Introduction: Anterior cruciate ligament (ACL) injuries are among the most common ligament injuries of the knee and often require reconstruction. The etiology of the molecular mechanisms of rupture of the anterior cruciate ligament (ACL) is poorly understood, and many external and internal factors have been associated with it, including genetics. This study aimed to investigate the association of sequence variants in the ELN and FMOD candidate genes with ACL ruptures based on the essential biological functions of these two proteoglycan-encoding genes in maintaining the structural integrity of tissues and regulating fibrillogenesis. Material and Methods: The partici-pants consisted of 229 (164 male and 65 female) individuals with a surgically diagnosed ACL rup-ture (ACLR) who qualified for ligament reconstruction and 192 (107 male and 85 female) healthy participants with no history of ACL injury (CON group). All 229 participants in the ACLR group sustained injuries through non-contact mechanisms. The chi-square tests were used for association analysis of ELN rs2071307 and FMOD rs7543148 between the anterior cruciate ligament rupture (ACLR) group and the control (CON) group. Results: It follows from the study that the tested group of athletes shows a statistically significantly more frequent AA genotype in the ELN rs2071307 gene polymorphism than the control group. However, looking at gender, one can observe that these are significantly more frequent. In the polymorphism of the FMOD rs7543148 gene, a significantly rarer TT genotype was observed in the study group compared to the control group and, similarly to the previous polymorphism, the TT genotype was significantly less frequent in the group of males com-pared to the control group. Conclusions: Genetic research in sports, especially concerning injuries connected to characteristic polymorphic variants of selected genes, is justified, particularly as regards gender-homogenous groups.

Fetal alcohol spectrum disorders (FASD) in a course of high prenatal alcohol exposure (hPAE) are among the most common causes of developmental disorders. The main reason for pharmacological treatment of FASD children is attention deficit hyperactivity disorder (ADHD), and methylphenidate (MPH) is the drug of choice. The aim of the study was to assess whether children born of hPAE with ADHD, with or without morphological FASD, differ in terms of catechol-O-methyltransferase (COMT) and dopamine receptor D2 (DRD2) gene polymorphisms, and if genetic predisposition affects response and safety of MPH treatment. The polymorphisms of COMT (rs4680) and DRD2 (rs1076560, rs1800497) were analyzed in DNA samples. A borderline significance was found for the correlation between MPH side effects and the G allele of COMT (rs4680) (p = 0.04994) in all ADHD children. No effect of COMT (rs4680) and DRD2 (rs1076560, rs1800497) polymorphisms and the treatment efficacy was observed. The analyzed DRD2 and COMT gene polymorphisms seem to play no role in MPH efficacy in ADHD children with hPAE, while low-activity COMT (Met158) variant carriers may be more intolerant to MPH. The MPH treatment is effective in ADHD independent of FASD, although the ADHD-FASD variant requires higher doses to be successful. These results may help in optimization and individualization in child psychiatry.

Prenatal alcohol exposure (PAE), which refers to alcohol consumption by pregnant women, is associated with the risk of numerous severe complications during fetal development. The State Agency for Alcohol Problem Solving reports that the incidence of fetal alcohol spectrum disorder (FASD) in Poland’s general population is over 1.7%, and the incidence of fetal alcohol syndrome (FAS) is estimated at more than 0.5%. This study aimed to evaluate the significance of alcohol exposure and focused on the pattern of alcohol intoxication exhibited by the mother during pregnancy and other environmental factors of the maternal environment contributing to the development of FASD. The study covered 554 subjects, including 251 mothers and 303 children (213 girls and 90 boys). The mother’s drinking problem was determined based on the information obtained from the case history. All children qualified for the study fulfilled the h-PAE (high alcohol exposure) criteria during their fetal life. The clinical diagnosis of FAS and pFAS (occurrence of morphological symptoms of fetal alcohol syndrome) was made using a four-digit diagnostic questionnaire validated in the Polish version of the Washington Questionnaire for the assessment of the spectrum of alcohol-related neurodevelopmental disorders or alcohol-related cognitive impairment (ARND/C). Statistical analysis of the obtained research results was developed using statistical software–STATISTICA PL, version 13.1 (StatSoft, Inc., Szczecin, Poland 2016, STATISTICA–data analysis software system, version 13.1). The most destructive drinking behaviors are compulsive intoxication (BD, binge drinking) during the first 6 weeks of pregnancy and chronic addiction throughout its duration (CHD, chronic drinking). Chronic alcohol intoxication (CHD) leads to a poorer nutritional status in mothers, which is reflected in a lower body mass index (BMI) (<18 kg/m²).

Background/Objectives: Impulsivity is a key psychological construct implicated in the onset and maintenance of behavioural addictions. Dysregulation of impulsivity is central to behavioural addictions, yet its genetic basis remains unclear. This study examined the association between the DAT1 variable number tandem repeat polymorphism and impulsivity in individuals with behavioural addictions. Methods: A total of 328 males (128 with behavioural addictions and 200 controls) completed the Barratt Impulsiveness Scale. DAT1 genotyping was performed via PCR and gel electrophoresis. Statistical analyses included chi-square tests, Mann–Whitney U-tests, and two-way ANOVA. Results: No differences in DAT1 genotype frequencies were found between groups. However, a significant interaction emerged for attentional impulsivity: individuals with behavioural addictions and the 9/9 genotype had the highest BIS-AI scores (F_{2, 322} = 5.48; p = 0.0046). Conclusions: The DAT1 9/9 genotype may increase vulnerability to attentional impulsivity, but only in the context of behavioural addictions. These findings highlight a gene–environment interaction and support the role of dopaminergic mechanisms in cognitive dysregulation. Future studies should validate these findings using longitudinal designs and neurobiological methods.

Behavioral addiction in digital environments is an increasingly relevant neurobehavioral phenomenon characterized by persistent engagement with high-frequency, algorithmically optimized reward stimuli. Although neural correlates of addictive behaviors have been widely studied, current models only partly explain how modern reinforcement environments reorganize behavior at the systems level. This review introduces Reward Instability Theory, a conceptual dynamical systems framework proposing that behavioral addiction may emerge as an attractor-like state within distorted reward landscapes shaped by high-density and high-variance reinforcement signals. The model shifts focus from static behavioral descriptions toward a systems account of motivation involving reinforcement learning, salience attribution, executive control, and environmental reward structure. We propose that digital environments may increase reinforcement density and reward variance, promoting dominant reward peaks and reducing behavioral diversity. To formalize these dynamics, we outline the Behavioral Reward Instability Index (BRII) as a heuristic systems construct integrating individual reward sensitivity, environmental reinforcement structure, and behavioral variability. The framework also situates established addiction models—including incentive sensitization, habit formation, and allostatic regulation—within a shared dynamical architecture. In addition, digital phenotyping is discussed as a potential empirical strategy for testing reward instability, while acknowledging limitations related to signal noise, ecological validity, bias, and privacy. This model is intended to explain problematic patterns characterized by reduced behavioral flexibility, persistence despite negative consequences, and functional impairment, rather than all forms of frequent digital use. Attractor-like terminology is used throughout as a conceptual heuristic to describe behavioral persistence and reduced flexibility, rather than as evidence of formally verified mathematical attractors.

Behavioral addiction in digital environments is an increasingly relevant neurobehavioral phenomenon characterized by persistent engagement with high-frequency, algorithmically optimized reward stimuli. Although neural correlates of addictive behaviors have been widely studied, current models only partly explain how modern reinforcement environments reorganize behavior at the systems level. This review introduces Reward Instability Theory, a conceptual dynamical systems framework proposing that behavioral addiction may emerge as an attractor-like state within distorted reward landscapes shaped by high-density and high-variance reinforcement signals. The model shifts focus from static behavioral descriptions toward a systems account of motivation involving reinforcement learning, salience attribution, executive control, and environmental reward structure. We propose that digital environments may increase reinforcement density and reward variance, promoting dominant reward peaks and reducing behavioral diversity. To formalize these dynamics, we outline the Behavioral Reward Instability Index (BRII) as a heuristic systems construct integrating individual reward sensitivity, environmental reinforcement structure, and behavioral variability. The framework also situates established addiction models—including incentive sensitization, habit formation, and allostatic regulation—within a shared dynamical architecture. In addition, digital phenotyping is discussed as a potential empirical strategy for testing reward instability, while acknowledging limitations related to signal noise, ecological validity, bias, and privacy.