Abstract
Introduction
The association between alcohol consumption and vitamin D status in young men remains controversial. Few data are available from sub-Saharan Africa, although necessary for better prevention of metabolic bone disease in adulthood. This study aimed to analyze the relationship between regular alcohol consumption and vitamin D status in young Cameroonian men.
Methods
It was a cross-sectional study on healthy males aged 18 to 45 with regular alcohol consumption within the last three months. We assessed their ethylic index (EI), hematological and hepatic biomarkers of chronic alcohol consumption, and 25 (OH) vitamin D (25(OH)D) concentrations, which were compared according to alcohol consumption (low < 20, moderate 20-39.9 and elevated ≥ 40 g/day) using ANOVA.
Results
155 participants were included, with a mean age of 31 (SD 6) years, a median alcohol consumption duration of 10 [7; 15] years and a median EI of 24 [14; 27] g/day. They mostly consumed beer (95%), with low (42%) and elevated (23%) predominant consumptions. Vitamin D deficiency (< 20ng/mL) was found in 63%. There was no difference in mean 25(OH)D concentrations between the three alcohol consumption groups. No correlation was found between the biomarkers of chronic alcohol consumption studied and 25(OH)D concentrations.
Conclusions
There appears to be no relationship between 25(OH)D concentrations and daily alcohol consumption in young Cameroonian men. Nevertheless, more data are needed, including vitamin D metabolism parameters to better understand this relationship.
Keywords: Alcohol, Vitamin D, Young men, Cameroon
Background
Alcohol is a widely consumed psychoactive substance in numerous cultures, and has been for millennia. Worldwide, the World Health Organization (WHO) estimates that over 2.3 billion adults consume alcohol, with a particularly high preponderance among men aged 15 to 49 [1, 2]. In Africa globally, and specifically in Cameroon, epidemiological data report impressive levels of consumption among young people, reaching 80% in some regions, two-thirds of whom are men [3, 4]. Alcohol consumption has been identified as an etiological factor in over 200 diseases, including neurological and liver disorders [5, 6]. However, it can also be associated with disorders of bone and calcium-phosphate metabolism, which may or may not be related to vitamin D status [7].
Vitamin D is an essential molecule in bone and calcium-phophate metabolism. The most significant related disturbance is vitamin D deficiency, defined biologically as a serum level of 25-hydroxy vitamin D below 20ng/mL [8]. It is a global health problem, affecting over a billion people in the general population [8, 9]. The relevance of vitamin D deficiency is not limited to osteomalacia. In young people, vitamin D deficiency can hinder the building of adequate bone capital, which is crucial for bone mass in adulthood, and is a risk factor for osteoporosis, which may affect men earlier than in old age [10, 11]. In the population with regular alcohol consumption, the prevalence of vitamin D deficiency ranges from 60.7 to 96.4% [12, 13]. Biologically, alcohol is thought to contribute to the genesis of this deficiency by interfering with the mechanisms of intestinal absorption and/or hepatic and renal conversion of vitamin D to its active form [14]. However, there is still some controversy when looking at the epidemiological data in the literature.
While some authors have found a positive association between alcohol consumption and vitamin D deficiency, others have not [12, 13, 15]. However, in sub-Saharan Africa overall, and in Cameroon more particularly, even though there is a high prevalence of alcohol consumption among young men and a high frequency of vitamin D deficiency in the general population, the potential link between these two situations remains poorly explored [4, 16, 17]. In the present study, we aimed to analyze the relationship between regular alcohol consumption and vitamin D status in Cameroonian men under 45, as they represent a key population for public health intervention. These data are important for improving early strategies at this age to prevent metabolic bone diseases and reduce their deleterious consequences later in adulthood.
Methods
Study design and setting
This study was carried out as part of the unfunded project EMAC (Etude des effets Métaboliques de l’Alcool chez l’homme Camerounais). This was a cross-sectional study conducted from October 2023 to February 2024 at the National Obesity Center located at the Yaoundé Central Hospital and at the Biochemistry Laboratory of the Yaoundé University Hospital Centre (Cameroon).
Participants
We included Cameroonian males aged 18 to 45 with regular and stable alcohol consumption who had consented to participate in the study. Regular consumption was defined as drinking at least once a week for at least one month. Stable drinking, was defined as drinking the same beverage, at the same frequency and in the same quantity, over the past three months. We excluded any participant receiving vitamin D supplementation or hypo- or hypercalcemic medication, as well as any participant with any chronic disease, such as impaired kidney or hepatic function or thyroid disease.
Sample size Estimation
The sample size was estimated using the formula adapted to our type of study contained in the manual by Whitley and Ball [18]. In the absence of data from Africa, we used the prevalence of vitamin D deficiency among male alcohol consumers contained in the Liu et al. study (60.7%) [19]. We used a 95% power and an 8% error rate, making a size of 143 participants.
Data collection
After obtaining administrative authorizations and ethical clearance, each potential participant was invited to the study by announcements in the general population residing in Yaoundé, the country’s capital. Data collection took place from October 1 to December 31, 2023. For all included participants, we collected age, clinical and biological data. Clinical data included:
Alcohol consumption: duration (since first consumption), type of alcohol consumed (beer, wine, whisky) and ethylic index (EI). EI was calculated in ethanol equivalence using the following formula: EI (g/day) = (average daily amount of alcoholic beverage consumed (ml) * degree of alcohol of beverage consumed * 0.8)/100. 0.8 representing the density of ethanol. Participants were stratified according to EI into: low consumption (< 20 g/day), moderate consumption (between 20 and 39.9 g/day) and elevated consumption (at least 40 g/day).
Lifestyle: tobacco consumption, sedentary lifestyle and physical activity. Physical activity was stratified by duration per week into: less than 30 min, 30 to 60 min, 60 to 90 min, 90 to 120 min, 120 to 150 min, and more than 150 min. Sedentary lifestyle was defined as physical activity of less than 30 min three times a week.
Other clinical data: family history osteoporosis, systolic and diastolic blood pressure (mmHg), weight, height to calculate body mass index (BMI), and abdominal circumference. BMI was classified according to WHO as normal (18 to 24.9), overweight (25 to 29.9), obesity grade 1 (30 to 34.9), grade 2 (35 to 39.9), and grade 3 (at least 40). Abdominal obesity was defined as an abdominal circumference of at least 94 cm according to the recommendations of the International Diabetes Foundation [20].
Biological data
Biological data were evaluated on a fasting venous blood sample collected without any tourniquet. They were:
Fasting blood glucose (8 h fasting, method of Trinder) and serum creatinine (modified Jaffé kinetic and colorimetric method), to exclude subjects with diabetes and those with a reduced glomerular filtration rate (GFR) of less than 60 ml/min. GFR was assessed according to the 4-parameter MDRD formula [21].
Biological markers of chronic alcohol consumption at the level of the liver (alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), and gamma glutamyltransferase (GGT)), and at the hematological level (hemoglobin level, mean corpuscular volume (MCV)). Liver enzyme activities were measured according to the recommendations of the International Federation of Clinical Chemistry and Laboratory Medicine [22–24]. We considered an elevation in ALAT or ASAT values to be from 40 IU/L, and GGT from 49 IU/L. The haemogram was performed using the Cyanhemato® automated system. MCV was considered normal between 80 and 100fL. Macrocytosis and microcytosis were defined as values below 80fL and above 100fL respectively. Anemia was defined as a hemoglobin level below 13 g/dL.
Calcemia measured by the CPC (O-Cresol Phthalein Complexon) method derived from Moorehead and Briggs, and albuminemia measured by the BCG (bromocresol green) method. We calculated corrected serum calcium from albumin values using the formula: Corrected serum calcium (mg/L) = measured serum calcium (mg/L) - albuminemia (g/L) + 35. Hypercalcemia was defined as a corrected serum calcium value exceeding 105 mg/L, and hypocalcemia as a value below 80 mg/L.
Serum 25 (OH) Vitamin D (25(OH)D) concentrations determined by competitive enzyme-linked immunosorbent assay (competitive ELISA) using a reagent manufactured by Pars Biochem Co. Ltd® in China. The reagents were validated by the Biochemistry Laboratory of the Yaoundé University Hospital Centre with an accuracy and precision at 10 ng/ml (95% CI ± 1.3), 20 ng/mL (95% CI ± 1.2), and 30 ng/ml (95% CI 1.15). We considered a normal value of 30 to 100ng/mL, an insufficiency of 20 to 29.9 ng/mL, a deficit of less than 20ng/mL, a severe deficit of less than 10 ng/mL, and an overdose for values above 100ng/mL [25].
Statistical analysis
The data collected were analyzed using SPSS software version 23.0. Graphics were designed using the same software. In the results, we present categorical variables with their count and percentages, continuous quantitative variables with their means and standard deviation (SD), and quantitative variables not following a normal distribution with median and interquartile range [q25; q75]. We investigated the association of clinical and biological data with ethylic index and 25(OH)D concentrations using Pearson’s correlation (r). Comparison of mean 25(OH)D levels between alcohol consumption groups was performed using the one-factor ANOVA test. For all tests used, the significance threshold was 0.05.
Results
We invited 200 participants, of whom 165 were eligible and 155 were finally selected. Their mean age was 31 (SD 6) years, with extremes of 19 and 45 years. The median ethylic index was 24 [14; 27] g/day, and the median duration of alcohol consumption was 10 [7 ; 15] years. Consumption was low in 64 (41%) and high in 35 (23%) participants. Beer was the most commonly consumed type of alcohol (95%). Sedentary lifestyle was found in 91 (59%); overweight and obesity in 54 (35%) and 36 (23%) respectively. Mean 25(OH)D concentrations were 19 (SD 18) ng/mL. Vitamin D deficiency was found in 98 (63%); it was severe in 58 (37%). Other laboratory abnormalities were elevated GGT (23%) and microcytosis (35%). Table 1 summarizes the characteristics of study participants.
Table 1.
CHARACTERISTICS of the sample
| Variables | Values |
|---|---|
| Age, mean (SD), years | 31 (6) |
| EI, median [IQ range], g/day | 24 [14 ; 27] |
| Type of alcohol beverages, n (%) | |
| Beer | 148 (95) |
| Whisky | 4 (3) |
| Wine | 3 (2) |
| EI level, n (%) | |
| Low (< 20 g/day) | 64 (41) |
| Moderate (20 to 39.9 g/day) | 56 (36) |
| Elevated (≥ 40 g/day) | 35 (23) |
| Tobacco consumption, n (%) | 21 (14) |
| Sedentary lifestyle, n (%) | 91 (59) |
| Physical activity per week, n (%) | |
| < 30 min | 42 (27) |
| 30 to 60 min | 25 (16) |
| 60 to 90 min | 24 (15) |
| 90 to 120 min | 23 (15) |
| 120 to 150 min | 12 (8) |
| ≥ 150 min | 31 (20) |
| Familial history of osteoporosis, n (%) | 3 (2) |
| SBP, mean (SD), mmHg | 126 (11) |
| DBP, mean (SD), mmHg | 82 (10) |
| BMI, mean (SD), kg/m² | 26.9 (5) |
| BMI class, n (%) | |
| Normal | 65 (42) |
| Overweight | 54 (35) |
| Grade 1 obesity | 25 (16) |
| Grade 2 obesity | 9 (6) |
| Grade 3 obesity | 2 (1) |
| Abdominal circumference, mean (SD), cm | 90 (13) |
| 25(OH) vitamin D, mean (SD), mg/L | 19 (18) |
| ASAT, mean (SD), UI/L | 25 (8) |
| ALAT, mean (SD), UI/L | 24 (9) |
| GGT, mean (SD), UI/L | 39 (27) |
| Calcemia, mean (SD), mg/L | 98 (10) |
| Hemoglobin level, mean (SD), g/dL | 13 (5) |
| MCV, mean (SD), fL | 81 (4) |
| Biological abnormalities, n (%) | |
| Vitamin D deficit | 98 (63) |
| Severe vitamin D deficit | 58 (37) |
| Vitamin D insufficiency | 23 (15) |
| Elevated ASAT | 7 (4) |
| Elevated ALAT | 11 (7) |
| Elevated GGT | 36 (23) |
| Anemia | 23 (15) |
| Microcytosis | 55 (35) |
| Macrocytosis | 0 (0) |
| Hypocalcemia | 5 (3) |
ALAT: alanine aminotransferase; ASAT: aspartate aminotransferase; BMI: body mass index; DBP: diastolic blood pressure; EI: ethylic index; GGT: gamma glutamyl-transferase; IQ: interquartile range [Q25; Q75]; MCV: Mean corpuscular volume; SD: standard deviation; SBP: systolic blood pressure
Among the relevant clinical variables and biomarkers measured, BMI (r = 0.2; p = 0.048) and GGT (r = 0.2; p˂0.01) were correlated with ethylic index, while age (r = 0.16; p = 0.01), abdominal circumference (r = 0.19; p = 0.01) and BMI (r = 0.2; p = 0.02) were correlated to 25(OH)D concentrations (Table 2).
Table 2.
Correlation between ethylic index, 25 (OH) vitamin D concentrations and relevant clinical and biological parameters
| Variables | Ethylic index | 25 (OH) vitamin D | ||
|---|---|---|---|---|
| r | p value | r | p value | |
| Age | 0.07 | 0.3 | 0.16 | 0.01 |
| Abdominal circumference | 0.1 | 0.1 | 0.19 | 0.01 |
| BMI | 0.2 | 0.048 | 0.2 | 0.02 |
| ASAT | 0.08 | 0.3 | 0.1 | 0.2 |
| ALAT | 0.01 | 0.8 | 0.03 | 0.6 |
| GGT | 0.2 | ˂0.01 | -0.04 | 0.6 |
| Hemoglobin level | 0.2 | 0.05 | 0.01 | 0.8 |
| MCV | 0.1 | 0.08 | -0.03 | 0.6 |
| Calcemia | 0.07 | 0.3 | 0.02 | 0.7 |
ALAT: alanine aminotransferase; ASAT: aspartate aminotransferase; BMI: body mass index; EI: ethylic index; GGT: gamma glutamyl-transferase; MCV: Mean corpuscular volume
There was no significant difference comparing 25(OH)D concentrations between low, moderate and high alcohol consumption groups (Fig. 1). Likewise, we found no association between 25(OH)D concentrations and biomarkers of chronic alcohol consumption (Table 2).
Fig. 1.
Comparison of mean 25 (OH) vitamin D concentrations between different alcohol consumption groups
Discussion
The metabolic consequences of alcohol consumption are numerous, set in gradually over time and linked to the quantity and duration of consumption; thus, young men are a key population for interventions aimed at preventing these complications. The relationship between alcohol and vitamin D is still poorly understood. The aim of the present study was to analyze the interaction between daily alcohol consumption and serum 25(OH)D concentrations in a sample of healthy young Cameroonian men. We found a prevalence of vitamin D deficiency of 63.2%, unrelated to daily alcohol consumption. We believe that these results are relevant and form the basis for future research on the subject, and already offer a glimpse into a number of possible avenues.
Our study showed that the mean 25(OH)D concentrations was 19 (SD 18) ng/mL; this is close to the mean levels (20ng/mL) found by Gill et al. 2014 in Australia [26] and Siddiqee et al. in 2023 in a meta-analysis in South Asian adults [27]. 25(OH)D concentrations were significantly associated with diet, which is known from the literature, as diet can contribute up to 25% of vitamin D concentrations [28]. In our population, we found a high prevalence of vitamin D deficiency (63.2%), i.e. almost two out of three people. The frequency of vitamin D deficiency in the general Cameroonian population varies between 10 and 40%. These data also raise the alarm about a greater deficiency among alcohol consumers [16, 29, 30]. These results are similar to those found by Duarte et al. in Portugal in 2020, where they estimated the prevalence of 25(OH)D concentrations below 20 ng/mL at 66.6% [13]. Similarly, Jiang et al, 2023 in Asia found a prevalence of 57.69% for vitamin D levels < 20 ng/mL [31]. Vitamin D deficit is highly prevalent in the general population worldwide, affecting 40–100% of adults [6]. Among alcohol consumers, Neupane et al. in 2013 in Nepal [12] found a prevalence of 64%; similarly, Liu et al. in 2023 [19] found a prevalence of vitamin D deficit of 60.7% in men suffering from alcohol dependence. This high prevalence of vitamin D deficiency should prompt the clinician to screen men who drink alcohol for it, and propose consistent supplementation with a view to correcting and preventing it by ensuring sufficient exposure to sunlight and an adequate diet.
On the analysis of the three alcohol consumption groups (low, moderate and high), we found no significant difference in 25(OH)D concentration. Similarly, we found no association with biomarkers of chronic alcohol consumption. These results are in line with those found by Neupane et al. in 2013; Aswathisasidharan et al. in 2022 in India; Tardelli et al. in 2017 in Brazil; Lee et al. in Korea in 2012 [12, 14, 32, 33]. They suggest that there is no direct link between alcohol consumption and serum vitamin D concentrations. However, there are a number of points to bear in mind. The balance between low and high consumers may come from the link between diet on the one hand and hepatic conversion of vitamin D on the other. Indeed, it has been shown that there is a link between alcohol consumption and an inadequate diet, which could have an impact on vitamin D intake [34–37]. It has also been suggested that at high daily consumption of alcohol may interferes with the conversion of 25(OH)D to 1,25 (OH) vitamin D, which could lead to a relatively higher 25(OH)D concentrations among alcohol consumers [33, 38]. Hence, we hypothesize that this result may reflect the balance between the lack of intake of vitamin D-rich foods and the lack of conversion of 25(OH) vitamin D with alcohol consumption. It will be crucial to evaluate this relationship taking into account the elements of vitamin D metabolism for a better interpretation.
Limitations of the study
A number of limitations need to be borne in mind when interpreting the results of our study. Firstly, the biological parameters assessed were measured only once, since their concentrations can vary over time. However, we used fairly strict selection criteria to limit measurement bias. Secondly, we did not assess vitamin D intake, sun exposure and other vitamin D metabolism parameters such as parathyroid hormone, as they are key determinants of 25(OH)D and needed to better understand the interaction with alcohol consumption. However, some parameters remain challenging to measure, and there is currently no validated standardized questionnaire for assessing vitamin D intake and sun exposure in our population. Nevertheless, this was a pilot study, which will enable us to put things into perspective and lay the foundations for a larger-scale study.
Conclusion
Vitamin D deficiency affects almost two out of three young men who regularly consume alcohol in our population. 25(OH)D concentrations do not appear to be influenced by the daily amount of alcohol consumed, nor by biological parameters linked to regular alcohol consumption. However, this relationship may be complex, and for a better understanding needs to be further investigated by integrating the evaluation of more parameters related to vitamin D metabolism.
Acknowledgements
The authors would like to thank Prof. Eugène Sobngwi, Dr. Claudine Jessica Yondo Ndedi, Dr Larissa Ange Tchuisseu Kwangoua, Dr Claude Bernard Yvan Momo and Dr Mbono Samba for their participation in data collection for the study.
Abbreviations
- 25 (OH) vitamin D
25(OH)D
- ALAT
Alanine aminotransferase
- ASAT
Aspartate aminotransferase
- BMI
Body mass index
- EI
Ethylic index
- GFR
Glomerular filtration rate
- GGT
Gamma glutamyltransferase
- MCV
Mean corpuscular volume
- WHO
World Health Organization
Author contributions
JRN: conceived the study, collected data, analyzed data, drafted and edited manuscript; DTT: collected and analyzed data; REYN: collected and analyzed data; DBE: collected data and revised manuscript; BF: revised manuscript; WNT: collected data; WTC: collected data; FA: collected data; VJAM: conceived the study, analyzed data and revised manuscript; MSN: conceived the study, analyzed data, revised manuscript and supervised the work. All authors read and approved final manuscript.
Funding
This research did not receive funds from any organization.
Data availability
All the dataset generated from this study are available from the corresponding author on request.
Declarations
Ethics approval and consent to participate
The study was approved by the Centre Regional Ethics Committee for Human Health Research in Cameroon (N°0721/CRERSHC/2023). All the participants read and signed a written informed consent before their inclusion in the study regarding the Helsinki declaration.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All the dataset generated from this study are available from the corresponding author on request.