Introduction
Male sexual victimization, despite its growing importance in victimology and criminology studies, remains one of the less addressed areas in scientific research and criminal policymaking. The historical focus of criminological literature on female victimization has led to the formation of a gender dichotomy in the analysis of sexual crimes; such that men are often perceived as powerful actors or potential perpetrators of violence, and the possibility of their sexual victimization is overlooked. This perspective, in addition to creating a theoretical gap in victimology, has led to the misinterpretation of many behavioral, psychological, and biological reactions exhibited by male victims within the criminal justice system. Consequently, reactions such as behavioral freezing, silence, delayed reporting, or impairments in recounting the incident are sometimes mistakenly interpreted as signs of consent or a lack of coercion. By focusing on the "biological contexts of male sexual victimization," this research seeks to demonstrate that sexual victimization is not merely the product of social and cultural factors; rather, biological, genetic, hormonal, physiological, and neurobiological factors also play a significant role in increasing or exacerbating male vulnerability. The main objective of the study is to identify and analyze the biological mechanisms affecting male sexual victimization and to elucidate how these mechanisms interact with high-risk environments and social structures. Furthermore, at an applied level, the research strives to explain the legal and judicial implications of these findings to achieve a more accurate understanding of the concepts of consent, coercion, involuntary reactions, and the evaluation of evidence in sexual crimes against men. The study is based on the premise that genetic characteristics, dysfunctions of the hypothalamic-pituitary-adrenal (HPA) axis, hormonal fluctuations, brain structure dysfunctions, and physiological vulnerabilities, in interaction with social and cultural contexts, can increase the probability of male sexual victimization. Therefore, the research seeks to provide a multidimensional model of male sexual victimization in which biological and environmental factors are analyzed concurrently.
Methods
The research was conducted using a mixed-methods approach, combining qualitative methods and theoretical studies to enable a multi-layered analysis of male sexual victimization. In the qualitative section, data were collected through semi-structured interviews and the Delphi technique. Participants included experts in the fields of victimology, psychiatry, psychology, neuroscience, criminal biology, and physiology, who were selected using purposive sampling. The Delphi process was conducted in three stages, involving a total of 18 experts. Additionally, interviews were conducted with some men who had lived experiences of sexual victimization; however, their data were not directly used in the final analysis due to limitations in verifying the narratives and the presence of psychological barriers. Data analysis was performed using MAXQDA software based on inductive coding. The data obtained from the interviews were categorized into conceptual categories and subcategories, and subsequently integrated with the theoretical findings. In the theoretical section, a systematic review of domestic and international scientific literature in the fields of behavioral genetics, neuroscience, psychobiology, victimology, and criminal law was conducted. The objective of this stage was to complete the conceptual framework of the study and elucidate the relationship between biological factors and male sexual victimization.
Results and Discussions
The study revealed that male sexual victimization is influenced by a complex set of biological factors categorized into four main domains: genetic, physiological, neurobiological, and hormonal. In the genetic dimension, the results demonstrated that certain gene polymorphisms, particularly the 5-HTTLPR gene and genes associated with the HPA axis such as FKBP5 and CRHR1, play a crucial role in regulating stress, emotion, and response to threat. Individuals possessing sensitive variants of these genes exhibit more severe reactions, such as fear, behavioral freezing, anxiety, or submissiveness, when confronted with stressful situations. The findings also support the "differential susceptibility" theory, meaning that some individuals are biologically more sensitive to their environment and, in high-risk situations, display greater vulnerability to victimization. In the realm of physiology, the research indicated that physical weaknesses, motor disabilities, developmental disorders, and sensory limitations can increase the likelihood of male sexual victimization. Men who have weak defensive reactions or greater dependence on others are more susceptible to abuse in power-centric relationships or environments lacking effective supervision. Furthermore, certain physical appearances and non-aggressive body language may be perceived by offenders as signs of weakness or an inability to report the crime. The findings showed that, in many cases, the primary motivation of the offender is not sexual desire, but domination, humiliation, and the exercise of power. At the neurobiological level, three key brain structures, including the amygdala, hippocampus, and prefrontal cortex, played a prominent role in increasing or decreasing vulnerability. Amygdala dysfunction can lead to deficient threat detection or the manifestation of a freezing response; a reaction that, in sexual crimes against men, might be misconstrued as implied consent. Additionally, hippocampal impairments can disrupt the victim's narrative memory, resulting in amnesia or distortion of the incident's details. Under such circumstances, inconsistencies in the narrative or inability to accurately recall the time and place should not be interpreted as deception. Moreover, dysfunction in the prefrontal cortex causes impaired decision-making, poor impulse control, and inability to respond effectively to danger. In the hormonal domain, the findings revealed that testosterone, cortisol, and oxytocin play a dual and complex role in male sexual victimization. Elevated testosterone levels can reduce sensitivity to social threats and drive individuals toward high-risk situations, whereas its reduction is associated with passivity, social anxiety, and silence in the face of victimization. Cortisol, as a biomarker of chronic stress, during prolonged activation of the HPA axis, causes structural brain changes, memory impairment, anxiety, and diminished coping capacity. Likewise, oxytocin, contrary to popular belief, is not solely the hormone of empathy and trust, but can also lead to "misplaced trust" or "trauma bonding," a condition wherein the victim develops emotional dependence on the perpetrator.
Conclusion
Male sexual victimization cannot be analyzed solely by relying on social or psychological explanations; rather, biological and neurobiological factors also play a fundamental role in shaping and exacerbating vulnerability. Genes, hormones, brain structures, and physiological characteristics, in interaction with cultural and social conditions, generate distinct patterns of threat response, silence, freezing, or an inability to defend oneself. These findings hold direct significance for the criminal justice system, as they can prevent the misinterpretation of male victims' behavior and prove effective in assessing consent, coercion, the credibility of testimony, and the analysis of evidence. The research results also underscore the necessity of training judges, law enforcement officers, and mental health professionals regarding the neurobiological reactions of victims. Ultimately, the present study demonstrates that preventive and therapeutic policies concerning male sexual victimization must be founded on an interdisciplinary approach, grounded in modern victimology, neuroscience, and criminal law, to facilitate more effective support for male victims and mitigate secondary victimization