Inodys

INODYS FERTILITY BOOSTS FEMALE FERTILITY IN CASE OF POLYCYSTIC OVARIES SYNDROME

3x MORE pregnancies with the original combination of Myo-DCI Inositol

3x LESS miscarriages with the original combination of Myo-DCI Inositol

Inodys Fertility Stick

 

   Female fertility booster

   Improvement of menstrual cycles and ovulation quality

   Patented combination of Myo-Inositol and D-Chiro-Inositol

   Enhanced in active folic acid (Quatrefolic®), zinc, glutathione and vitamin D

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Polycystic ovary syndrome, the main cause of infertility and anovulation


Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine-metabolic disorder. As the name indicates, PCOS is a syndrome and not a disease, meaning it is a set of signs and symptoms with no known, specific aetiology and for which no single test can be used for diagnosis.
PCOS is one of the most frequent endocrine pathologies encountered in women of reproductive age and it is the principal cause of sterility and anovulation. It affects up to 10% of women of reproductive age in which hyperandrogenism, enlarged cystic ovaries, and chronic anovulation often coexist in close relation with metabolic syndrome (obesity, hypertension, dyslipidemia, and glucose metabolism alterations), which makes it a serious threat to public health.

Women with PCOS have often a higher body mass index (BMI) than the general population while a reduction in weight has been shown to improve insulin resistance and PCOS symptoms1. The long term consequences of PCOS include cardiovascular disease (CVD), type II diabetes mellitus (DM2), sleep apnoea, psychological complications and low self-esteem as well as reproductive, fertility and pregnancy complications2. PCOS itself accounts for 19 to 28% of DM2 in reproductive aged women3.

PATHOGENESIS AND AETIOLOGY

The pathophysiology of PCOS is complex (figure 1) with its aetiology remaining unclear but likely genetic, being influenced later by environmental factors such as nutrition, lifestyle or obesity. Insulin resistance (IR) and compensatory hyperinsulinemia are known to be key components of the syndrome, affecting 75% of lean PCOS affected individuals and 95% of obese individuals1,4. The degree of IR experienced by women with PCOS has also been shown to be above what would be expected given their BMI1. IR affects both hyperandrogenaemia and ovulation by acting on the pituitary and ovaries arresting follicular development and increasing androgen production5,6 Insulin further inhibits the production of hepatic sex hormone binding globulin (SHBG) at the liver contributing to the higher serum concentration of free androgens commonly seen in PCOS7. Decreasing IR through weight loss, lifestyle interventions or with insulin sensitising agents improves the clinical features of PCOS while excess weight worsens IR and symptom severity1.

CLINICAL MANIFESTATIONS

The clinical manifestations of this syndrome are polymorphous and vary according to the age and characteristics of each patient. Within this range of presentations, we can find:

  • Hyperandrogenism, one of the principal characteristics of PCOS; consist of an excess of androgens in the blood (hyperandrogenemia) and the exacerbation of its effects throughout the body.
  • Hirsutism, an excess presence of hair in androgen dependent areas, where women do not typically present hair, and is found in around 70% of patients with PCOS8.
  • Menstrual alterations, characterised by patterns of oligomenorrhea or secondary amenorrhea due to the absence of ovulation. The appearance of these symptoms usually occurs in the prepuberty period, close to the age of the first menstrual period. In 70% of patients patterns of oligomenorrhea with bleeding with intervals of more than 45 days or fewer than nine annual menstruation periods, alternated with intervals of secondary amenorrhea (absence of menstruation during, at least, 3 consecutive months)9. An absence of ovulation or dysovulation implies an alteration of fertility, present in 30-70% of patients, which entails a longer period of time to achieve pregnancy.
  • Ovary alterations. The ovaries of patients with PCOS present a specific appearance, with multiple small preantral and antral follicles localised peripherical, with an increase in stromal volume. At the histological level, there is a thickening and sclerosis of the ovarian cortex which give them their characteristic appearance.
  • Obesity, present in around 35-50% of patients with PCOS10,11, however the prevalence varies according to the population studied, which is likely related to genetic factors, lifestyle and diet. The presence of obesity itself is associated with alterations of the menstrual cycle12,13. In obese patients with PCOS, menstrual alterations are greater than in thin patients with PCOS13.
  • Hyperinsulinaemia and insulin resistance, are more common in patients with PCOS, be they obese or thin, however, insulin resistance is worsened by the presence of obesity14,15. The risk of diabetes mellitus type 2 is greater in patients with PCOS, above all in those patients with a first-degree family history of type 2 diabetes16,17. Patients with PCOS present an increased prevalence of metabolic syndrome34,35,36.
  • Further clinical symptoms are hyperprolactinaemia, endometrial hyperplasia & endometrial carcinoma, acne and alopecia.

OBSTETRIC PATHOLOGY

The risk of complications during pregnancy for these women is increased. The miscarriage rate is 20 to 40% higher than with normal women21.

Women with PCOS also present a greater risk of hypertensive disorders of pregnancy, preeclampsia, gestational diabetes, foetal macrosomia, intrauterine growth retardation, preterm birth, the need for caesarean section, and their children are at a higher risk of needing admission to neonatal intensive care units22.

Table 3. Diagnostic criteria for polycystic ovary syndrome
NIH/NICHD-1990 ESHRE/ ASRM Rotterdam 2003 AE-PCOS Society 2006
Exclusion of other disorders that cause excessive androgen secretion Exclusion of other disorders that cause excessive androgen secretion Exclusion of other disorders that cause excessive androgen secretion
Clinical hyperandrogenism and/or biochemistry Clinical hyperandrogenism and/or biochemistry Clinical hyperandrogenism and/or biochemistry
Menstrual alterations

(Both criteria are necessary)

 Oligovulation or anovulation
Ultrasound: polycystic ovaries(Two of the three criteria are necessary)		 Ovarian dys-function and/or Ultrasound: polycystic ovaries<br/<
(Both criteria are necessary)

Accoring to The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group Revised 2003 consensus on diagnostic criteria and long-term health risks related to poly-cystic ovary syndrome (PCOS). Hum-Reprod. 2004;19:41-7.

TREATMENT OPTIONS

Where classical treatment of infertility in PCOS patients for a long time was based on Myo-Inositol, modern treatments have the potential to improve all symptoms, signs, and laboratory anomalies of PCOS. They should be able to correct systemic insulin resistance treating the metabolic features of PCOS. Simultaneously, they will create a healthy intra-ovarian milieu, which will correct hyperandrogenism, improve menstrual regularity, and promote ovulation and fertility.
The first step in a treatment often is to lose weight, specifically for obese or overweight patients. Weight loss of 2 to 5% can improve hyperinsulinemia as well as hyperandrogenism23,24,25 which at their turn improve the metabolic level and is also related with increased rates of ovulation recovery and pregnancy26,27.
More than 50% of PCOS patients present resistance to insulin and insulinaemia which justifies the use of insulin sensitizers increasing cellular susceptibility to insulin, improving endocrine functions and restoring follicle producing cycle and ovulation. Classical insulin sensitizer is metformin which is recommended in cases of patients with glucose intolerance or type 2 diabetes and in cases of Clomiphene citrate therapy which often fails in PCOS patients.

INOSITOL AS NEW TREATMENT OPTION FOR PCOS

The Inositol isomers are a group of insulin sensitizing agents derived from vitamin B8. These substances are naturally present in the cell membranes and exist in nine isomers with Myo-Inositol (MYO) and D-Chiro-Inositol (DCI) as most frequent. Inositol is, among a lot of other functions, facilitating the metabolization of fat in the liver and contributes to a proper function of muscles and nervous system.
MYO is the most abundant inositol in the human body and naturally converts into DCI.
The role of both substances as well as single ingredients as well in combination are well investigated in relation to PCOS.

Inositol and hyperinsulinaemia

MYO and DCI act by increasing the cell’s insulin sensitivity by activating the enzymes that control glucose metabolism. In patients with PCOS and insulin resistance, a defect in tissue bioavailability or in the metabolism of inositol can favour the maintenance of this insulin resistance. Administering inositols in PCOS patients results in an increased sensitivity to insulin at the cellular level, which translates to an improvement in ovulatory function and hyperandrogenism.

The Inositols in PCOS fertility treatment

Supplementation with MYO In patients with PCOS, improves levels of prolactine (PRL), testosterone, LH and insulin. It also produces a variation of the FSH/LH quotient, improves insulin resistance and restores cycles in amenorrheic patients28. Both MYO and DCI have been shown to improve metabolic factors in women with PCOS, reducing insulin resistance, improving ovarian function, and reducing androgen levels.
Supplementation with MYO has been demonstrated to improve oocyte and embryo quality in patients treated with in vitro fertilisation (IVF). And it has achieved lower requirements of recombinant FHS and fewer canceled cycles29,30. Effective doses for MYO are as high as 4g/day as being demonstrated in various clinical trials31,32,33,34.
Supplementation with DCI in PCOS patients appears to improve levels of progesterone by 35%, increase the ovulation rate 3 times versus a placebo35, and regulate cycles in 64% of patients after six cycles of DCI36. DCI supplements reduce levels of LH by 55% and improve the FSH/ LH ratio by 44% in patients with PCOS. They also appear to reduce oxidative stress within the ovarian follicles.
In patients with diabetes mellitus type 2, the DCI/MYO ratio and the synthesis of DCI are lower due to the lesser activity of the epimerase converting MYO to DCI, except in the ovary where cells do not develop insulin resistance. As a result, there is an increase in the epimerisation of MYO into DCI. This phenomenon has been described as the “DCI paradox”37. High intraovarian concentrations of DCI seem to negatively affect oocyte quality38. Supplementation with DCI also led to a decrease in hirsutism by 12%, measured using the Ferriman-Gallwey scale.
As for the glycaemic profile, DCI decrease hyperinsulinemia by lowering levels in blood and improves resistance by 48%35. It seems to improve cell sensitivity to insulin by 71% and the glucose/insulin ratio by 43%39.
By improving cellular sensitivity to glucose, a decrease in cardiovascular risk, along with a decrease of total cholesterol by 27% against a placebo and a reduction of tryglycerides by 41%, are achieved38.
Comparing the action of MYO supplements with DCI in patients subjected to IVF, MYO supplements appear to be more effective40.

MYO – DCI combinations

According to clinical trials, combination inositol therapy (MYO and DCI) has the potential to improve all symptoms, signs, and laboratory anomalies of PCOS. Both inositols, prescribed together, should be able to improve the required inositol concentrations in both systemic circulation and the ovary, thus addressing the ovary inositol paradox. The correction of systemic insulin resistance by MYO will treat the metabolic features of PCOS. Simultaneously, adequate DCI levels will create a healthy intra-ovarian milieu, which will correct hyperandrogenism, improve menstrual regularity, and promote ovulation and fertility.
Recent studies have indeed confirmed the superiority of combined use of MYO and DCI rather than MYO alone for the treatment of PCOS41,42,43. These studies propose a very low proportion of DCI, with a ratio of 40:1, based on the proportion found in the human body.
However in an overview article of Barthi Kalra in the Indian Journal of Endocrinology44, she remarked that current evidence is still inadequate to provide a definite answer regarding the optimal MYO/DCI ratio. While MYO is necessary for metabolic management, DCI is equally important for menstrual, ovulatory, and cutaneous hyperandrogenic resolution. Therefore, the ratio may be less important than the absolute concentrations of both inositols. It is clear, therefore, that a high concentration of DCI is necessary to circumvent epimerase deficiency and ensure adequate levels in the ovary. Most actual pharmaceutical preparations provide very low amounts of DCI, which are insufficient to achieve adequate levels in the ovary. Hence, formulations with relatively higher levels of DCI are preferred. In 2019, very recently a new study was reported using a ratio of 3.6:1. However more important is the absolute concentration which is used in this trial (300 mg DCI)45.

INODYS FERTILITY, INNOVATIVE INOSITIOL COMBINATION

A Natural Comprehensive Approach for Women with Polycystic Ovary Syndrome
“INODYS FERTILITY” is a novel combination of high MYO and high DCI combination. According to experts these are the absolute concentrations of MYO and DCI which are more important than the physiological ratio. The suggested actual dosage of 40:1 is not enough to get the maximum benefit to the use of inositols for improvement of fertility in women suffering PCOS.
“INODYS FERTILITY” contains 1.100 mg MYO and 300 mg DCI, or expressed as a ratio: 3,6:1
This results in a strong increase in numbers of pregnancies in a comparative clinical trial between these ratios45:

This clearly demonstrates the superiority of the 3.6:1 ratio over the physiological 40:1 ratio, presenting the 3.6:1 ratio as most advanced treatment for PCOS infertility.

Composition of “INODYS FERTILITY”
1 stick Components
1.100 mg
300 mg		 CARONOSITOL
– Myo-inositol
– D-Chiro Inositol
20 mg Glutathione
7,5 mg Zinc
400 µg Folic acid (as Quatrefolic)
5 µg Vitamin D3

Presented in a box of 20 sticks.

OTHER COMPONENTS

QUATREFOLIC®

Quatrefolic® is the glucosamine salt of (6S)-5- methyltetrahydrofolate and is structurally analogous to the reduced and active form of folic acid so Quadefolic® completely bypasses the «damaged»

MTHFR conversion step and delivers a «finished» folate the body can immediately use without any kind of metabolization. Many studies have shown synergy between inositol and folic acid in PCOS (Raffone et al, 2010).

VITAMIN D IN PCOS

Vitamin D is most crucial in PCOS. Vitamin D acts in the body as a hormone and has receptors in about every organ. Vitamin D has been shown to play a role in egg quality, development, and overall fertility.

GLUTATHIONE

INODYS FERTILITY product contains glutathione for better efficacy. Glutathione is one of the body’s greatest antioxidants, protecting cells from attack by free radicals.

ZINC

Zinc contributes to normal fertility and reproduction. Inodys Fertlity contains zinc as bisglycinate form which shows a vastly superior bioavailability in comparaison with other forms of zinc.

LITTERATURE

  1. Lucinda C.D. Blackshaw, Irene Chlour, Nigel K. Stepto, Siew S. Lim. Barriers and Facilitators to the Implementation of Evidence-Based Lifestyle Management in Polycystic Ovary Syndrome: A Narrative Review Med. Sci. 2019, 7(7), 76;
  2. Teede, H.; Deeks, A.; Moran, L. Polycystic ovary syndrome: A complex condition with psychological, reproductive and metabolic manifestations that impacts on health across the lifespan. BMC Med. 2010, 8, 41. [Google Scholar] [CrossRef]
  3. Rodgers, R.J.; Avery, J.C.; Moore, V.M.; Davies, M.J.; Azziz, R.; Stener-Victorin, E.; Moran, L.J.; Robertson, S.A.; Stepto, N.K.; Norman, R.J.; et al. Complex diseases and co-morbidities: Polycystic ovary syndrome and type 2 diabetes mellitus. Endocr. Connect. 2019, 8, R71–R75.
  4. Legro RS, Driscoll D, Strauss III JF, Fox J, Dunaif A. Evidence tor a genetic basis for hyperandrogenemia in polycystic ovary syndrome. ProcNat Acad Sci U SA. 1998;95:14956-60.
  5. Robert L. Barbieri, Anastasia Makris, Rebecca W. Randall, Gilbert Daniels, Robert W. Kistner, Kenneth J. Ryan Insulin Stimulates Androgen Accumulation in Incubations of Ovarian Stroma Obtained from Women with Hyperandrogenism. The Journal of Clinical Endocrinology & Metabolism, Volume 62, Issue 5, 1 May 1986, Pages 904–910,
  6. Fauser BC, Tarlatzis BC, Rebar RW, Legro RS, Balen AH, Lobo R, et al. Consensus on women’s health aspects of polycystic ovary syndrome (PCOS): the Amsterdam ESHRE/ASRM-Sponsored 3rd PCOS Consensus Workshop Group. 2012 Jan;97(1):28-38.
  7. John E. Nestler, Linda P. Powers, Dennis W. Matt, Kenneth A. Steingold, Stephen R. Plymate, Roger S. Rittmaster, John N. Clore, William G. Blackard A Direct Effect of Hyperinsulinemia on Serum Sex Hormone-Binding Globulin Levels in Obese Women with the Polycystic Ovary Syndrome. The Journal of Clinical Endocrinology & Metabolism, Volume 72, Issue 1, 1 January 1991, Pages 83–89
  8. Morán C, Tapia MC, Hernández E, Vázquez G, García Hernández E. Etiological review of hirsutism in 250 patients. Arch Med Res. 1994;25:311-4.
  9. Balen AH, Conway GS, Kaltsas G, Techatsak K, Manning PJ, West C, et al. Polycystic ovary syndrome: the spectrum of the disorder in 1741 patients. Hum Reprod. 1995;10:2107-11.
  10. Kiddy DS, Sharp PS, White DM, Scanlon MF, Mason HD, Bray CS, et al. Differences in clinical and endocrine features between obese and non-obese subjects with polycystic ovary syndrome: an analysis of 263 consecutive cases. Clin Endocrinol (Oxf). 1990;32:213-20.
  11. GambineriA, Pelusi C, Vicennati V, Pagotto U,Pasquali R. Obesity and the polycysticovary syndrome. nt J ObesRelatMetabDisord.2002;26:883-96.
  12. Mitchell GW, RogersJ. The influence of weight reduction on amenorrhea in obese women. N Eng J Med. 1935;249:835-7.
  13. Hartz AJ, BarboriakPN, Wong A, Katayama KP, Rimm AA. The association of obesity with infertility and related menstrual abnormalities in women. Int J Obes. 1979;3:57-73.
  14. Moller DE, Flier JS. Insulin resistance mechanisms syndromes and implications. N Engl J Med. 1991;325:938-48.
  15. Dunaif A. Insulin resistance and the polycystic ovary syndrome: mechanism and implications for pathogenesis. Endocr Rev. 1997;18:774-800.
  16. Ehrmann DA, Barnes RB, Rosenfield RL, Cavaghan MK, Imperial J. Prevalence of impaired glucose tolerance and diabetes in women with polycystic ovarysyndrome. Diabetes Care. 1999;22(1):141-6.
  17. Ford ES, Giles WH, Mokad AH. Increasing prevalence of the metabolic syndrome among U. S. Adults. Diabetes Care. 2004;27:2444-9.
  18. Apridonidze T, EssahPa, IuornoMJ, Nestler JE. Prevalence and characteristics of the metabolic syndrome n women with polycystic ovary syndrome. J Clin Endocrinol Metab.2005;90:1929-35.
  19. Dokras A, Bochner M, Hollinrake E, Markham S, Vanvoorhis B, Jagasia DH.Screening in polycystic ovary syndrome for metabolic syndrome. Obstet Gynecol. 2005;106:131-7.
  20. J oham AE, Ranasinha S, Zoungas S, Moran L, TeedeHJ. Gestational diabetes and type 2 diabetes in reproductive-aged women with polycystic ovary syndrome. J Clin EndocrinolMetab. 2014 Mar;99(3):E447-52.
  21. Glueck CJ, Wang P, Goldenberg N, Sieve-Smith L. Pregnancy outcomes among women with polycystic ovary syndrome treated with metformin. Hum Reprod. 2002;17(11):2858-64.
  22. Qin JZ, Pang LH, Li MJ, Fan XJ, Huang RD, Chen HY.Obstetric complications in women with polycystic ovary syndrome: a systematic review and meta-analysis. ReprodBiol Endocrinol. 2013;11:56.
  23. Kiddy DS, Hamilton-Fairley D, Sepälä M, Koistinen R, James VHT, Reed MJ, et al. Diet- induced changes in sex hormone binding globulin and free testosteronein women with normal o polycystic ovaries: correlation with serum insulin and insulin like-growth factor- I. Clin Endocrinol (Oxf). 1989 Dec;31(6):757-63.
  24. Kiddy DS, Hamilton-Fairley D, Bush A, Short F, AnyaokuSJ, Reed MJ, et al. Improvement in endocrine and ovarian function during dietary treatment of obese womenwith polycystic ovary syndrome. Clin Endocrinol. 1992;36:105-11.
  25. Guzik DS, Wing R, Smith D, Berga S, Winters SJ. Endocrineconsequences of weight loss in obese, hyperandrogenic anovulatory women. FertilSteril. 1994;61:598-604.
  26. Clarck AM, Ledger W, Galletly C, Tomlison L, Blaney F, Wang X, et al. Weight loss results in significant improvement in pregnancy and ovulation rates in anovulatory obese women. Hum Reprod.1995;10:2705-12.
  27. Hollmann M, Runnebaum B, GerhardI. Effects of weight loss son the hormonal profile in obese infertile women. Hum Reprod. 1996;11:1884-91.
  28. Genazzani AD, Lanzoni C, Ricchieri F, JasonniVM. Myo-inositol administration positively affects hyperinsulinemia and hormonal parameters in overweight patients with polycystic ovary syndrome. GynecolEndocrinol. 2008 Mar;24(3):139-44.
  29. Papaleo E, Unfer V, Baillargeon JP, Fusi F, Occhi F, De Santis L. Myo-Inositol may improve oocyte quality in intracytoplasmatic sperm injection cycles. A prospective, controlled, randomized trial. FertilSteril. 2009;91:1750-4.
  30. Ciotta L, Stracquadanio I, Pagano I, Carbonaro A, Palumbo M, Gulino F. Effects of myo-inositol supplementation on oocyte’s quality in PCOS patients: a double blind trial. Eur RevMedPharma Col Sci. 2011;15:509-14.
  31. V. Unfer1, G. Carlomagno1, G. Dante & F. Facchinetti. Effects of myo-inositol in women with PCOS: a systematic review of randomized controlled trials. Gynecological Endocrinology, 2012; 1–7, Early Online
  32. Enrico Papaleo et al. Myo-inositol in patients with polycystic ovary syndrome: A novel method for ovulation induction. Gynecological Endocrinology, December 2007; 23(12): 700–703
  33. M. Bizzaril, G. Carlomagno. Inositol: history of an effective therapy for Polycystic Ovary Syndrome. Eur Rev Med Pharmacol Sci. 2014; 18: 1896-1903
  34. Pedro-Antonio Regidor1 and Adolf Eduard Schindler. Myoinositol as a Safe and Alternative Approach in the Treatment of Infertile PCOS Women: A German Observational Study. International Journal of Endocrinology Volume 2016, Article ID 9537632, 5 pages
  35. Luorno MJ, Jakubowicz DJ, Baillageon JP, Dillon P, Gunn RD, Allan G, et al. Effects of D-Chiro-Inositol in lean women with polycystic ovary syndrome. EndocrPract. 2002;8(6):417-23.
  36. Pizzo A, Laganà AS, Barbaro L. Comparison between effects of myo-inositol and d-chi-inositol on ovarian function and metabolic factors in women with PCOS. Gynecol Endocrinol. 2014;30(3):205-8.
  37. Carlomagno G, Unfer V, Roseff S. The D-chiro-inositol paradox in the ovary. FertilSteril. 2011;95:2515-6.
  38. Asplin I, Galasko G, Larner J. Chiro-inositol deficiency and insulin resistance: a comparison of the chiro- inositol and the myo-inositol-containing insulin mediators isolated from urine, hemodialysate, and muscle of control and type II diabetic subjects. Proc Natl Acad Sci U SA. 1993 Jul 1;90(13):5924-8.
  39. Genazzani AD, Santagni S, Rattighieri E, Chierchia E, Despini G, Marini G, et al. Modulatory role of D-Chiro inositol (DCI) on LH and insulin secretion in obese PCOS patient. Gynecol Endocrinol. 2014;30(6):438-43.
  40. Unfer V, Carlomagno G, Rizzo P, Raffone E, Roseff S. Myo-inositol rather than D-chiro-inositol is able to improve oocyte quality in intracytoplasmic sperm injection cycles. A prospective, controlled, randomized trial. Eur Rev Med Pharmacol Sci. 2011;15(4):452-7.
  41. Colazingari S, Treglia M, Najjar R, Bevilacqua A. The combined therapy myo-inositol plus d-chiro-inositol, rather than D-chiro-inositol, isable to improve IVF outcomes: results from a randomized controlled trial. Arch Gynecol Obstet.2013;288:1405-11.
  42. Bevilacqua A, Carlomagno G, Gerli S, Montanino Oliva M, Devroey P, Lanzone A, et al. Results from the International Consensus Conference on myo-inositol and D-chiro-inositol in Obstetrics and Gynecology–assisted reproduction technology. Gynecol Endocrinol.2015;31:441-6.
  43. Unfer V, PorcaroG. Updates on the myo-inositol plus D-chiro-inositol combined therapy in polycystic ovary syndrome. Expert Rev ClinPharmacol.2014;7(5):623-31.
  44. Bharti Kalra, Sanjay Kalra1, J. B. Sharma. The inositols and polycystic ovary syndrome. Indian Journal of Endocrinology and Metabolism / Sep-Oct 2016 / Vol 20 | Issue 5.
  45. Mendoza et al. “Comparison of the effect of a combination MYO:DCI with low DCI proportion (40:1) versus the combination with higher DCI proportion (3.6:1) on oocyte quality and pregnancy rates in women suffering Polycystic ovary syndrome (PCOS)”. Gynecol. Endocrin. 35:8, 695-700, DOI:10.1080/09513590. 2019.1576620