Based on a conglomeration of basic science research studies a model of hypothetical mechanisms of how the fetal semi-allograft can develop into a live baby was created. One of the tenets of the model is that it is necessary to remodel some of the typically thick-walled uterine arteries found during the proliferative phase into thin-walled spiral arteries to allow nutrient exchange between mother and fetus through an autoimmune mechanism during the luteal phase. The model suggests that the rise in progesterone inhibits dopamine. One function of dopamine is to diminish cellular permeability allowing irritants to infuse into the endometrium thus evoking an inflammatory reaction. The body must suppress these cellular immune cells from attacking the fetus. Progesterone activates membrane progesterone receptors which produces immunomodulatory proteins e.g., the Progesterone Induced Blocking Factor (PIBF), which negates the killing effect of cellular immunity. One hypothesis suggested that PIBF may be secreted by malignant tumors facilitating these tumors with foreign antigens to escape immunosurveillance and thus metastasize. Progesterone receptor antagonists e.g., mifepristone, which suppresses PIBF, have successfully increased length and quality of life in patients with a large variety of end stage treatment resistant cancers. Excessive permeability of various tissues was hypothesized to be related to possible relative deficiency of dopamine. A large variety of medical conditions have been ameliorated significantly by the use of dopaminergic drugs e.g. dextroamphetamine or cabergoline. The model explains why certain conditions may get worse premenstrually e.g., pelvic pain or headaches by the added suppressive effect of progesterone on dopamine. Though possibly further research may modify this model, based on the present hypothesis, a large number of treatment refractory conditions had very successful improvement based on treating with drug releasing dopamine thus correcting tissue permeability disorders.