Alkoholizm i Narkomania

Full text

3/2025 vol. 38
Original article

Biochemical indicators of alcohol and physiological hunger in alcohol-dependent men – a preliminary study

Damian Czarnecki 1
,
Anna Długosz 2
,
Jacek Budzyński 3
,
Jan Chodkiewicz 4
,
Ewa Żekanowska 5
,
Zofia Rosińska 6
,
Napoleon Waszkiewicz 7
,
Małgorzata Sidor 1
,
Joanna Wróblewska 8
,
Marcin Ziółkowski 1

  1. Department of Preventive Nursing, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

  2. Department of Food Industry Technology and Engineering, Bydgoszcz University of Science and Technology, Bydgoszcz, Poland

  3. Department of Vascular and Internal Diseases, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

  4. Institute of Psychology, Department of Clinical Psychology, University of Lodz, Lodz, Poland

  5. Department of Pathophysiology, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

  6. Department of Nutrition and Dietetics, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

  7. Department of Psychiatry, Medical University of Białystok, Poland

  8. Department of Medical Biology and Biochemistry, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Torun, Poland

Alcohol Drug Addict 2025;38(3):131-144

DOI: https://doi.org/10.5114/ain.2025.161820
Data publikacji online: 2026/05/29
Article file
AIN-Czarnecki.pdf
Confronting perimenopausal women’s knowledge of coronary heart disease with their health behaviours. Controversial role of hormone replacement therapy in the protection of coronary heart disease


■ Introduction

Recurring alcohol use is a severe and frequent element when alcohol-dependence treatment fails. One of the most essential factors of relapse in alcohol treatment therapy is alcohol hunger [1, 2]. There is a large body of research devoted to explaining the factors determining the desire to drink alcohol [3, 4]. Earlier analyses have suggested that the occurrence of alcohol hunger may be related to physiological mechanisms regulating appetite (hunger and satiety) [5-9]. 

We already know that the appetite regulation process is complex and depends on external sti­muli like taste, smell, temperature, culture and social behaviour; internal factors including hormones from fat tissue and digestive tract neuropeptides also play a part [10-13]. 

The regulating mechanisms of pre-meal hunger include control of appetence at the central level
by neuropeptide orexin and proopiomelanocortin (POMC) [14]. A higher concentration of orexin increases pre-meal appetite, stimulating food intake while POMC is considered to be an anorectic agent, stimulating the feeling of satiety [14, 15]. 

The intensity of pre-meal appetite is also mo­dulated by ghrelin concentration, and the feeling of satiety is induced by leptin and interleukin 6 (IL-6). Ghrelin stands in opposition to POMC while simultaneously acting as a stimulator of neuropeptides. Leptin is produced by adipocytes, stimulating central POMC secretion and reducing the secretion of neuropeptide Y (NPY) and Agouti protein, which ultimately increases the feeling of satiety [5-8, 14, 16]. IL-6 participates in the inhibition of appetite [17]. The appetite and satiety control mechanism involving these biochemical mediators is illustrated in Figure 1. The Figure shows selected factors regulating hunger and satiety, including those not considered in this study. 

We assume that alcohol consumption might activate similar mechanisms of food-intake regulation as any other food, with the only difference being in alcoholic drinks with specific properties of taste and brain reward-system interaction. There is strong evidence suggesting that the same neuronal structures responsible for food hunger participate in modulating alcohol craving [21-23]. It is noteworthy that our earlier analyses showed that over 18% of alcohol-dependent patients confuse alcohol hunger with pre-meal hunger. Moreover, approximately 54% of patients believe that the confusion of these hungers may increase the risk of alcohol drinking relapse [24]. All the current scientific evidence justifies the search for standard mechanisms of nutrition and recurrences of alcohol drinking and provides a rationale for planning new, efficient therapeutic strategies.

This study aimed to compare the serum concentrations of selected appetite-regulating neuropeptides and cytokine including orexin, ghrelin, leptin, POMC and IL-6 between alcohol-dependent men and healthy controls. Additionally, the study examined the associations between these biochemical markers and the intensity of alcohol craving, pre-meal physiological hunger and anthropometric parameters (waist-to-hip ratio – WHR, body fat percentage – %FM, body mass index – BMI). 

We hypothesised that alcohol-dependent individuals exhibit dysregulation in appetite and satiety mechanisms, characterised by changes in ghrelin levels and IL-6 concentrations, which may contribute to heightened alcohol craving and the risk of relapse.

This exploratory study sought to answer the following research questions: 

1. Do alcohol-dependent individuals differ significantly from healthy controls in terms of appetite-regulating neuropeptide and IL-6 levels (central or peripheral)? 

2. Are these biomarkers associated with the intensity of alcohol craving and physiological hunger?

3. Do anthropometric parameters correlate with biomarker concentrations and the subjective experience of hunger?

Generally, we tried to assess which of the selected biochemical factors in the central or peri­pheral areas play a role in the initiation of alcohol craving. We need this information to improve treatment for alcohol-dependent individuals.

The analysis was not pre-registered and the results should be considered exploratory.

■ Material and methods


Characteristics of the studied sample

The study was carried out on 54 males in the addiction treatment unit, who were of an average age of 45 (in the range 27-72) and on 20 males of an average age of 43 (in the range 22-72) as a control group; all were under examination at an occupational health centre. Patients and control subjects were each studied once (patients to the seventh day of hospitalisation). 

The inclusion criteria for the alcohol-dependent patient group were alcohol dependence diagnoses according to the International Classification of Diseases (ICD-10) [25] and patients’ consent to participate in the study. The patients’ exclusion criteria were metabolic disorders (e.g. diabetes) and cognitive deficits that would make informed consent impossible. 

The criteria for inclusion in the control group were an absence of alcohol and drug dependence, a “0” score on the Short Alcohol Dependence Data Questionnaire (SADD) [26], age or BMI level similar to the patient group and consent to participate in the study. The control group exclusion criteria were metabolic disorders (diabetes), a score higher than “0” on the SADD scale and cognitive deficits that would make conscious consent impossible.

Methods

The study was cross-sectional. Each examined patient was evaluated for age and clinical variables. These included the frequency and intensity of incidents of pre-meal hunger and alcohol craving measured using the Visual Analogue Scale (VAS) [27] where 0 indicated absence of hunger and 10 indicated very intense hunger. Hunger and craving were treated as motivations for appetitive behaviours that increase the risk of relapse. These variables were expressed as episodes per week. 

Additionally, the duration of alcohol consumption during the 30 days prior to the examination was recorded as well as the intensity of alcohol drinking over the same period. A standard drink was defined as 10 g of pure ethanol, which corresponds to 30 ml of 40% vodka, 100 ml of 12% wine and 250 ml of 5% lager beer. 

Alcohol dependence severity was measured using the SADD questionnaire. The SADD allows the severity of alcohol dependence to be categorised where the sum of 1-9 points indicates mild dependence, 10-19 moderate dependence and 20-45 points severe dependence [26]. 

Anthropometric data, including measurements of body mass (in kilograms), height (in centimetres) and waist and hip circumferences (in centimetres) were obtained using standard techniques and calibrated equipment. We measured skin-fat folds with skinfold callipers above the triceps and biceps above the suprailiac muscles and above the hip. We expressed our measurements in millimetres (mm). The BMI (kg/m²) was calculated based on body mass and stature measurements. The index of body fat tissue distribution was calculated as a WHR with the widely accepted norm of ≤ 0.9 for males [28]. The Durnin and Womersley method was used to calculate the percentage of body-fat mass [29, 30]. 

Every participant had blood drawn from the antecubital vein into a dry test tube before consuming their first meal between 7:00 and 8:00 a.m. We measured the concentration of orexin (orexin-A – OXA), POMC, IL-6, leptin, ghrelin and insulin in patients’ serum with the ELISA method (Cloud-Clone Corp. and LDN Labour Diagnostika Nord GmbH & Co. KG). The serum was obtained from these blood probes. After the serum was drawn, we initiated the centrifugation procedure at 4°C at 3600 rpm. The obtained serum was kept at –80°C.

Bioethics

The subjects had provided written informed consent and the study protocol was approved by the institute’s human research committee. The study was carried out with the permission of the Bioethical Committee (No. KB243/2008). Each patient provided informed consent for the examinations, which were performed in accordance with the Helsinki Declaration.

Statistical analysis

The distribution of variables was checked using a Kolmogorov-Smirnov test. Due to the small number of patients in the selected subpopulations, we used the non-parametric Mann-Whitney U test, Spearman’s ρ correlation test and the χ2 test (Fisher’s Exact test) with a p-value of ≤ 0.05 adopted as the statistical significance level. Statistical analysis was performed using the IBM SPSS 27 (IMAGO7) statistical package.

■ Results

As shown in Table I, neither the patient subpopulation nor the control group differed in terms of POMC, orexin, leptin, blood insulin concentration, body mass, BMI. However, alcohol dependent patients had lower ghrelin, %FM (% fat mass), higher IL-6 serum concentrations and higher WHR, a higher number of drinking days and standard drinks during the last 30 days, a higher SADD score and a higher prevalence of smoking cigarettes than the control group (Table I). 

As Table II shows, POMC was positively and statistically significantly but weakly correlated with the number of standard drinks consumed in the 30 days before the treatment, with the number of drinking days 30 days before the treatment and with the number of alcohol craving episodes per day. The number of alcohol craving episodes per day is significantly positively correlated with serum POMC concentration and significantly negatively correlated with IL-6 levels. In contrast, the number of alcohol craving episodes per week is significantly negatively correlated with WHR. It should also be noted that the number of alcohol-craving episodes per day is positively correlated with the intensity of alcohol craving as measured using a VAS (correlation data not shown in the table; r = 0.448, p = 0.001). Orexin was negatively and statistically significantly correlated with leptin (r = –0.334), and showed a trend towards a relationship between orexin and the intensity of pre-meal hunger (r = 0.250). The patient group showed a negative correlation between IL-6 and number of alcohol craving episodes per day (r = –0.376) or a positive correlation with length of alcohol dependence (r = 0.325). Insulin was negatively and statistically significantly correlated with the intensity of pre-meal hunger (r = –0.266) and positively correlated with leptin (r = 0.528). Leptin was positively and statistically significantly correlated with BMI (r = 0.393), %FM (r = 0.404), and WHR (r = 0.316) and negatively correlated with smoking cigarettes (r = –0.319). %FM was negatively correlated with the intensity of pre-meal hunger (r = –0.310), length of alcohol dependence (r = –0.325) or smoking cigarettes (r = –0.319) and positively with BMI (r = 0.582). BMI was negatively correlated with the intensity of pre-meal hunger (r = –0.261) and smoking cigarettes (r = –0.347).

■ Discussion

In the present study, we analysed the links between serum concentrations of hunger and satiety neuromodulators (orexin, leptin, POMC, ghrelin and IL-6) and alcohol craving as well as with pre-meal appetite, the quantity of alcohol consumed 30 days before analysis and the severity of alcohol dependence. We did not directly show differences in concentrations of orexin, leptin and POMC between patients and the control group participants. However, alcohol dependent male patients had lower ghrelin and higher IL-6 serum concentrations (Table I). These results can partly suggest the role of hunger and satiety neuromodulators in the pathomechanism of alcohol dependence and craving, probably via modulation of the reward limbic system that regulates eating behaviours, reproduction and psychoactive substance intake [31-37]. On the other
hand, two axies of food intake regulation are mentioned: short-lived, which comes from the current eating and has to do with the satiety feeling and inhibition of food intake and long-lived, hormonally regulated (leptin, insulin, ghrelin) eating, which has to do with appetence modulation as well as control of energy resources [13, 38]. It is possible that the absence of the above-mentioned relation (ghrelin vs. orexin, leptin, POMC) observed in this study may result from the fact that the analysis involved total ghrelin, which consists of acylated and deacylated ghrelin. The action of both ghrelin forms is, as assumed, often synergistic; anyhow, it is also, importantly, independent [39]. However, the relationship between alcohol misuse or dependence and alterations in appetite-regulating signals like reduced levels of orexigenic ghrelin and elevated levels of IL-6 remains complex and may reflect underlying inflammatory mechanisms [40, 41]. 
A potential explanation for this involves disrupted ghrelin signalling, either through impaired secretion or diminished receptor sensitivity, possibly resulting from damage to the gastric mucosa, the primary site of ghrelin synthesis. In turn, elevated IL-6 levels may originate from increased visceral adiposity, as suggested by higher WHR observed in alcohol-dependent individuals (Table I) [36].
A study by Rose et al. [42] found that drinking alcohol increases the desire to eat; in addition, alcohol can disrupt the natural appetite and satiety regulations associated with the need to eat. Alcohol consumption contributes to unhealthy eating behaviours, including the consumption of low- quality foods. Rose et al. [42] suggest that indivi­duals who display a tendency to lack control over eating may be particularly susceptible to unhealthy eating behaviours as a result of alcohol intake and the influence of disinhibiting environments. Rose et al. [42] clearly highlight the close relationship between alcohol drinking and eating behaviour. 

We did not find differences in orexin and POMC serum concentrations between patients with alco­hol dependence and persons from the control group (Table I). These observations do not corrobo­rate the reference data, which showed that POMC intensifies the orexige­nic action of orexin [43] and suggest a link between alcohol craving and levels of POMC and orexin (it can be an indirect link). POMC is secreted by the arcuate nucleus and is a precursor of cocaine and amphetamine-regulated transcript peptide (CART) and the melanocyte- stimulating hormone (MSH), present in neuro­transmitters causing the feeling of satiety [44]. The sense of satiety also results from the activation of melanocortin receptors (type 4) in the ventromedial nucleus through POMC and CART [45]. In turn, Y neuropeptide (NPY) and Agouti protein, as an antagonist of melanocortin receptor, are excreted in a different type of neurons of the arcuate nucleus, inducing orexin A and B secretion in the lateral nucleus of the hypothalamus, which increases pre-meal appetite [45]. Morello et al.’s [46] studies showed that the cross-talk between orexin, the endocannabinoid system and melanocortin influences hyperphagia, thereby contributing to obesity and hepatic steatosis. Those data corroborate our observations concerning WHR, which was higher in alcohol dependent patients than in the control group (abdominal obesity). Abdominal distribution of adipose tissue in alcohol dependent patients can be explained by a higher frequency of alcohol drinking, quantity and quality of alcohol drunk, higher prevalence of cigarette smoking habit, more prevalent non-regular eating and poor quality, pro-inflammatory diet in alcohol dependent patients compared to the control group participants. Some role might be played by the associations we found between orexin-IL-6 serum concentrations and the intensity of hunger, and fat mass and the intensity of hunger (Table I and II). Additionally, researchers suggest that alcohol intake itself favours longer food intake, changes the tempo of eating and delays the onset of satiety [47, 48]. It could be evidence of the dysregulation of centres responsible for food intake by alcohol-dependent patients. Morello et al.’s [46] analyses of the biochemical aetiology of obesity in animal models showed that the relationships between orexin, POMC, and cannabinoid pathways play a significant role in food intake disturbances. The patient group may have a higher WHR value than the control group due to a higher blood cortisol concentration [49, 50]. Meanwhile, the low percentage of fat mass in patients compared to the control group could be related to the increased excretion of nutritional contents like fats.

Spearman’s correlations revealed that the number and standard drinks consumed in the 30 days preceding treatment were positively associated with POMC concentration in the serum of our patients (Table II). 

We found a positive correlation between “intensity of pre-meal hunger (VAS, 0-10)” and orexin-A
concentration and a negative link with insulin concentration or % fat mass body and BMI. However, more number alcohol craving episodes per day may be linked with higher POMC and lower IL-6 concentration in the serum of patients with alcohol dependence. And “number of alcohol craving episodes in the week” may have a negative link with WHR (Table II). Interestingly, the posi­tive correlation with POMC concentration was observed only for the daily frequency of alcohol craving episodes but not for the weekly frequency or for the intensity of alcohol craving although the analyses demonstrated a relatively strong positive correlation between the frequency and intensity of alcohol craving. This may suggest that higher POMC concentrations are more closely associated with greater exposure to alcohol craving episodes irrespective of their severity. It is worth adding that WHR and %FM were positively correlated with BMI (Table II). The explanation of these connections may be as follows: low %FM due to heavy drinking (negative link between length of alcohol dependence and %FM) in patients with alcohol dependence is connected with more “intensity pre-meal hunger”, which is a connection with higher orexin concentration. Higher POMC concentration, with a simultaneous high orexin concentration, can balance its orexigenic action [51].
Because of low POMC concentration favours high alcohol cravings [43, 52]. Whereas, Lei et al. [53] suggested that orexin signalling plays an important role in “compulsive-like alcohol drinking”. Researchers have shown that OX-1R (orexin 1 receptor) activation contributes to the increased biosynthesis of 2-arachidonoylglycerol (2-AG) in POMC neurons [46]. Therefore endocannabinoid system activation by orexin-A causes a fall in
α-melanocyte-stimulating hormone (α-MSH), which consequently leads to a search for food (in non-
obese mice the mechanism is physiological) [46]. In obesity, incorrect endocannabinoid activation by orexin-A in POMC neurons, which is induced by leptin deficit through a vicious circle, blocks POMC synthesis and leads to hyperphagia and increases in body mass [46]. This interpretation of the results corroborates those published by other authors [54]. We showed that the confusion factor of smoking cigarettes was connected with a lower level of leptin, fat mass and BMI. The previous studies showed that cigarette smoking leads to weight loss in individuals with alcohol dependence [55, 56].

Practical applications of results

Despite our study involving a small group of subjects, the results caste light on our knowledge of the mechanisms of alcohol craving and hunger regulation and motivate us to continue research that, in the future, will help to determine new tools (biochemical and questionnaires) to distinguish alcohol and pre-meal hungers as ways to minimise alcohol craving in therapy and reduce the risk of alcohol drinking relapse. A substantial body of scientific evidence already exists on the use of agonists for neuronal POMC receptors in the treatment of obesity and addiction [2, 4, 14, 57, 58]. Future research should consider the marking of both orexin (A and B) and ghrelin (acylated and deacylated) fractions [59-62].

Limitations of the study

The main limitation of the study was the small sample size. Therefore this study should be treated as preliminary, requiring continuation on a larger and more homogenous group in relation to clinical factors, especially the length of the abstinence period and the quantity of alcohol drunk before the study. Another confounding limitation may be the lack of analyses of mood and anxiety disorders in the studied patient group; also, the statistical analysis fails to  account for multiple testing and lacks both a correction for multiple tests of signi­ficance and multivariable tests due to the low number of patients studied. The research should be considered as a preliminary or a pilot study. The study used the VAS, which may be difficult to interpret in people with mild cognitive impairment [63]. 

Another limitation may be the use of a control group that is not representative in terms of alcohol consumption intensity compared to the Polish population. However, the selection of a control group characterised by low alcohol intake was a deliberate methodological decision by the authors, aimed at maximising the ability to demonstrate the effects of alcohol on the physiology of both heavy and light drinkers.

■ Conclusions

Due to the presence of lower levels of ghrelin and higher levels of IL-6 in alcohol-dependent patients than those in the non-alcohol-dependent group (control group), it can be assumed that there is a dysregulation of appetite due to alcohol dependence. We may very cautiously propose that alcohol-dependent patients develop at least two regulating mechanisms like lower ghrelin and higher IL-6 serum concentrations. The obtained results suggest that patients with alcohol dependence exhibit dysregulation of hunger, including lower ghrelin levels and higher IL-6 concentrations. This may indicate a connection between appetite-regulating mechanisms.

The relationships between the amount of consumed standard drinks or the number of drinking days and high POMC concentration suggest the role of orexigenic and anorexigenic neuropeptides in the pathology mechanism of alcohol craving and probably drinking relapse.

Conflict of interest/Konflikt interesów

None declared./Nie występuje. 

Financial support/Finansowanie

This research was funded by Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz from the university grant for young scholars. / Badanie finansowane ze środków własnych Uniwersytetu Mikołaja Kopernika w Toruniu Collegium Medicum w Bydgoszczy.

Ethics/Etyka  

The study was approved by the Ethics Committee of Nicolaus Copernicus University in Toruń, Collegium Medicum in Bydgoszcz (No. KB243/2008). / Badanie zostało zaakceptowane przez Komisję Etyczną Uniwersytetu Mikołaja Kopernika w Toruniu, Collegium Medicum w Bydgoszczy nr KB243/2008.

The work described in this article has been carried out in accordance with the Code of Ethics of the World Medical Association (Declaration of Helsinki) on medical research involving human subjects, Uniform Requirements for manuscripts submitted to biomedical journals and the ethical principles defined in the Farmington Consensus of 1997. 

Treści przedstawione w pracy są zgodne z zasadami Deklaracji Helsińskiej odnoszącymi się do badań z udziałem ludzi, ujednoliconymi wymaganiami dla czasopism biomedycznych oraz z zasadami etycznymi określonymi w Porozumieniu z Farmington w 1997 roku.

Availability of data and materials/Dostępność danych

The data presented in this study are available on request from the corresponding author. The data are not publicly available due to ethical reasons. / Dane przedstawione w niniejszym badaniu są dostępne na żądanie u autora korespondencyjnego. Dane nie są publicznie dostępne ze względów etycznych.

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