OTC. Right Sugarpie, sugar may not be your problem but certainly hashimotos is partly due to high testosterone? Maybe there's some good drugs for that? Insulin resistance, high testosterone, there's a whole schwack of things involved with PCOS right? Insulin resistance seems to be a biggie from the studies done and from my understanding insulin is not necessarily how much sugar you eat, it's how your body copes with processing the sugar (for every human, it's a natural part of aging-we get worse at processing it). In my opinion you don't need to have an issue with sugar it to help your body cope but I don't have PCOS. Anyway, these were the studies relating to PCOS, I'm no expert and would only suggest the links as a good read!
"PCOS affects up to 10% of American women. In PCOS, reduced insulin sensitivity leads to an increase in circulating insulin. This excess insulin triggers an increase in luteinizing hormone (LH), which signals testosterone levels to rise. The high levels of insulin, LH and testosterone are responsible for reduced fertility and miscarriage.
Obesity causes PCOS
Overweight and obese women appear five times as likely as lean women to have PCOS.
https://www.sciencedaily.com/releases/2010/06/100621143602.htm
Insulin resistance causes excess testosterone seen in PCOS
The combination of having ovaries which are responsive to insulin and high insulin levels in the blood, can result in the overproduction of testosterone.
https://www.uchospitals.edu/specialties/pcos/pcos.html
Elevated insulin causes more potent testosterone to be produced in PCOS
Insulin seems to enhance 5alpha reduction of steroids (conversion of testosterone into the more potent dihydrotestosterone) in PCOS but was not associated with the elevated cortisol production rate.
https://www.ncbi.nlm.nih.gov/pubmed/14671189
Insulin resistance in PCOS causes GnRH levels to go up
Hyperinsulinemia increases GNRH pulse activity leading to disorderly LH and FSH activity, as seen in Polycystic ovary syndrome (PCOS).
https://en.wikipedia.org/wiki/Gonadotropin-releasing_hormone
Myo-inositol restores normal ovulatory activity and fertility in women with PCOS
Myo-inositol combined with folic acid (Inofolic) 4 g a day was administered continuously for 6 months. RESULTS: Twenty-two out of the 25 (88%) patients restored at least one spontaneous menstrual cycle during treatment, of whom 18 (72%) maintained normal ovulatory activity during the follow-up period. A total of 10 singleton pregnancies (40% of patients) were obtained. Nine clinical pregnancies were assessed with fetal heart beat at ultrasound scan. Two pregnancies evolved in miscarriage. CONCLUSION: Myo-inositol is a simple and safe treatment that is capable of restoring spontaneous ovarian activity and consequently fertility in most patients with PCOS.
https://pubget.com/profile/author/Guido Marelli
4 g/day myo-inositol improves egg quality and pregnancy rate in women with failed IVF
Recently, a number of studies have shown that the presence of several compounds in the follicular fluid positively correlates with oocyte quality and maturation (i.e., myo-inositol and melatonin). In the present study, we aim to evaluate the pregnancy outcomes after the administration of myo-inositol combined with melatonin in women who failed to conceive in previous in vitro fertilization (IVF) cycles due to poor oocyte quality. Materials and methods. Forty-six women were treated with 4 g/day myo-inositol and 3 mg/day melatonin (inofolic® and inofolic® Plus) for 3 months and then underwent a new IVF cycle. Results. After treatment, the number of mature oocytes, the fertilization rate, the number of both, total and top-quality embryos transferred were statistically higher compared to the previous IVF cycle, while there was no difference in the number of retrieved oocyte. After treatment, a total of 13 pregnancies occurred, 9 of them were confirmed echographically; four evolved in miscarriage. Conclusion. The treatment with myo-inositol and melatonin improves ovarian stimulation protocols and pregnancy outcomes in infertile women with poor oocyte quality.
https://www.ncbi.nlm.nih.gov/pubmed/21463230
Inositol improved pregnancy rate and lowered cancellation rate in PCOS infertility patients:In an attempt to evaluate the role of inositol supplementation in insulin-resistant patients with polycystic ovary syndrome (PCOS), undergoing gonadotropin ovulation induction using the low-dose step-down regimen, we conducted a prospective longitudinal study comparing the stimulation characteristics of 15 patients treated with inositol, to a cohort, matched by age and body mass index (BMI), without inositol. Inositol nutritional supplementation produced very good clinical results with a significant reduction in cancellation rate (0 vs. 40%) and the consequent improvement in clinical pregnancy rate (33.3% vs. 13.3%).
Myo-inositol begins working within one week, restores ovulation, induces weight loss
Of the 92 patients randomized, 47 received 400 mcg folic acid as placebo, and 45 received myo-inositol plus folic acid (4 g myo-inositol plus 400 mcg folic acid). The ovulation frequency assessed by the ratio of luteal phase weeks to observation weeks was significantly higher in the treated group (25%) compared with the placebo (15%), and the time to first ovulation was significantly shorter [24.5 d compared with 40.5 d]. The number of patients failing to ovulate during the placebo-treatment period was higher in the placebo group, and the majority of ovulations were characterized by normal progesterone concentrations in both groups. The effect of myo-inositol on follicular maturation was rapid, because the estrogen circulating concentration increased over the first week of treatment only in the myo-inositol group. A significant increase in circulating high-density lipoprotein was observed only in the myo-inositol-treated group. Metabolic risk factor benefits of myo-inositol treatment were not observed in the morbidly obese subgroup of patients. After 14-wk myo-inositol or placebo therapy, no change in fasting glucose concentrations, fasting insulin, or insulin responses to glucose challenge was recorded. There was an inverse relationship between body mass and treatment efficacy. In fact, a significant weight loss (and leptin reduction) was recorded in the myo-inositol group, whereas the placebo group actually increased weight. These data support a beneficial effect of myo-inositol in women with oligomenorrhea and PCOS in improving ovarian function.
https://www.europeanreview.org/pdf/458.pdf
Myo-inositol lowers testosterone, FSH, LH, cholesterol, and insulin resistance
Forty-six hirsute women were enrolled and evaluated at baseline and after receiving myo-inositol therapy for 6 months. No changes in BMI were observed. The hirsutism decreased after therapy. Total testosterone, FSH and LH concentrations decreased while estrogen concentrations increased. There was a slight non-significant decrease in total cholesterol concentrations, an increase in HDL cholesterol concentrations and a decrease in LDL cholesterol concentrations. No significant changes were observed in serum triglyceride, apolipoprotein B and lipoprotein(a) concentrations. Insulin resistance, analysed by homeostasis model assessment, was reduced significantly after therapy. Administration of oral myo-inositol significantly reduced hirsutism and hyperandrogenism and ameliorated the abnormal metabolic profile of women with hirsutism.
https://www.ncbi.nlm.nih.gov/pubmed/18854115
Inositol and Insulin Resistance
High insulin associated with low inositol, regardless of PCOS or obesity
Women with or without PCOS, display increased urinary clearance of D-chiro-inositol and decreased area under the curve of D-chiro-inositol-containing inositolphosphoglycan in association with higher insulin levels but independent of adiposity. Increased clearance of inositols might reduce tissue availability of D-chiro-inositol and decrease the release of D-chiro-inositol-containing inositolphosphoglycan mediator, which could contribute to insulin resistance and compensatory hyperinsulinemia.
https://humrep.oxfordjournals.org/cgi/reprint/23/6/1439.pdf"