Vitamin D is known as the main regulator of calcium homeostasis. Recent studies have demonstrated that vitamin D3 is a potent antitumor agent that shrinks uterine fibroids in vitro and in appropriate preclinical animal studies; however, human trials are yet to be conducted in this important area of women’s health, which should be considered a high clinical research priority to verify these important preclincial observations. 1,25(OH)2D3 is the biologically active form of vitamin D3 and, in cell systems, functions through interacting with the VDR. VDR is a cell membrane as well as a nuclear transcription factor that includes growth arrest, differentiation and/or induction of apoptosis demonstrating the involvement of vitamin D signaling in the inhibition of cell growth. Vitamin D3 reduces the expression levels of cell proliferation marker PCNA; MKI67 protein expressions; antiapoptotic BCL2, BCL2L1, ESR1, PGR-A, PGR-B protein expressions; and the expression levels of cell cycle regulatory proteins (CDK1, CDK2 and CDK4) in fibroid tumors, but increases the expression of the proapoptotic Bad protein and the VDR itself. Vitamin D3 also functions as a strong antifibrotic factor as it dramatically inhibit the expression of collagen and other TGF-β3-dependent key profibrotic factors in human fibroid cells in a dose-dependent fashion. Finally, there is a paradoxical increase in MMPs in uterine fibroids. The MMP system is responsible for ECM homeostasis and a decrease in the expression of MMPs caused by 1,25 dihydroxyvitamin D3 is associate with fibroid shrinkage. We believe vitamin D and/or its nonhypercalcemic potent analogs, pending appropriate clincial trials evaluation, could be viable options for medical orally adminstered treatment of symptomatic uterine fibroids. Read more
Sandra Ishkanes is a Functional Medicine specialist. She takes a whole-body approach to healthcare, combining nutrition, lifestyle and cutting-edge medical testing.
Find out if it’s right for you.