Research - Journal of Drug and Alcohol Research ( 2022) Volume 11, Issue 10
Effects of Alcohol Use Disorder on Biochemical and Hematological Parameters of Adolescents
Eleazar Chukwuemeka Anorue1*, Parker Elijah Joshua1, Chioma Assumpta Anosike1 and Adama Grace Ngozi22Department of Education, University of Nigeria, Nigeria
Eleazar Chukwuemeka Anorue, Department of Biochemistry, University of Nigeria, Nigeria, Email: eleazar.anorue.02464@unn.edu.ng
Received: 03-Oct-2022, Manuscript No. JDAR-22-70201;;Accepted Date: Oct 24, 2022; Editor assigned: 05-Oct-2022, Pre QC No. JDAR-22-70201 (PQ); Reviewed: 19-Oct-2022, QC No. JDAR-22-70201; Revised: 24-Oct-2022, Manuscript No. JDAR-22-70201 (R); Published: 31-Oct-2022, DOI: 10.4303/JDAR/236204
Abstract
Background: Alcohol use disorder is becoming an increasing problem among adolescents. As a result, it has been reported that abuse of alcohol contributes to over 3 million deaths each year globally and is one of the world’s leading risk factors of morbidity, mortality and disability among adolescents.
Aim: Therefore, investigation was carried out to know the effects of alcohol use disorder on hematological and biochemical parameters of adolescents.
Method: The study was categorized into 3 groups comprising of non-drinkers (0 g/day), low drinkers (≤ 46 g/day), and high drinkers (≥ 46 g/day).
Result: It was found that biochemical and hematological parameters of high drinkers (≥ 46 g/day) were significantly lower (p<0.05) compared to that of non-drinkers and low drinkers.
Conclusion: The results of this study suggest that alcohol use disorder can lead to anemia, vulnerability to infection, liver toxicity, kidney failure, and other pathophysiological conditions among adolescents given to high intake of alcohol.
Keywords
Abuse; Adolescents; Alcohol use disorder; Biochemical; Hematological; Hemoglobin
Abbreviations
(EDTA) Ethylene diaminetetraacetic acid; (PCV) Packed cell volume; (RBC) Red blood cell; (WBC) White blood cell; (HB) Hemoglobin; (MDA) Malondialdehyde; (SOD) Superoxide dismutase; (CAT) Catalase; (GPx) Glutathione peroxidase; (GSH) Reduced glutathione; (ADH) Alcohol dehydrogenase; (ALT) Alanine aminotransferase; (ALP) Alkaline phosphatase; (TB) Total bilirubin; (DB) Direct bilirubin; (TAG) Triacylglycerol; (HDL) High density lipoprotein; (LDL) Low density lipoprotein
Introduction
Alcohol use disorder is a condition in which a person desires to consume alcohol even when it has negative impact on the health of the individual. A person with this condition does not have the willpower to stop drinking even when it is detrimental to the health of the individual. Although alcohol in itself is not bad, it becomes problematic when it takes precedence over all other activities. There are many problems associated with alcohol use disorder. Over time, regular alcohol consumption can disrupt the balance of gamma- aminobutyric acid (GABA) and glutamate [1]. GABA is a neurochemical that controls impulsiveness, while glutamate on the other hand stimulates the nervous system. Disruption of GABA balance can lead to impulse-drinking while disruption of glutamate can stimulate the nervous system leading to intoxication.
Furthermore, dopamine levels could rise, making the drinking experience more gratifying; hence the person loses control over how much alcohol consumed. Obviously, this comes with its own side effects. Some of the complications of alcohol use disorder include; alteration of the drinkers’ thought, emotions and general behavior, loss of muscle coordination, inability to speak properly, coma, fatigue, memory loss, liver diseases, hypertension, cardiovascular diseases, diabetes, erectile dysfunction, fetal alcohol syndrome, thinning bones, cancer, numbness, dementia, confusion, gastro-intestinal complication etc.,. The impact of alcohol use disorder in the society is increasing at an alarming rate. Inappropriate use of alcohol is one of the world’s leading risk factors of morbidity, mortality and disability. According to the National Institute of Health (NIH) in 2015, 15.1 million American adults had an alcohol use problem. According to World Health Organization, over 3.3 million deaths occur every year globally from the harmful use of alcohol. Only in the USA, acute intoxication directly results in about 2,200 deaths per year [2]. Also, according to Centers for Disease Control (CDC) data released January 2013, an average of 6 people died of alcohol poisoning each day in the USA from 2010 to 2012. This social vice is ever increasing, especially among adolescents. Therefore, this study was conducted to investigate the effects of alcohol use disorder on biochemical and hematological parameters of adolescents categorized as non-drinkers, low drinkers and heavy drinkers.
Materials and Method
Chemicals and reagents
The chemical and reagents used for this study were of analytical grade: 39.4% sodium chloride, 95% methylated spirit, 97% potassium phosphate salts, 92.5% sodium hydroxide, 35% concentrated hydrochloric acid (All Panhong Chemical Co., Shenzhen, Guangdong, China) and 100% distilled water (Energy Centre University of Nigeria, Nsukka, Enugu, Nigeria) [3].
Equipment, apparatus and instruments
Allegra X-14R centrifuge, (Beckman Coulter Co., Indianapolis, Indiana, USA), Spectrum Lab 23A spectrophotometer (Spectrum Laboratories, Stamford, Connecticut, USA), cotton wool (Jinniu District Hengnuan Cotton Plant, Chengdu, Sichuan, China), hypodermic syringes (Troge Medical GmbH, Hamburg, Germany), micropipettes (Globe Scientific Inc., Mahwah, New Jersey, USA), Pasteur pipettes (Globe Scientific Inc.), pH meter (Hanna Instruments, Woonsocket, Rhode Island, USA), refrigerator (Thermo-cool Public Ltd Co., Ilupeju, Lagos, Nigeria), water bath (Qinhuangdao YuanchenHardwares, Qinhuangdao, Hebei, China) [4].
Collection of blood sample
Whole blood (5 mL) was collected from each student volunteer using venepuncture into a Venoject tube containing ethylene diaminetetraacetic acid (EDTA) as an anticoagulant.
Experimental design
This study was conducted in a federal university in Nigeria among 30 undergraduate students aged 16-19 years. These students were categorized as non-drinkers, low drinkers and high drinkers [5]. Non-drinkers were students who have never taken alcohol; low drinkers were students who have taken ≤ 46 g/day between January to March 2022 while high drinkers were students who have taken ≥ 46 g/ day between January to March 2022. The frequency of alcohol consumption within the period of study was categorized thus;
Group 1: Non-drinkers (0 g/day)
Group 2: Low drinkers (≤ 46 g/day)
Group 3: High drinkers (≥ 46 g/day)
The ethanol equivalent intake in gram was calculated as follows: 633 ml beer=23 grams, 60 ml whisky=23 grams, 120 ml wine=11.5 grams, 180 ml sake=23 grams and 180 ml shochu=38 grams.
Determination of hematological parameters
Whole blood samples were collected intravenously. Hematological parameters such as Packed cell volume (PCV), Red blood cell (RBC), White blood cell (WBC), Hemoglobin (HB) and platelet were determined by standard methods as outline in the RANDOX commercial kit [6].
Determination of anti-oxidant parameters
Whole blood samples were collected intravenously and centrifuged to obtain the serum. Antioxidant and lipid peroxidation biomarkers such as malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione peroxidase (GPx) were determined by standard methods as outlined in the RANDOX commercial kit.
Determination of liver function parameters
Whole blood samples were collected intravenously and centrifuged to obtain the serum. Liver function biomarkers such as alcohol dehydrogenase (ADH), aspartate transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total bilirubin (TB) and direct bilirubin (DB) were determined by standard methods as outlined in the RANDOX commercial kit [7].
Determination of kidney function parameters and electrolytes
Whole blood samples were collected intravenously and centrifuged to obtain the serum. Kidney function parameters and electrolytes such as creatinine, urea, chloride, sodium, potassium and bicarbonate were determined by standard methods as outlined in the RANDOX commercial kit.
Determination of lipid profile
Whole blood samples were collected intravenously and centrifuged to obtain the serum. Lipid profile parameters such as Total cholesterol (CHOL), Triacylglycerol (TAG), High-Density Lipoprotein (HDL) and Low-Density Lipoprotein (LDL) were determined by standard methods as outlined in the RANDOX commercial kit [8].
Statistical analyses
One-Way ANOVA and Duncan Multiple Range Test (DMRT) were used to determine the biochemical and hematological effects of alcohol use disorder among these undergraduate students. Generally, statistical significance was carried out at p<0.05. Results were shown as mean ± standard deviation (SD) [9].
Results
Effects of alcohol use disorder on hematological parameters of undergraduate students
The result of the effect of alcohol use disorder on hematological parameters of the subjects showed that there was no significant difference (p>0.05) between non-drinkers and low drinkers [10]. However, hematological results of high drinkers were significantly lower (p<0.05) than non-drinkers and low drinkers (Table 1).
| Group | PCV (%) | RBC × 1012/L | WBC × 109/L | Platelet × 109/L | HB g/dL |
|---|---|---|---|---|---|
| Non-drinkers | 59.00 ± 1.00a | 300.52 ± 0.23a | 80.34 ± 0.11a | 100.29 ± 0.25a | 19.09 ± 0.09a |
| Low drinkers | 55.41 ± 0.39a | 295.44 ± 0.11a | 77.40 ± 0.38a | 97.56 ± 0.29a | 18.25 ± 0.10a |
| High drinkers | 13.78 ± 6.21b | 41.30 ± 0.06b | 11.15 ± 9.46b | 20.33 ± 0.10b | 4.74 ± 2.06b |
Note: Results are presented as Mean ± STD of 10 replications. Mean values with different letters as superscripts across column are considered significant at p<0.05.
Table 1: Effects of alcohol use disorder on hematological parameters of adolescents
Effects of alcohol use disorder on antioxidant parameters of undergraduate students
The result of the effect of alcohol use disorder on antioxidant parameters of the subjects showed that there was no significant difference (p>0.05) between non-drinkers and low drinkers [11]. However, antioxidant results of high drinkers were significantly lower (p<0.05) than non-drinkers and low drinkers except MDA which showed a significant (p<0.05) increase (Table 2).
| Group | SOD U/mg | CAT U/mg | GP × U/mg | GSH mg/dL | MDA mg/mL |
|---|---|---|---|---|---|
| Non-drinkers | 11.49 ± 0.45a | 2.41 ± 0.52a | 44.01 ± 4.52a | 5.65 ± 1.88a | 0.79 ± 0.29a |
| Low drinkers | 11.28 ± 0.72a | 2.31 ± 0.01a | 43.10 ± 0.09a | 4.55 ± 1.16a | 0.81 ± 0.03a |
| High drinkers | 3.02 ± 3.40b | 0.99 ± 0.07b | 7.05 ± 5.87b | 0.87 ± 0.37b | 4.82 ± 3.33b |
Note: Results are presented as Mean ± STD of 10 replications. Mean values with different letters as superscripts across column are considered significant at p<0.05.
Table 2: Effects of alcohol use disorder on antioxidant parameters of adolescents
Effects of alcohol use disorder on liver function parameters of undergraduate students
The result of the effect of alcohol use disorder on liver function parameters of the subjects showed that there was no significant difference (p>0.05) between non-drinkers and low drinkers [12]. However, liver function results of high drinkers were significantly lower (p<0.05) than non-drinkers and low drinkers (Table 3).
| Group | ADH iu/L | AST iu/L | ALT iu/L | ALP iu/L | TB mg/dL | DB mg/dL |
|---|---|---|---|---|---|---|
| Non-drinkers | 48 ± 1a | 42 ± 1a | 34.38 ± 0.47a | 36.42 ± 0.41a | 0.45 ± 0.25a | 0.25 ± 0.01a |
| Low drinkers | 46.03 ± 0.05a | 40.42 ± 0.39a | 32.58 ± 0.17a | 33.27 ± 0.16a | 0.53 ± 0.15a | 0.32 ± 0.2a |
| High drinkers | 8 ± 06b | 10 ± 5b | 15.41 ± 0.17b | 12.49 ± 3.26b | 1.78 ± 1.10b | 2.82 ± 1.86b |
Table 3: Effects of alcohol use disorder on liver function parameters of adolescents
Effects of alcohol use disorder on kidney function parameters and electrolytes of undergraduate students
The results of the effect of alcohol use disorder on kidney function parameters and electrolytes of the subjects showed that there was no significant difference (p>0.05) between non-drinkers and low drinkers. However, kidney function and electrolytes result of high drinkers were significantly lower (p<0.05) than non-drinkers and low drinkers (Table 4).
| Group | UR mg/dL | Creat mg/dL | CL mmol/L | HC03 mmol/L | K mmol/L | Na mmol/L |
|---|---|---|---|---|---|---|
| Non-drinkers | 36.48 ± 0.44a | 1.35 ± 0.05a | 97.29 ± 0.51a | 24.15 ± 0.16a | 6.72 ± 0.03a | 169.18 ± 0.16a |
| Low drinkers | 35.15 ± 0.24a | 1.24 ± 0.35a | 96.48 ± 0.49a | 24.44 ± 0.40a | 6.62 ± 0.03a | 167.19 ± 0.17a |
| High drinkers | 10.12 ± 0.17b | 0.47 ± 0.31b | 32.39 ± 0.34b | 7.15 ± 0.17b | 2.39 ± 0.43b | 42.34 ± 0.48b |
Note: Results are presented as Mean ± STD of 10 replications. Mean values with different letters as superscripts across column are considered significant at p<0.05.
Table 4: Effects of alcohol use disorder on kidney function parameters and electrolytes of adolescents
Effects of alcohol use disorder on lipid profile of undergraduate students
The result of the effect of alcohol use disorder on lipid profile parameters of the subjects showed that there was no significant difference (p>0.05) between non-drinkers and low drinkers. However, liver function results of high drinkers were significantly lower (p<0.05) than non-drinkers and low drinkers (Table 5).
| Group | CHOL mmol/L | TAG mmol/L | LDL mmol/L | HDL mmol/L |
|---|---|---|---|---|
| Non-drinkers | 2.56 ± 1.32a | 1.20 ± 0.20a | 2.13 ± 0.35a | 1.70 ± 0.30a |
| Low drinkers | 2.97 ± 1.05a | 1.40 ± 0.40a | 2.40 ± 0.40a | 1.50 ± 0.10a |
| High drinkers | 35.07 ± 1.53b | 39.1 ± 0.10b | 44.50 ± 0.50b | 0.12 ± 0.10b |
Table 5: Effects of alcohol use disorder on lipid profile of adolescents
Discussion
Analysis was done to know the effects of alcohol use disorder on biochemical and hematological parameters of undergraduate student volunteers. The result showed that there was significant decrease (p<0.05) in packed cell volume, red blood cell, white blood cell, platelet and total hemoglobin of high drinkers compared to none and low drinkers. Packed cell volume is the percentage of red blood cells in circulating blood. A decreased PCV is indicative of loss of circulating red blood cell as a result of destruction of the cells [13]. This suggests that alcohol use disorder (>46 g/ day) could lead to destruction of the circulating red blood cells such that there won’t be enough red blood cell in circulation. The mechanism behind this could be by induction of hemolysis which causes constant breakdown of red blood cells and this will ultimately lead to anemia. On the other hand, white blood cells are part of the body’s immune system that helps the body fight infection and other diseases. Decrease in white blood cell suggests that alcohol use disorder (>46 g/day) can lower the immune system, thereby lowering the body’s ability to fight infection and other diseases. Platelets are pieces of very large cells in the bone marrow called megakaryocytes. Generally, they form blood clots to slow or stop bleeding and help wound healing. Decreased platelet suggests that alcohol use disorder (>46 g/day) could lower production of platelet and hence delay wound healing. These findings corroborate the results of Gacouin (2012), Nakanishi (2003), Ballard (1997) and Girard et al. (1987) who also reported decreased packed cell volume, red blood cells, white blood cells and platelet of heavy alcohol drinkers. Decrease in total hemoglobin suggests that high alcohol use disorder (>46 g/day) exacts deteriorative effects on hemoglobin leading to breakdown of the heme group and loss of its oxygen carrying ability. This is in line with the result of an unpublished study on the effect of alcohol use disorder on human oxyhemoglobin that showed that high blood alcoholic concentrations led to decrease in oxyhemoglobin concentrations and oxidation of oxyhemoglobin.
Furthermore, the result of the study showed that alcohol use disorder (>46 g/day) led to significant (p<0.05) decrease in all the antioxidant parameters except MDA which showed a significant (p<0.05) increase. Antioxidant enzymes catalyze reactions to neutralize free radicals and reactive oxygen species [14]. They form the body’s endogenous defense mechanism to help protect against free radical-induced cell damage. In the occasion of generation of free radical and reactive oxygen species, they tend to increase in their concentration in order to neutralize the free radicals and reactive oxygen species generated. However, when the free radicals and reactive oxygen species generated are too much, they tend to overwhelm the enzymes repair capacity and causes depletion in their concentration [15]. Therefore, the significant (p<0.05) decrease in antioxidant enzyme concentrations observed in this study suggests that alcohol use disorder (>46 g/day) causes generation of free radicals and reactive oxygen species too much for the antioxidant enzymes to neutralize, thus, overwhelming the antioxidant repair capacity and leading to their depletion. This accounts for the lipid peroxidation indicated by significant (p<0.05) increase in malonaldehyde concentration observed in this study. Thus, increase in malonaldehyde concentration suggests that alcohol use disorder (>46 g/day) can lead to oxidation of lipids; a mechanism implicated in many pathological conditions such as cardiovascular diseases, liver damage and kidney failure. This corroborates the results of Wei et al. (2013) and Baraona and Lieber (1979) that reported increased MDA in rats treated with alcohol.
Liver function parameters are used to study the health of the liver. High or low levels of these parameters indicate liver disease or damage [16]. The result of our study showed that alcohol use disorder (>46 g/day) led to significant (p<0.05) decrease in alcohol dehydrogenase, aspartate transaminase, alanine aminotransferase and alkaline phosphatase but a significant (p<0.05) increase in total bilirubin and direct bilirubin. Alcohol dehydrogenase initiates the step for the breakdown of alcohol to a less harmful form in the body. Decrease in alcohol dehydrogenase concentration suggests that alcohol use disorder (>46 g/day) could lead to depletion of the enzyme, thus making the liver prone to damage. Interestingly, the significant increase in total and direct bilirubin support the reduction in red blood cell observed in this study. Since decrease in red blood cell is due to excessive breakdown of RBC, there tend to be elevated level of bilirubin due to excessive breakdown of RBC [17]. This observation corroborates the result of Rosoff et al. (2019) who also reported decrease in alcohol dehydrogenase, aspartate transaminase, alanine aminotransferase, alkaline phosphatase, and increase in total and direct bilirubin of rats treated with high concentration of alcohol.
Moreso, the result of this study showed that alcohol use disorder (>46 g/day) could lead to significant decrease (p<0.05) in creatinine and urea. Creatinine is a waste product made by the muscles as part of regular everyday activity while urea is a nitrogenous waste product of protein and ammonia in the body [18]. Normally, the kidneys filter creatinine and urea from the blood and send it out of the body in the urine; too much or very low creatinine and urea are indicative of kidney disorder. Therefore, the significant (p<0.05) decrease in creatinine and urea observed in this study suggests that alcohol use disorder (>46 g/day) could cause kidney dysfunction. On the other hand, electrolytes are elements and compounds that occur naturally in the body and usually present in the blood. They control important physiological functions in the body and any imbalance in their concentration can affect their physiological functions, which could lead to other pathological conditions. This study showed that alcohol use disorder (>46 g/day) led to significant (p<0.05) decrease in chloride, bicarbonate, potassium and sodium. This suggests that alcohol use disorder (>46 g/day) could cause electrolyte imbalance leading to condition such as hyponatremia, hypokalaemia, hydration, anaemia, hypertension, muscle disorder, neurological disorder, heart problem and kidney disorder. This corroborates the result of Molla et al. (2020) who reported decreased electrolytes, urea and creatinine in rats treated with high concentrations of alcohol.
Finally, the result of the study showed that alcohol use disorder (>46 g/day) led to significant (p<0.05) increase in total cholesterol, triacylglycerol, and low-density lipoprotein concentrations except high density lipo-protein which showed significant (p<0.05) increase in concentrations [19]. High concentrations of total cholesterol, triacylglycerol, low-density lipoprotein and decreased high density lipoprotein are usually implicated in diseases such as sclerosis, cardiovascular diseases, obesity and diabetes. This suggests that alcohol use disorder (>46 g/day) could make an individual vulnerable to cardiovascular diseases, obesity and diabetes. This corroborates the results of George et al. (2019) and Rosoff et al. (2019) who also reported increased total cholesterol, triacylglycerol, low density lipo- protein and decreased high density lipo-protein in rats treated with high concentrations of alcohol.
Conclusion
In this study, investigation was carried out to know the effect of alcohol use disorder (>46 g/day) on biochemical and hematological parameters of adolescents. It was found that alcohol use disorder (>46 g/day) led to deleterious effects on biochemical and hematological parameters of adolescents categorized as high drinkers (>46 g/day) [20].
Acknowledgement
Thanks to Department of Biochemistry, University of Nigeria, Nsukka for providing the chemical reagents and equipment for this study.
Author Contributions
All authors made significant contributions to the conceptualization and design of the study, read and approved the final manuscript.
Consent for Publication
All authors have gone through the manuscript and given their consent for publication.
Ethical Approval and Consent to Participate
The subjects gave their consent to participate and the study was conducted in accordance to the regulations and approval of the Ethics and Biosafety Committee of the Faculty of Biological Sciences, University of Nigeria, Nsukka.
Availability of Data and Materials
Not applicable.
Competing Interests
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Funding
No funding was received for this work.
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