Erectile dysfunction (ED) is among the most prevalent male sexual disorders worldwide, with an estimated 322 million affected men in 2025. Although phosphodiesterase type 5 inhibitors (PDE5is) remain the first-line pharmacological treatment, approximately 30% of patients show inadequate response or intolerable adverse effects, and tadalafil unresponsiveness at one month has been reported in 48.1% of a clinical cohort, with elevated systemic inflammatory response index (SIRI) independently associated with failure (OR = 2.420). This clinical reality indicates that the pathophysiological burden of ED cannot be fully reduced to a single NO–cGMP signaling deficit; mitochondrial bioenergetic impairment, redox imbalance, endothelial inflammation, and tissue remodeling constitute a heterogeneous pathological chain spanning molecular, cellular, tissue, and systemic levels. Existing ED assessment frameworks—centered on history, IIEF-EF/SHIM, EHS, morning testosterone, and selective specialized investigations—remain clinically pragmatic but lack an explicit integrative language that organizes multi-system information and submits itself to independent statistical testing. This paper develops a Prim-Lex Eight-Dimensional ED Assessment Framework. The framework uses the Fivefold Prim-Fire of Prim-Lex Theory as theoretical background, the Eight-Dimensional Coherence structure as the state-description layer, and the Prim-Nexus Guidance as a decision-support layer, mapping energy metabolism, vascular–redox balance, cross-scale communication, disease stage, five functional modules, spatial structure, temporal rhythm, and information integration onto observable or operationalizable ED-related variables. The paper does not claim that Prim-Lex Theory has identified the “root mechanism” of ED, nor does it propose that any eight-dimensional score should replace current guidelines. Its core contribution is threefold: (1) theory development—specifying the mapping between the eight-dimensional structure and established ED pathophysiology, together with explicit boundaries of applicability; (2) clinical evidence mapping—using PRISMA 2020 and TRIPOD-SRMA as methodological anchors to distinguish dimensions supported by reliable clinical evidence, dimensions that are mechanistically plausible but lack human ED validation, and dimensions requiring instrument development; and (3) a falsifiable validation protocol—formulating five pre-registered hypotheses, with incremental predictive value (H1) as the primary test, and specifying benchmark models, failure conditions, and reporting standards. All mathematical expressions are constrained by explicit definitions, units, directionality, missing-data rules, and evidence grading. Thresholds that have not undergone independent calibration are presented as exploratory parameters only. The anticipated contribution is not a therapeutic revolution, but an operationalizable, falsifiable, and methodologically auditable theory–measurement–validation loop for the multi-system assessment of ED.
No takes yet. Share an insight, caveat, or question.
Shen Xiaowang (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: