Our study aimed at establishing substance use and clinical correlates of opioid dependence among adolescents visiting LUTH. In our study one of the variables that was strongly associated with opioid use was alcohol abuse. The strong independent association of alcohol abuse with the outcome corroborates prior research demonstrating its role in exacerbating chronic health conditions through pathways such as metabolic disruption, immune dysregulation, and poor adherence to medical care [29]. Alcohol abuse, a prominent risk factor identified in this analysis, aligns with evidence from Zambia by matenga et al, where community-based studies have highlighted its role in driving chronic disease burdens and opioid use particularly in urban settings [30]. Local research underscores alcohol’s societal and health impacts, exacerbated by limited access to addiction treatment services and cultural norms surrounding consumption[30,31]. Regionally, similar patterns emerge across sub-Saharan Africa, where alcohol misuse intersects with socioeconomic disparities and healthcare inequities, amplifying its adverse effects [32]. For instance, Rehm et al. (2017) highlighted alcohol’s dose-dependent relationship with multi-organ toxicity in a landmark Global Burden of Disease study, further validating its systemic health impacts[33]. Globally, large-scale epidemiological studies reinforce alcohol’s systemic harms, though challenges in estimating precise effects in smaller or heterogeneous cohorts such as those in low-resource settings emphasize the need for context-specific methodological adaptations [34].

Other variables that were worth mentioning as they proved to show relationship with opioid use were systolic and diastolic blood pressure. The observed relationships between systolic and diastolic blood pressure and the studied outcome reflect a complex interplay of hemodynamic, clinical, and contextual factors, echoing findings from diverse epidemiological and clinical studies. The inverse association of systolic blood pressure (SBP) with the outcome, while seemingly counterintuitive, aligns with paradoxical patterns documented in populations with advanced cardiovascular disease or comorbidities [35]. For instance, studies in aging cohorts have proposed that lower SBP in adjusted models may signal underlying pathologies such as reduced cardiac output in heart failure or compensatory mechanisms in chronic kidney disease, rather than a true protective effect [36]. This phenomenon has been reported in sub-Saharan African settings, where undiagnosed comorbidities like HIV or tuberculosis may confound traditional hypertension risk profiles, as noted in Ugandan and South African research[37].

While the current analysis did not explicitly measure opioid use, existing literature highlights its relevance to DBP dynamics and cardiovascular risk. A Zambian study by Lorenz et al. (2022) reported elevated DBP among individuals using tramadol, a commonly misused synthetic opioid, hypothesizing that its noradrenergic effects may increase peripheral resistance [38]. Similarly, Akande-Sholabi et al. (2019) documented higher DBP in Nigerian cohorts using codeine-containing cough syrups, underscoring the need for region-specific investigations into opioid [39]. These studies align with the current findings on DBP’s role as a risk factor, suggesting that substance-specific mechanisms (e.g., opioid-induced vasoconstriction or autonomic dysregulation) may amplify cardiovascular risk in vulnerable populations.