Co: 3 vs. 96; p = 0.007), vibration notion impairment (Ca: 41 vs. 113; Co: 15 vs. 84; p = 0.03), better with historical past of AUD. |
| Zambelis (2005) [86] | Cross-Sectional Study | Greece | 98 | 22:17 | 45.2 ± 9.9 (27–70) | Chronic alcohol dependence ± PoN | Daily alcohol consumption (g); length of alcohol abuse | Duration of alcohol consumption considerably increased in these with PoN vs. with out (19.19 vs. 14.14, p = 0.03). |
| Zambelis (2016) [87] | Cross-Sectional Study | Greece | 99 | 23:76 | 47 ± 19.6 | Alcohol dependence ± Ulnar Ne | Duration of alcohol dependence | UNE considerably related to length of alcohol dependence (1.09 [1.04–1.15], p < 0.001). |