Treatment With a Patented 3.6:1 Myo-Inositol to D-chiro-Inositol Ratio, Antioxidants, Vitamins and Minerals Food Supplement in Women With a History of Assisted Reproductive Technique (ART) Failures: A Series of Case Reports

Abstract

Infertility affects 15% of couples in reproductive age worldwide. In women in particular, infertility can be caused by various abnormalities, with polycystic ovary syndrome (PCOS) being the most common. Currently, there are many assisted reproductive techniques (ART) available to combat the burden of infertility. However, positive results are not guaranteed. The administration of inositol has been shown to increase positive reproductive outcomes in women undergoing ART. Here we present a series of clinical cases in which women with a history of infertility and previously failed ART, supplemented with a specific 3.6:1 MYO:DCI ratio, antioxidants, vitamins, and minerals for a period of 1 to 3 months before undergoing in vitro fertilization (IVF). In this series of case reports, we provide preliminary evidence that supplementation with a specific 3.6:1 MYO to DCI ratio, as well as antioxidants, vitamins, and minerals may contribute positively to female fertility in women undergoing IVF, with a history of primary or secondary infertility and previously failed ART.

Keywords: In vitro fertilization (IVF); MYO:DCI ratio; female infertility; inositol; polycystic ovary syndrome (PCOS).

Figure 1.

Four follicles visualized in the right ovary through ultrasound (Case 2).

Figure 2.

MYO to DCI epimerase conversion in the presence of insulin resistance at both the systemic and ovarian levels. In normal conditions, after insulin binds to the insulin receptor, inositol derivatives—inositol phosphoglycans—are hydrolyzed from cytoplasmic membrane, releasing MYO which induces glucose internalization via Glut-4 receptor. Meanwhile, the epimerase enzyme catalyzes the isomerization of MYO to DCI, which induces glycogen synthesis. Intracellularly, insulin resistance down-regulates insulin signaling in classic insulin target tissues leading to a systemic deficiency of DCI. As ovaries maintain the normal insulin sensitivity (deemed “ovarian paradox”), the overstimulation of the insulin receptor increases the isomerization of MYO to DCI, resulting in a pathological increase of DCI.

Figure 3.

After Ovosicare^® supplementation, the endogenous concentration of both metabolic derivatives of MYO and DCI—inositol phosphoglycans—are restored, recovering glycogen synthesis and therefore, reducing systemic hyperglycemia and hyperinsulinemia. After recovering insulin signaling, epimerase enzyme catalyzes the conversion of MYO to DCI. Once the homeostatic metabolic regulation is restored at the systemic level, the insulin receptor is no longer overstimulated and normalizes the concentration of DCI at the ovarian level.