The female reproductive system encompasses organs and structures  responsible for reproduction and hormone regulation. Key components  include the ovaries, fallopian tubes, uterus, cervix, and vagina. The  ovaries produce eggs (ova) and release hormones such as estrogen and  progesterone, essential for menstrual cycle regulation and pregnancy  maintenance. The fallopian tubes transport eggs from the ovaries to the  uterus, where fertilization typically occurs. The uterus, or womb, is  where a fertilized egg implants and develops into a fetus during  pregnancy. The cervix is the lower part of the uterus, connecting it to  the vagina, and serves as a barrier to the uterus. The vagina is a  muscular canal that leads from the cervix to the external genitalia and  serves as the birth canal during childbirth. Together, these organs  enable the processes of ovulation, fertilization, pregnancy, childbirth,  and menstruation, contributing to female reproductive health and  fertility. 

1. Cervical Dysplasia: Abnormal changes in the cells on the cervix, often caused by human papillomavirus (HPV) infection, which can progress to cervical cancer if left untreated.
2. Endometriosis: A condition where tissue similar to the lining of the uterus grows outside the uterus, causing pelvic pain, painful periods, infertility, and sometimes bowel and bladder problems.
3. Fibroids: Noncancerous growths in the uterus that can cause heavy menstrual bleeding, pelvic pressure or pain, and frequent urination.
4. Infertility: Difficulty conceiving despite regular unprotected intercourse, which can be caused by various factors including ovulatory disorders, blocked fallopian tubes, or uterine abnormalities.
5. Menstrual Disorders: Including irregular periods, heavy menstrual bleeding (menorrhagia), and absence of menstruation (amenorrhea).
6. Ovarian Cysts: Fluid-filled sacs that form on the ovaries, which may cause pelvic pain, bloating, and irregular menstrual periods.
7. Pelvic Inflammatory Disease (PID): An infection of the female reproductive organs, often caused by sexually transmitted bacteria, leading to pelvic pain, infertility, and ectopic pregnancy.
8. Pelvic Organ Prolapse: When pelvic organs such as the uterus, bladder, or rectum slip out of place, causing pelvic pressure or bulging.
9. Polycystic Ovary Syndrome (PCOS): A hormonal disorder characterized by enlarged ovaries with multiple small cysts, leading to irregular menstrual periods, excessive hair growth, acne, and infertility.
10. Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD): Conditions characterized by emotional and physical symptoms before menstruation, such as mood swings, fatigue, and bloating.

1. Cervical Dysplasia:
   
   • Hyperinsulinemia, insulin resistance, and metabolic syndrome may indirectly impact cervical dysplasia by increasing the risk of human papillomavirus (HPV) infection, which is a major cause of cervical dysplasia. Insulin resistance-related inflammation and impaired immune function may also contribute to HPV persistence and the progression of cervical dysplasia to cervical cancer.
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1. Endometriosis:
   
   • While the direct impact of hyperinsulinemia, insulin resistance, and metabolic syndrome on endometriosis is not well-established, these metabolic disorders may exacerbate inflammation and hormonal imbalances associated with endometriosis. Insulin resistance-related factors such as obesity and dyslipidemia may also contribute to the development or progression of endometriosis.

1. Fibroids:
   
   • Hyperinsulinemia, insulin resistance, and metabolic syndrome may contribute to the development or growth of fibroids through mechanisms such as increased estrogen levels, inflammation, and altered growth factor signaling. Obesity, a common feature of metabolic syndrome, is associated with an increased risk of fibroids and may exacerbate hormonal imbalances and uterine inflammation.

1. Infertility:
   
   • Insulin resistance and hyperinsulinemia can disrupt ovarian function and hormone regulation, leading to ovulatory disorders and infertility. Metabolic syndrome-related conditions such as obesity and dyslipidemia may further impair fertility by disrupting hormone balance and promoting inflammation. Additionally, insulin resistance-related oxidative stress may affect oocyte quality and embryo implantation, compromising fertility.

1. Menstrual Disorders:
   
   • Insulin resistance, hyperinsulinemia, and metabolic syndrome may contribute to menstrual disorders by disrupting normal hormone regulation and ovarian function. Insulin resistance-related factors such as obesity and dyslipidemia may exacerbate hormonal imbalances and irregular menstrual cycles. Chronic inflammation associated with insulin resistance and metabolic syndrome may also contribute to menstrual abnormalities.

1. Ovarian Cysts:
   
   • While the direct impact of hyperinsulinemia, insulin resistance, and metabolic syndrome on ovarian cysts is not well-established, these metabolic disorders may indirectly influence cyst formation through hormonal imbalances and altered ovarian function. Insulin resistance-related factors such as obesity may exacerbate ovarian dysfunction and increase the risk of cyst formation.

1. Pelvic Inflammatory Disease (PID):
   
   • Insulin resistance, hyperinsulinemia, and metabolic syndrome may increase the risk of pelvic inflammatory disease by promoting inflammation and impairing immune function. Conditions associated with metabolic syndrome, such as obesity and diabetes, are known to increase susceptibility to infections, including sexually transmitted bacteria that can cause PID.

1. Pelvic Organ Prolapse:
   
   • Hyperinsulinemia, insulin resistance, and metabolic syndrome may indirectly impact pelvic organ prolapse by contributing to conditions such as obesity and chronic coughing, which are risk factors for pelvic floor dysfunction and prolapse. Additionally, insulin resistance-related inflammation and connective tissue abnormalities may contribute to pelvic floor weakness and prolapse.

1. Polycystic Ovary Syndrome (PCOS):
   
   • PCOS is closely associated with insulin resistance and hyperinsulinemia, which contribute to hormonal imbalances and ovarian dysfunction characteristic of the condition. Insulin resistance and hyperinsulinemia stimulate androgen production by the ovaries, leading to symptoms such as irregular menstrual cycles, ovarian cysts, and infertility. Metabolic syndrome components such as obesity and dyslipidemia further exacerbate insulin resistance and hormonal imbalances in PCOS.

1. Premenstrual Syndrome (PMS) and Premenstrual Dysphoric Disorder (PMDD):

• While the direct impact of hyperinsulinemia, insulin resistance, and metabolic syndrome on PMS and PMDD is not well-established, these metabolic disorders may exacerbate hormonal fluctuations and neurotransmitter imbalances associated with these conditions. Insulin resistance-related factors such as obesity and dyslipidemia may also contribute to mood disturbances and physical symptoms characteristic of PMS and PMDD.

 Female infertility refers to the inability of a woman to conceive or carry a pregnancy to term. While female infertility can have various causes, including anatomical, hormonal, and ovarian factors, metabolic abnormalities have been implicated in its development and progression.

Obesity and Insulin Resistance: Obesity and insulin resistance are significant risk factors for female infertility. Excess adiposity, particularly central obesity, is associated with hormonal imbalances, including elevated insulin levels and androgen excess, which can disrupt ovarian function and menstrual cycles. Insulin resistance can lead to hyperinsulinemia, which may further exacerbate ovarian dysfunction, impair follicular development, and disrupt ovulation.

Polycystic Ovary Syndrome (PCOS): PCOS is a common endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. Insulin resistance and hyperinsulinemia are central features of PCOS and contribute to ovarian dysfunction and anovulation. Elevated insulin levels stimulate androgen production by the ovaries and inhibit sex hormone-binding globulin (SHBG) production by the liver, leading to increased bioavailability of androgens. Androgen excess disrupts follicular development and ovulation, contributing to infertility in women with PCOS.

Inflammation and Oxidative Stress: Metabolic abnormalities such as obesity and insulin resistance are associated with chronic inflammation and oxidative stress, which can negatively impact ovarian function and fertility. Inflammatory cytokines and reactive oxygen species (ROS) can impair oocyte quality, disrupt follicular development, and contribute to ovarian aging. Oxidative stress may also damage ovarian tissue and reduce ovarian reserve, further compromising fertility in women with metabolic abnormalities.

Hormonal Imbalances: Metabolic factors can disrupt the hypothalamic-pituitary-gonadal (HPG) axis and alter sex hormone levels, leading to hormonal imbalances that affect ovarian function and fertility. Insulin resistance and hyperinsulinemia can disrupt gonadotropin secretion and impair follicular maturation and ovulation. Additionally, dysregulation of sex hormone levels, including elevated androgen levels and reduced estrogen levels, can disrupt menstrual cycles and impair fertility.Treatment Considerations: Management of female infertility associated with metabolic factors typically involves lifestyle modifications, including weight management, regular physical activity, and dietary changes, to improve metabolic health and optimize fertility outcomes. In some cases, medications targeting metabolic abnormalities, such as insulin sensitizers or anti-androgen medications, may be used to restore ovulatory function and improve fertility. Assisted reproductive technologies (ART), such as in vitro fertilization (IVF) or ovulation induction, may also be recommended for women with infertility refractory to conventional treatments.

In summary, metabolic factors such as obesity, insulin resistance, and hormonal imbalances play important roles in the development of female infertility. Understanding the underlying metabolic dysregulation in infertility is crucial for identifying high-risk individuals, implementing targeted interventions, and optimizing fertility outcomes for affected women.

1. McGrice  M, Porter J. The Effect of Low Carbohydrate Diets on Fertility Hormones  and Outcomes in Overweight and Obese Women: A Systematic Review.  Nutrients. 2017;9(3). doi:10.3390/nu9030204
2. Camajani, E. et al. (2023) ‘Ketogenic Diet as a Possible Non-pharmacological Therapy in  Main Endocrine Diseases of the Female Reproductive System: A Practical  Guide for Nutritionists’, Current Obesity Reports [Preprint]. Available at: https://doi.org/10.1007/s13679-023-00516-1.
3. Salcedo, A.C. et al. (2023) ‘Therapeutic Carbohydrate Restriction as a Metabolic Modality  for the Prevention and Treatment of Abnormal Uterine Bleeding’, Nutrients, 15(17), p. 3760. Available at: https://doi.org/10.3390/nu15173760.
4. Pasca, L. et al. (2023) ‘Ketonemia variability through menstrual cycle in patients undergoing classic ketogenic diet’, Frontiers in Nutrition, 10. Available at: https://www.frontiersin.org/articles/10.3389/fnut.2023.1188055.
5. Maseroli, E. et al. (2023) ‘(055) Application of a Very Low Calorie Ketogenic Diet (VLCKD)  Protocol in Women’s Endocrinology: Psychosexual Correlates of Weight  Loss’, The Journal of Sexual Medicine, 20(Supplement_2), p. qdad061.051. Available at: https://doi.org/10.1093/jsxmed/qdad061.051.
6. Hantoushzadeh, S. et al. (2023) ‘Glucose metabolism tests and recurrent pregnancy loss: evidence from a systematic review and meta-analysis’, Diabetology & Metabolic Syndrome, 15(1), p. 3. Available at: https://doi.org/10.1186/s13098-022-00973-z.
7. Cai, W.-Y. et al. (2022) ‘Insulin resistance in women with recurrent miscarriage: a systematic review and meta-analysis’, BMC Pregnancy and Childbirth, 22(1), p. 916. Available at: https://doi.org/10.1186/s12884-022-05256-z.
8. Alghamdi,  A.A. and Alotaibi, A.S. (2023) ‘High Insulin Resistance in Saudi Women  with Unexplained Recurrent Pregnancy Loss: A Case–control Study’, Saudi Journal of Medicine & Medical Sciences, 11(4), p. 314. Available at: https://doi.org/10.4103/sjmms.sjmms_82_23.
9. Grieger  JA, Grzeskowiak LE, Smithers LG, et al. Metabolic syndrome and time to  pregnancy: a retrospective study of nulliparous women. BJOG: An  International Journal of Obstetrics & Gynaecology.  2019;126(7):852-862. doi:10.1111/1471-0528.15647
10. Hilali  NG, Sak S, Incebiyik A, et al. Recurrent pregnancy loss and metabolic  syndrome. Ginekologia Polska. 2020;91(6):320-323. doi:10.5603/GP.a2020.0063 PDF
11. Shehata  H, Berry A, Riba C, Salcedo AC. Insulin Resistance and Other Risk  Factors of Cardiovascular Disease in Abnormal Uterine Bleeding. In  Review; 2021. doi:10.21203/rs.3.rs-604656/v1 (concepts expanded and discussed by Dr Salcedo in this podcast – Protecting Your NEST with Dr. Tony Hampton – Dr. Andrea Salcedo & the Metabolic/Gynecologic Connection)
12. Wang H, Zhang Y, Fang X, Kwak-Kim J, Wu L. Insulin Resistance Adversely Affect IVF Outcomes in Lean Women Without PCOS. Frontiers in Endocrinology. 2021;12. doi:10.3389/fendo.2021.734638
13. Liu  Y, Du M, Gan Y, Bao S, Feng L, Zhang J. Triglyceride Induced Metabolic  Inflammation: Potential Connection of Insulin Resistance and Recurrent  Pregnancy Loss. Front Endocrinol (Lausanne). 2021;12. doi:10.3389/fendo.2021.621845

Anemia: Iron deficiency anemia occurs when the body  doesn't have enough iron to produce hemoglobin, resulting in decreased  oxygen delivery to tissues. Symptoms may include fatigue, weakness, pale  skin, shortness of breath, dizziness, and cold hands and feet. 

Impaired Immune Function: Iron is necessary for proper  immune function, and iron deficiency can weaken the immune system,  making individuals more susceptible to infections and impairing wound  healing. 

Cognitive Impairment: Iron deficiency can affect  cognitive function, including memory, attention, and learning abilities.  In children and adolescents, iron deficiency may impair cognitive  development and academic performance. 

 Fatigue and Decreased Physical Performance: Iron deficiency can lead to fatigue and decreased physical endurance, affecting exercise tolerance and overall quality of life. 

Complications during Pregnancy: Iron deficiency during  pregnancy increases the risk of preterm birth, low birth weight, and  maternal complications such as preeclampsia. 

 Increased Menstrual Blood Loss: Hyperinsulinemia,  insulin resistance, and metabolic syndrome may exacerbate iron  deficiency in females by contributing to heavy menstrual bleeding  (menorrhagia). Insulin resistance-related factors such as obesity and  dyslipidemia can disrupt normal hormonal regulation of the menstrual  cycle, leading to irregular or heavy periods and increased blood loss. 

 Impaired Iron Absorption: Insulin resistance and  hyperinsulinemia may impair iron absorption in the intestine, leading to  reduced uptake of dietary iron. Chronic inflammation associated with  insulin resistance and metabolic syndrome can also interfere with iron  absorption and utilization. n, including memory, attention, and learning abilities.  In children and adolescents, iron deficiency may impair cognitive  development and academic performance. 

 Increased Risk of Inflammation-Induced Iron Deficiency: Metabolic syndrome-related conditions such as obesity and insulin  resistance are associated with chronic low-grade inflammation, which can  lead to functional iron deficiency. Inflammatory cytokines released  during chronic inflammation can sequester iron within cells, impairing  its availability for hemoglobin synthesis 

 Altered Iron Metabolism: Insulin resistance and  hyperinsulinemia may disrupt iron metabolism by affecting the expression  and activity of proteins involved in iron transport and storage.  Dysregulation of these processes can contribute to iron deficiency or  impaired utilization of iron stores. 

 Menstrual disorders encompass a range of abnormalities in menstrual  cycles, including irregular periods, heavy menstrual bleeding  (menorrhagia), and absence of menstruation (amenorrhea). 

 Hyperinsulinemia, insulin resistance, and metabolic syndrome may  contribute to menstrual disorders by disrupting normal hormone  regulation and ovarian function, potentially exacerbating irregularities  and symptoms. 

 Mitochondria are essential for maintaining the health and functionality of the female reproductive system, including the ovaries, fallopian tubes, uterus, and cervix. Within the cells of these reproductive organs, mitochondria provide the energy necessary for follicular development, oocyte maturation, fertilization, implantation, and pregnancy maintenance. Additionally, mitochondria regulate cellular processes critical for reproductive function, including hormone production, oxidative stress response, and embryo development.

Dysfunction in these cellular powerhouses due to poor dietary choices can lead to impaired ovarian function, irregular menstrual cycles, reduced fertility, and pregnancy complications. This dysfunction may contribute to female infertility, reproductive disorders, and pregnancy loss. Nutrient-dense foods support optimal mitochondrial function, while processed foods may compromise reproductive health.

Prioritizing a diet rich in whole foods is essential for preserving mitochondrial health and reducing the risk of reproductive system disorders in women. By nourishing the female reproductive system with essential nutrients, individuals can help maintain hormonal balance, support fertility, and reduce the risk of pregnancy complications. This underscores the critical role of dietary choices in supporting female reproductive health and overall fertility.

Throughout history, aging has been a major concern for  society. Healthcare advances and the distribution of vaccines have  contributed to the increase in life expectancy from 35 years in the 18th  century to 72.6 years today (Nakamura et al., 2017; Mansouri Torghabeh et al., 2022).  Based on numerous observations, it has been hypothesized that the poor  quality of reproductive cells can result in accelerated aging and a  shorter healthspan (Loose et al., 2022).  The state of the reproductive system is not only essential for  fertility, but also for overall health. Reproductive aging is a  universal developmental process conserved across species coinciding with  age-related fertility depletion and decline of gamete quality,  culminating in infertility and deleterious consequences on the offspring  (Drori and Folman, 1976; Drewry et al., 2011; Archie et al., 2014; Sinha and Rae, 2014).  Reproduction is an energy-costly undertaking that profoundly impacts on  multiple individual characteristics at molecular, cellular, and  endocrine levels (Loose et al., 2022; Secomandi et al., 2022).  Nevertheless, reproductive fitness also offers notable physiological  benefits. For instance, it is commonly discovered that women who remain  reproductively healthy until their late 30 years or even 40 years have  longer lifespans compared to younger women who give birth in their late  20 years (Murphy, 2023). Similarly, research on humans indicates that early menopause may be associated with increased mortality (Shuster et al., 2010).  Despite the presence of numerous intrinsic and extrinsic factors that  may contribute to aging traits in an organism’s germline, the intricate  cellular mechanisms underlying reproductive aging remain poorly  understood and warrant further investigation to fully comprehend the  complex interactions involved.

In recent academic  research, there is a growing emphasis on the role of mitochondria as a  central component in cellular events associated with reproductive aging  primarily due to oxidative stress (OS) caused by the progressive  accumulation of ROS, as a result of oxidative phosphorylation (OxPhos) (Gumienny et al., 1999; Terman et al., 2007; Roger et al., 2017).  Nevertheless, OS is not the sole contributing factor to  mitochondria-dependent changes in reproductive aging; energy metabolism,  mitochondrial dynamics, and the integrity of mitochondrial DNA (mtDNA)  also play significant roles (Terman et al., 2007; Noh et al., 2023).  Delayed blastocyst development and reduced quality in gametes are  associated with accumulated oxidative damage and inefficient clearance  of dysfunctional mitochondria (Shen et al., 2021; Khan et al., 2023). Importantly, there is a high probability that these issues are interconnected.

 Ovarian cysts are fluid-filled sacs that form on the ovaries. They can  cause pelvic pain, bloating, and irregular menstrual periods. 

 While the direct impact is uncertain, hyperinsulinemia, insulin  resistance, and metabolic syndrome may indirectly influence cyst  formation through hormonal imbalances and altered ovarian function,  potentially increasing the risk and severity of symptoms. 

 Pelvic organ prolapse occurs when pelvic organs such as the uterus,  bladder, or rectum slip out of place, causing pelvic pressure or  bulging. 

 Hyperinsulinemia, insulin resistance, and metabolic syndrome may  indirectly impact pelvic organ prolapse by contributing to conditions  such as obesity and chronic coughing, which are risk factors for pelvic  floor dysfunction and prolapse. 

 Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. While the exact cause of PCOS is not fully understood, metabolic factors play a significant role in its pathogenesis.

Insulin Resistance and Hyperinsulinemia: Insulin resistance and hyperinsulinemia are central features of PCOS and contribute to its development and clinical manifestations. Insulin resistance impairs glucose uptake by cells, leading to compensatory hyperinsulinemia. Elevated insulin levels stimulate androgen production by the ovaries and inhibit sex hormone-binding globulin (SHBG) production by the liver, leading to increased bioavailability of androgens. Hyperinsulinemia further exacerbates insulin resistance, creating a vicious cycle that contributes to the pathogenesis of PCOS.

Obesity and Metabolic Syndrome: Obesity and metabolic syndrome are commonly associated with PCOS and contribute to its metabolic and reproductive abnormalities. Excess adiposity, particularly central obesity, is associated with insulin resistance and dysregulation of glucose and lipid metabolism, exacerbating the metabolic dysfunction seen in PCOS. Metabolic syndrome, characterized by a cluster of metabolic abnormalities including central obesity, dyslipidemia, hypertension, and insulin resistance, is more prevalent in women with PCOS and may contribute to its clinical manifestations.

Hormonal Imbalances: Metabolic factors such as insulin resistance and hyperinsulinemia can disrupt the hypothalamic-pituitary-gonadal (HPG) axis and alter sex hormone levels, leading to hormonal imbalances characteristic of PCOS. Elevated insulin levels stimulate ovarian theca cells to produce excess androgens, leading to hyperandrogenism and hirsutism. Insulin resistance may also disrupt follicular development and ovulation, contributing to anovulation and menstrual irregularities in women with PCOS.

Inflammation and Oxidative Stress: Metabolic abnormalities associated with PCOS, such as insulin resistance and hyperinsulinemia, are associated with chronic low-grade inflammation and oxidative stress. Inflammatory cytokines and reactive oxygen species (ROS) can impair insulin signaling, exacerbate insulin resistance, and contribute to ovarian dysfunction in PCOS. Oxidative stress may also damage ovarian tissue and reduce ovarian reserve, further compromising fertility in women with PCOS.

Treatment Considerations: Management of PCOS typically involves lifestyle modifications, including weight management, regular physical activity, and dietary changes, to improve metabolic health and reproductive outcomes. Medications targeting metabolic abnormalities, such as insulin sensitizers like metformin, may be used to improve insulin sensitivity and regulate menstrual cycles in women with PCOS. Hormonal contraceptives may also be prescribed to regulate menstrual cycles and reduce hyperandrogenism in women with PCOS.

 PCOS, or polycystic ovarian syndrome, affects between 5 to 10 percent of all women. 

PCOS symptoms include irregular or heavy periods, acne, facial hair, scalp hair loss, increased belly fat, and increased levels of testosterone. 

It is also strongly correlated with infertility. While conventional medicine typically views PCOS as a gynaecological issue, it is actually commonly driven by things such as diet, environmental toxins, genetics, and more.

In summary, polycystic ovary syndrome (PCOS) is closely associated with metabolic factors such as insulin resistance, hyperinsulinemia, obesity, and metabolic syndrome. Understanding the underlying metabolic dysregulation in PCOS is crucial for effective management and optimizing reproductive outcomes for women affected by this condition.

Systematic Reviews, Meta-analyses & Narrative Reviews

1. Khalid, K. et al. (2023) ‘Effects of Ketogenic Diet on Reproductive Hormones in Women With Polycystic Ovary Syndrome’, Journal of the Endocrine Society, 7(10), p. bvad112. Available at: https://doi.org/10.1210/jendso/bvad112.
2. Zhang  X, Zheng Y, Guo Y, Lai Z. The Effect of Low Carbohydrate Diet on  Polycystic Ovary Syndrome: A Meta-Analysis of Randomized Controlled  Trials. Int J Endocrinol. 2019;2019. doi:10.1155/2019/4386401 
3. Shang  Y, Zhou H, He R, Lu W. Dietary Modification for Reproductive Health in  Women With Polycystic Ovary Syndrome: A Systematic Review and  Meta-Analysis. Frontiers in Endocrinology. 2021;12:1408. doi:10.3389/fendo.2021.735954 
4. Saadati, N. et al. (2021) ‘The effect of low glycemic index diet on the reproductive and  clinical profile in women with polycystic ovarian syndrome: A systematic  review and meta-analysis’, Heliyon, 7(11), p. e08338. doi:10.1016/j.heliyon.2021.e08338
5. Frary  JMC, Bjerre KP, Glintborg D, Ravn P. The effect of dietary  carbohydrates in women with polycystic ovary syndrome: a systematic  review. Minerva Endocrinol. 2016;41(1):57-69. PMID: 24914605 ABSTRACT
6. Porchia  LM, Hernandez-Garcia SC, Gonzalez-Mejia ME, López-Bayghen E. Diets with  lower carbohydrate concentrations improve insulin sensitivity in women  with polycystic ovary syndrome: a meta-analysis. European Journal of  Obstetrics & Gynecology and Reproductive Biology. Published online  March 6, 2020. doi:10.1016/j.ejogrb.2020.03.010 ABSTRACT
7. Pateguana  NB, Janes A. The contribution of hyperinsulinemia to the  hyperandrogenism of polycystic ovary syndrome. Journal of Insulin  Resistance. 2019;4(1):3. doi:10.4102/jir.v4i1.50 
8. Douglas  CC, Gower BA, Darnell BE, Ovalle F, Oster RA, Azziz R. Role of diet in  the treatment of polycystic ovary syndrome. Fertility and Sterility.  2006;85(3):679-688. doi:10.1016/j.fertnstert.2005.08.045 

Trials/Studies

1. Mei, S. et al. (2022) ‘Mediterranean Diet Combined With a Low-Carbohydrate Dietary  Pattern in the Treatment of Overweight Polycystic Ovary Syndrome  Patients’, Frontiers in Nutrition, 9, p. 876620. doi:10.3389/fnut.2022.876620.
2. Pandurevic, S. et al. (2022) ‘Efficacy of very low calorie ketogenic diet in obese PCOS: a randomized controlled study’, in Endocrine Abstracts. ECE 2022, 24th European Congress of Endocrinology, Bioscientifica. doi:10.1530/endoabs.81.P193.
3. Li  J, Bai W-P, Jiang B, et al. Ketogenic diet in women with polycystic  ovary syndrome and liver dysfunction who are obese: A randomized,  open-label, parallel-group, controlled pilot trial. J Obstet Gynaecol Res. Published online January 18, 2021. doi:10.1111/jog.14650
4. Palafox-Gómez, C. et al. (2023) ‘Adding a ketogenic dietary intervention to IVF treatment in  patients with polycystic ovary syndrome improves implantation and  pregnancy’, Reproductive Toxicology (Elmsford, N.Y.), 119, p. 108420. Available at: https://doi.org/10.1016/j.reprotox.2023.108420.
5. Paoli  A, Mancin L, Giacona MC, Bianco A, Caprio M. Effects of a ketogenic  diet in overweight women with polycystic ovary syndrome. Journal of  Translational Medicine. 2020;18(1):104. doi:10.1186/s12967-020-02277-0
6. Magagnini, M.C. et al. (2022) ‘Does the Ketogenic Diet Improve the Quality of Ovarian Function in Obese Women?’, Nutrients, 14(19). Available at: https://doi.org/10.3390/nu14194147.
7. Pohlmeier  AM, Phy JL, Watkins P, et al. Effect of a Low Starch/Low Dairy Diet on  Fat Oxidation in Overweight and Obese Women with Polycystic Ovary  Syndrome. Appl Physiol Nutr Metab. 2014;39(11):1237-1244. doi:10.1139/apnm-2014-0073
8. Moran  LJ, Noakes M, Clifton PM, Tomlinson L, Norman RJ. Dietary Composition  in Restoring Reproductive and Metabolic Physiology in Overweight Women  with Polycystic Ovary Syndrome. J Clin Endocrinol Metab.  2003;88(2):812-819. doi:10.1210/jc.2002-020815 
9. Gower  BA, Chandler-Laney PC, Ovalle F, et al. Favourable metabolic effects of  a eucaloric lower-carbohydrate diet in women with PCOS. Clin Endocrinol  (Oxf). 2013;79(4):550-557. doi:10.1111/cen.12175 
10. Yang, M. et al. (2022) ‘Metabolic effects of a ketogenic diet in overweight/obese women  with polycystic ovary syndrome with different uric acid levels: a  prospective cohort study’, Reproductive BioMedicine Online [Preprint]. doi:10.1016/j.rbmo.2022.03.023.
11. Mavropoulos  JC, Yancy WS, Hepburn J, Westman EC. The effects of a low-carbohydrate,  ketogenic diet on the polycystic ovary syndrome: a pilot study. Nutr  Metab (Lond). 2005;2:35. doi:10.1186/1743-7075-2-35 
12. Missel  AL, O’Brien AV, Maser H, et al. Impact of an Online Multicomponent Very  Low-Carbohydrate Program in Women with Polycystic Ovary Syndrome: A  Pilot Study. F&S Reports. Published online September 4, 2021. doi:10.1016/j.xfre.2021.08.008
13. Galletly  C, Moran L, Noakes M, Clifton P, Tomlinson L, Norman R. Psychological  benefits of a high-protein, low-carbohydrate diet in obese women with  polycystic ovary syndrome—A pilot study. Appetite. 2007;49(3):590-593.  doi:10.1016/j.appet.2007.03.222 ABSTRACT 

 Summarized by Dr Michael Fox, fertility specialist at the Jacksonville Center for Reproductive Medicine  in Florida https://jcrm.org/