Connective tissue morphogenesis has long been interpreted through a fibroblast-centric paradigm. However, this view harbors a fundamental spatial paradox: it requires local cells, which lack sensory organs to perceive macroscopic tissue axes, to perform global geometric planning. This study proposes the "Poisson Compression Theory (PCT)," fundamentally restructuring connective tissue morphogenesis through a strict three-tier causal hierarchy: "Boundary Conditions → Physics → Biology." This theory restores the correct causal sequence: specific boundary conditions dictate mechanical constraints ("molds"), which ignite physical generators (anomalous Poisson effect and poroelastic syneresis) to establish geometric templates, which biology ultimately stabilizes and fixes. Growth-induced tension, arising from the geometric mismatch between volumetric expansion (V∝r³) and surface area (S∝r²), provides the fundamental fuel for this system. When this expansion is confined within a closed geometric frame, striking orthogonal Poisson compression occurs within the hydrated collagen network. This compression expels interstitial fluid, collapsing porosity and forcing fibers into flattened, aligned configurations. Under different boundary conditions, this identical physical mechanism generates entirely distinct fascial architectures. A natural subtraction experiment using CT scans of congenital unilateral renal agenesis demonstrates that the parietal layer of the posterior renal fascia autonomously forms in its predicted anatomical position despite the lifelong absence of organ-dependent hoop stress (local field), supporting the mechanical origin of a system-level global field. From an evolutionary perspective, the acquisition of human-specific bipedalism (iliac flare) demands an evolutionary delay in iliac ossification (back-loading). To compensate for this structural and mechanical vulnerability, the stiffening of connective tissue is accelerated (front-loading), concentrating the mammalian-universal spinal elongation energy into a multiaxial tension field and amplifying the mid-gestational Poisson compression. The same principle persists into adulthood, redefining tissue remodeling as continuous adaptive mechanomorphogenesis driven by a sustained Poisson Compression field. This study supports the hypothesis that fascial architecture is a mechanical consequence dictated primarily by tension fields and Poisson compression, rather than exclusively by cellular traction. The novelty of this study is twofold. First, it identifies anomalous Poisson compression and poroelastic syneresis as the primary physical engines driving connective tissue flattening. Second, it specifies that the fundamental fuel igniting this physical engine is the growth-induced tension generated by the r³−r² geometric mismatch.