Ultra-weak photon emissions (UPEs) including those from human have been experimented for decades. The photo-genic origin of UPE has also been attributed to the oxidative stress or free radical production that is unique to metabolically active states of biological organisms. However, there are considerable gaps in quantitative understanding of UPE. In this work, I propose an analytical framework of hypothesis for the initial objective of modeling a few superficial presentations of UPE of human, including the systematic dependency on age, the diurnal variation, and the geometric asymmetry associated with serious asymmetrical pathological conditions. The hypothesis which is currently limited to human assumes a new form of energy state, termed vivo-nergy, which resides only in metabolically active organisms that are also under neuronal control. The hypothesis projects a decrease of the vivo-nergy in human during growth beyond puberty, with the rate of decrease dictated by a critical time-scale---the age of the first opposite-sex sexual intercourse (FOSSI). The hypothesis also proposes a modification of the vivo-nergy by the phases of systematic or homeostatic physiology. The hypothesis further postulates that the deviation of the physiology-modified vivo-nergy from the pre-puberty level is deteriorated by acquired organ-specific pathological conditions. Any reduction of vivo-nergy from the pre-puberty level is hypothesized to proportionally cause oxidative stress that functions as the physical source of UPE. The resulted steady-state diffusion of the photon emitted from a photo-genic source of UPE in a human geometry simplified as a homogeneous spherical domain is modeled by photon diffusion principles incorporating an extrapolated zero-boundary condition. The age and systematic physiology combined determines the intensity of the centered physiological photo-genic source. The acquired (single) pathology sets both the intensity and the off-center position of the (single) pathological photo-genic source. When the age-related, physiology-commanded, and pathology-controlled modifications of the photo-genetic sources are implemented in the photon diffusion model, the photon fluence rate at the surface of the simplified human-representing spherical domain reveals the dependency on age, the temporal variation corresponding to systematic physiology, and the geometric asymmetry associated with significant asymmetric pathological condition as reported previously for UPE. The hypothesis, as it provides analytical conveniences for quantitative estimation of UPE patterns, may be useful to further model-based interpretation of the spatial-temporal characteristics of UPE.