Aug 2015|Vol 12|Is 8

Dynamic Perspectives on Polycystic Ovarian Syndrome


AKP Homoeopathic Clinical Research Centre
6, Lloyd's II Lane,
Royapettah, Chennai
Tamil Nadu- 600014
PH: 044 -28113300



         Polycystic ovarian syndrome (PCOS) is a "multifactorial" disorder suspected in patients with irregular menses and clinical signs of hyperandrogenism such as acne, seborrhoea, hirsutism, infertility and alopecia. It is considered as the most common endocrine disorder amongst reproductive-age women and emerging health crisis of young females. It affects multiple systems, and requires a comprehensive perspective on health care for effective treatment. This article focuses on the understanding of the background, pathophysiology, hormonal facets, clinical features and efficient homoeopathic management of PCOS.


      Polycystic ovarian syndrome, Anovulation, Irregular menses, Hirsutism, Insulin Resistance (IR), Infertility, Obesity, Multifactorial, Hyperandrogenism, Hormone imbalance, Diabetes mellitus, Metabolic syndrome, Testosterone, SHBG, Androgen, LH, FSH, Prolactin, TSH, Psychological features, Stress, Life style, Homoeopathy.

      Stein–Leventhal syndrome; Polycystic Ovarian disease; Hyperandrogenic Anovulation(HA)


      PCOS is a multifaceted disease caused by complex interactions between environmental factors and predisposing polygenic backgrounds. It has become one of the leading causes of oligo-ovulatory infertility among premenopausal women. Over the past 3 decades, research has launched it from relative medical obscurity to a condition increasingly recognized as common in internal medicine practices. It has significant and diverse clinical implications including Reproductive, Metabolic and Psychological features. With the complex and varied manifestations of the disorder a patient may present to any one of several providers: an internist, a family practitioner, a gynecologist, a dermatologist, an endocrinologist, a dietician etc. It is an infuriating experience for women, often multifarious for managing clinicians and is a scientific challenge for researchers.

Origin and Evolution

      It is an ancient disorder, arising from ancestral gene variants. It was first described by Valisnere in 1721 as, “Young, married peasant women, moderately obese, and infertile with two larger than normal ovaries, bumpy, shiny and whitish, just like pigeon eggs”. In 1935, American gynecologists Irving F. Stein, Sr., and Michael L. Leventhal reported a series of 7 women who presented with oligo/amenorrhoea, hirsutism, obesity, infertility, and bilateral polycystic ovaries (Stein-Leventhal syndrome). Bilateral wedge resection of the enlarged ovaries was therapeutic in normalizing the menses and fertility of the women studied. They concluded that there was a primary ovarian defect, and the disorder was known as polycystic ovarian disease (PCOD). Today, PCOD has been associated with various metabolic disorders, and is now known as polycystic ovarian syndrome (PCOS).


      The precise definition of PCOS remains unclear because of the heterogeneity of this abnormality. Polycystic Ovarian Syndrome (PCOS) is a chronic heterogeneous endocrinopathy characterized by oligo-anovulation, hyperandrogenism and polycystic ovaries. It is associated with metabolic syndrome.


      PCOS is of clinical and public health importance as it is very common, affecting up to one in five women of reproductive age. The exact prevalence is not known as the syndrome is not defined precisely and generally ill-diagnosed. Several studies have suggested a prevalence of PCOS of 5%–10% in women of reproductive age, using the diagnostic criteria of the US National Institutes of Health. Recent studies shows the prevalence of PCOS in Indian adolescents is about 9.13%


      The exact cause of PCOS is unknown, but it's thought to be related to abnormal hormone levels. The imbalance is fashioned by both insulin resistance and hyperandrogenism. The schema of aetiology and features of PCOS is elicited in the Figure.1

Figure.1. Schema of aetiology and features of PCOS

Insulin Resistance

      Insulin is a hormone produced by the pancreas to control the amount of sugar in the blood. It helps to move glucose from blood into cells, where it's broken down to produce energy. Insulin resistance means the body's tissues are resistant to the effects of insulin. The body therefore has to produce extra insulin to compensate. High levels of insulin cause the ovaries to produce too much testosterone, which interferes with the development of the follicles and prevents normal ovulation. Insulin resistance can also lead to weight gain, which can make PCOS symptoms worse, because having excess fat causes the body to produce even more insulin. Insulin resistance is a pathophysiological contributor in around 50% to 80% of women with PCOS, especially in overweight women. Conversely, lean women and women with milder PCOS appear to have less severe hyperinsulinaemia and insulin resistance. Insulin resistance contributes to metabolic features but also to reproductive features through augmenting androgen production and increasing free androgens by reducing sex hormone binding globulin (SHBG).

Hormone imbalance

      Many women with PCOS are found to have an imbalance in certain hormones. It includes
• Raised levels of Testosterone(T) – a hormone often thought of as a male hormone, although all women usually produce small amounts of it
• Raised levels of Luteinizing hormone (LH) – this stimulates ovulation, but may have an abnormal effect on the ovaries if levels are too high
• Low levels of Sex hormone-binding globulin (SHBG) – a protein in the blood, which binds to testosterone and reduces its effect
• Raised levels of Prolactin– hormone that stimulates the breast glands to produce milk in pregnancy (only in some women with PCOS)


      PCOS is a multi-factorial disease sometimes runs in families. If any relatives, such as your mother, sister or aunt, have PCOS, then the risk of developing it is often increased. This suggests there may be a genetic link to PCOS, although specific genes associated with the condition are still under research. The several genes proposed and investigated as the main and possibly PCOS-related genes include those that regulate the HPO axis and those associated with peripheral insulin resistance and its sequelae. Genetic and environmental contributors to hormonal disturbances combine with other factors, including obesity, ovarian dysfunction and hypothalamic pituitary abnormalities to contribute to the aetiology of PCOS. In this panorama of unclear aetiology and mechanisms of insulin resistance and abnormal hormonal levels further research is clearly needed.


      The primary pathophysiological defect is unknown, but important characteristics include insulin resistance, androgen excess and impaired gonadotropin dynamics. The heterogeneity of PCOS reflects the participation of multiple pathophysiological mechanisms however, how much each mechanism contributes to developing PCOS is still unknown. Figure.2
1. Hypothalamus-pituitary-ovary-adrenal axis (HPOA Axis)
2. Androgen Biosynthesis, factors related to its Production
3. The Role of Insulin

Figure.2. Pathophysiology of Polycstic Ovarian Syndrome

1. Hypothalamus-Pituitary-Ovary-Adrenal axis

      The hypothalamus and the pituitary gland are the structures that regulate the endocrine system. The sensorial and endocrine information is processed and integrated in the brain, by means of connections between the pituitary gland and hypothalamic or portal system neurons. In the pituitary anterior lobe, the portal system produces peptides that bind to specific cell membrane receptors, thus initiating hormone release (HR) or Hormone inhibition (HI). The hypothalamus stimulates the production of gonadotropins in the pituitary through pulsatile gonadotropin-release hormone (GnRH), increasing the transcription of gonadotropin genes (luteinizing hormone - LH and follicle-stimulating hormone - FSH). Hence, the frequency of pulsatile GnRH stimulus partly determines the relative proportion LH and FSH synthesis. The increased frequency of GnRH pulse favors the transcription of LH ? -subunit over FSH; conversely, decreased GnRH pulse frequency favors the transcription of FSH ?-subunit, reducing the transcription rate of LH over FSH.

2. Androgen biosynthesis and factors related to its production

      Hyperandrogenism is a well established contributor to PCOS aetiology, detected in around 60% to 80% of cases. The androgens are derived from cholesterol and in females synthesized by the ovaries, adrenal glands and in extraglandular sites like liver, muscles, skin and adipose tissue. Androgen aromatization occurs in muscle and adipose tissues, that is, testosterone and androstenedione are converted into estrogens - estrone and estradiol, whereas, in the pilosebaceous unit and skin, T is converted into dihydrotestosterone (DHT) by the enzyme 5-a-reductase 1 or 2. The pilosebaceous unit and skin represent target-structures for androgen, which explains the pathophysiology of hyperandrogenism cutaneous manifestations (hirsutism, acne, seborrhea and alopecia). 3-a-androstenediol glucuronide derives from the conversion of DHT and A, by means of 5-a-reductase. It is considered a marker of androgen biological action in the pilosebaceous unit and the skin its main production site. Androgen biosynthesis is mediated by cytochrome P-450c-17, an enzyme with 17a -hidroxylase, 17, 29-lyase and 17?-hydroxysteroid dehydrogenase activities. The androgens are aromatized to estrone by the enzyme aromatase (cytochrome p-450 aromatase).In the ovaries, the androgens are precursors of estrogens and their production is controlled by LH/FSH. Normal ovarian function is determined by a combined action of LH in the theca cells, corpus luteum and stroma, and of FSH in granulosa cells. FSH stimulates the synthesis of estrogens, inhibin, activin and follistatin in granulose cells. SHBG, IGF, inhibin, activin and follistatin release by granulose cells modulate the amount of androgens made in response to LH. Insulin and the insulin-like growth factor (IGF) enhance the action of FSH in granulosa cells. 80% of circulating T is bound to a protein produced by the liver-?-globulin (SHBG), 19% is bound to albumin, and only 1% is free and responsible for the peripheral effect of androgens. Increased levels of ?-globulin are related to higher levels of estrogens and thyroid hormones, while androgens, obesity, glucocorticoids, growth hormone and insulin inhibit its synthesis.

3. The role of insulin

      Insulin is a polypeptide secreted by ?-cells of the pancreas, and plays an important role in glucose homeostasis. The classic target tissues include liver, muscles and adipose tissue. The terms insulin sensitivity and insulin resistance (IR) refer to the action of insulin in glucose homeostasis. Biochemical abnormalities were described and it seems that the primary defect is Insulin Resistance in muscles and adipose tissue, associated with compensatory hyperinsulinemia although the ovaries remain sensitive to insulin. Furthermore, IR may be related to an intrinsic dysfunction of pancreatic ?-cells. The genetic etiology may be observed in mothers and sisters of PCOS patients, mainly because of higher frequency of the syndrome and IR. Nevertheless, the mode of inheritance remains uncertain and unknown, as well as the influence of several environmental factors, such as diet and life style. Another important characteristic in PCOS is changes in gonadotropin metabolism.

The theories proposed to explain the pathophysiology of PCOS could be divided into four categories:
A. Single defect in action and secretion of insulin, causing Insulin Resistance and hyperinsulinemia
B. Primary neuroendocrine defect, leading to increased pulse frequency and amplitude of LH
C. Defect in androgen synthesis, resulting in increased production of ovarian androgens
D. Alteration in cortisol metabolism, resulting in increased production of adrenal androgens

A. Insulin Resistance and Hyperinsulinemia

      Hyperinsulinemia is believed to be a biochemical, central and probably hereditary alteration of PCOS. Insulin may act through insulin receptors, which are distributed in the ovaries, through IGF-1 receptors or even by means of hybrid receptors that contain a combination of a and ? units of insulin and IGF-1 receptors. It increases the production of androgens in the ovaries and of IGFs in the liver. The direct effect of insulin and IGF-1 is increased 17-hydroxilase activity in the ovaries, causing an excessive production of androgens, particularly A and T and its precursor, 17-hydroxyprogesterone (17-OHP). IGF-1 inhibits the enzyme aromatase and hence prevents the conversion of T into estrogens. Indirectly, insulin seems to potentialize the action of LH in the ovaries. Another effect of hyperinsulinemia, and similar to obesity, is to decrease the hepatic production of SHBG and of IGFBP-1, thus contributing to a broader action of free testosterone (FT) and IGF-1, respectively in target-cells. Figure.3

Figure.3. Schema of Insulin Resistance

      Glucose, leptin and lipid intolerance: PCOS is a risk factor more important for glucose intolerance than race ethinicity. Leptin seems to have a direct effect in ovarian steroidogenesis due to the presence of leptin receptors in thecal and granulosa cells; moreover, granulose cells are able to synthesize leptin. Peripheral insulin resistance probably accounts for reduction in leptin and resistin concentration in the adipocytes of women with PCOS. In PCOS, total cholesterol is increased because of raised low-density lipoprotein (LDL); however, high-density lipoprotein (HDL) is decreased. Blood levels of triglycerids are elevated, as well as plasminogen activator inhibitor (PAI). The increase in PAI levels and alteration in lipid levels seem to be responsible for the increased incidence of hypertension, coronary artery disease and thrombosis in PCOS.

B. Defect in the Neuroendocrine System

      By and large, the inappropriate secretion of gonadotropins is associated to the classical PCOS. The increased secretions of gonadotropins is related to increased activity of GnRH pulse generator and to pituitary response to GnRH. LH and FSH synthesis and secretion depend on GnRH stimulus, which is characterized by fast and slow frequencies that, respectively, favor their secretion. In the PCOS, during the follicular phase, there is a disproportion of gonadotropins, that is, LH pulsatile secretion is increased and that of FSH is reduced.

C. Defect in ovarian steroid synthesis

      PCOS patients present an increase in GnRH and LH pulse frequency and, consequently, in ovarian androgen synthesis. In PCOS women, follistatin levels are elevated and activin levels are lower than in non-PCOS women. The peripheral metabolism of steroids is altered in PCOS, primarily in adipose and muscular tissues and in the pilosebaceous unit. Hence, hirsutism, acne, seborrhea and alopecia are common and reflect hyperandrogenism, which may be progressive or not. The adipose tissue is able to form T and estrone from inactive precursors, contributing to increased steroid levels. In the pilosebaceous unit, there is an increase in activity of the enzyme 5a-reductase, converting T into DHT. The activity of 5a-reductase is mediated by IGF-1 and may be intensified by hyperinsulinemia, thus aggravating hirsutism. Insulin seems to have a direct and stimulating effect in the pilosebaceous unit (hirsutism, acne, seborrhea and alopecia) and in the epidermis (acanthosis nigricans).

D. Peripheral increase in cortisol metabolism

      Increased androgen production by adrenal glands is observed in 25% of PCOS patients, probably as a result of genetic influence or secondary to abnormal secretion of ovarian androgens.

Risk Factors

      Research has shown that a number of factors may contribute to development of the syndrome like genetics, environmental factors, metabolic factors, and the in utero environment etc.
• Genetic (inherited) risk factor; a family history of someone with the condition
• High insulin levels
• Lack of physical activity
• Obesity
• Increased dietary consumption of Plastic-packaged foods.etc

Clinical Features

      Women with PCOS may present with a variety of clinical upshots including Reproductive manifestations like Menstrual irregularaties, Hirsutism, Infertility and Pregnancy complications; Metabolic implications like Insulin resistance, Obesity, Metabolic syndrome, IGT, DM2 and Potentially CVD and Psychological problems includes reduced quality of life, poor self-esteem, depression, anxiety etc.( Table.1 & Figure.4). Features of PCOS may manifest at any age, ranging from childhood (premature puberty), teenage (Hirsutism, Menstrual irregularities), early adulthood and middle life (infertility, Glucose intolerance) in later life (Diabetes Mellitus and Cardiovascular disease)

Reproductive Manifestations of PCOS

Ovarian dysfunction
      Ovarian dysfunction usually manifests as oligomenorrhoea/amenorrhoea resulting from chronic oligo-ovulation/anovulation. However, prolonged anovulation can lead to dysfunctional uterine bleeding which may mimic more regular menstrual cycles. The majority of PCOS patients have ovarian dysfunction, with 70% to 80% of women with PCOS presenting with oligomenorrhoea or amenorrhoea. Oligomenorrhoea occurs usually in adolescence, with onset later in life often associated with weight gain. Menorrhagia can occur with unopposed oestrogen and endometrial hyperplasia, further exacerbated by elevated oestrogen levels in obesity.

      It is the most common cause of anovulatory infertility. It accounts for 90% to 95% of women attending infertility clinics with anovulation. However 60% of women with PCOS are fertile, although time to conceive is often increased. Obesity independently exacerbates infertility, and induces a greater risk of miscarriage.

      The clinical and biochemical signs of androgen excess in PCOS result from increased synthesis and release of ovarian androgens. Clinical hyperandrogenism primarily includes Hirsutism, Acne & seborrhea and Male pattern alopecia.

      PCOS is a common cause of hirsutism occurring in approximately 60% of cases; however this varies with race and degree of obesity. Hirsutism is defined as the presence of excessive terminal hair in areas of the body that are androgen-dependent and usually hairless or with limited hair growth, such as the face, upper lip, chin chest, abdomen, back, areolas, thighs and arms. It refers to a male pattern of body hair (androgenic hair) and it is therefore primarily of cosmetic and psychological concern. Normally, in females after pubarche the major androgenic molecules are Dehydroepiandrosterone sulfate (DHEAS), Androstenedione, Dehydroepiandrostenedione, Testosterone, and Dihydrotestosterone (DHT), in descending order of serum concentration. Only the Testosterone and DHT can bind to the androgen receptor and promote hair follicle changes. Terminal hair should be differentiated from vellus hair. Terminal hair development requires androgen stimulation—as seen in pubarche, where androgens trigger vellus to mature into terminal hair and thus, hirsutism can be seen as the result of the interaction hyperandrogenemia and its influence in the hair follicle unit. Hirsutism can be evaluated through the “Ferriman-Gallwey Score”.

Acne and Seborrhea
      Acne affects one third of cases and is not particularly specific for PCOS. Sebaceous glands are also androgen-dependent structures, with sebocytes being highly sensitive to androgen signaling, which is exacerbated in PCOS, leading to the development of acne, oily skin and seborrhea. Androgens stimulate sebocyte proliferation—especially in the mid-back, forehead, and chin and secretion of sebum. Local bacteria further complicate the process by secreting lypolytic enzymes which break down triglycerides produced in the sebocyte.

Figure.4. Clinical Presentation of PCOS

Male pattern Hair loss (Androgenic alopecia)

      Hair is miniaturized, due to an increased telogen:anagen ratio with telogen hair being at mitotical rest and anagen hair being mitotically active—and associated to genetic susceptibility related to increased 5a -reductase activity in the hair follicle. This increased enzymatic activity would favor the local conversion of testosterone into DHT, a more powerful androgen. The balding pattern is dominated by the frontal and parietal scalp zones, leaving the occipital area with great hair density, as opposed to thinner and scarcer hair in the crown area.

Acanthosis Nigricans
      Acanthosis nigricans, a dark and hyperpigmented hyperplasia of the skin typically found at the nape of the neck, axilla, groins is a marker for insulin resistance. Many adolescents with PCOS have higher levels of insulin in their blood, excess circulating androgens leads to dark patches.

      Other features of hyperandrogenism include virilisation, which, especially if presenting with clitoromegaly and rapid onset, requires exclusion of other causes including adrenal or ovarian androgen-secreting tumours.
Metabolic Manifestations of PCOS

      It is a key magnifying factor of PCOS. It may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact, insulin possesses true gonadotrophic function and increased insulin availability at the level of ovarian tissue may favour excess androgen synthesis. Obesity, particularly the abdominal phenotype, may be partly responsible for insulin resistance and associated hyperinsulinemia in women with PCOS. Therefore, obesity-related hyperinsulinemia may play a key role in favouring hyperandrogenism in these women. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe hyperandrogenism and related clinical features than normal-weight PCOS women.

      Dyslipidaemia is common in PCOS compared to weight matched controls, with higher triglycerides and lower high density lipoprotein cholesterol. It occurs independent of body mass index, however there is a synergistic deleterious effect of obesity and insulin resistance in PCOS analogous to that seen in DM2. The causes of dyslipidaemia in PCOS are again multifactorial. Insulin resistance appears to have a pivotal role mediated in part by stimulation of lipolysis and altered expression of lipoprotein lipase and hepatic lipase.

Insulin resistance and abnormal glucose metabolism
      Insulin resistance occurs in around 50% to 80% of women with PCOS. Primarily in the more severe NIH diagnosed PCOS and in those who are overweight. Lean women and milder Rotterdam diagnosed PCOS appear to have less severe insulin resistance. It results in hyperinsulinaemia with its associated diverse and complex effects on regulating lipid metabolism, protein synthesis and modulation of androgen production. Women with PCOS are at increased risk of developing IGT and DM2 with prevalence rates of 31.3% and 7.5%, respectively. Also develop abnormal glucose metabolism at a younger age and may demonstrate a more rapid conversion from IGT to DM2

Cardiovascular disease risk
      Alongside insulin resistance, metabolic syndrome, IGT and DM2, women with PCOS also have increased novel cardiovascular risk factors (inflammation, oxidative stress and impaired fibrinolysis). Also, increased early clinical and subclinical markers of atherosclerosis seen in PCOS (endothelial dysfunction, impaired pulse wave velocity, increased carotid intima media wall thickness, presence of carotid plaque and increased coronary artery calcification) are further exacerbated by obesity

Psychological Manifestations of PCOS
      The challenges to feminine identity and body image due to obesity, acne and excess hair, as well infertility and long-term health-related concerns compromise quality of life and adversely impact on mood and psychological well-being. PCOS women are more prone to depression, anxiety, low self-esteem, negative body image, and psychosexual dysfunction. The other critical aspect of psychosocial impact in PCOS is the negative impact of mood disturbance, poor self-esteem and reduced psychological well-being on motivation and on ability to implement and sustain successful lifestyle changes that are critical in this condition. These issues all need to be explored and addressed as part of PCOS assessment and management.

Diagnostic Criteria

      PCOS has undergone multiple iterations of Diagnostic criteria. Since 1990, various bodies have laid down criteria for the diagnosis of PCOS, based on oligo or anovulation, signs of hyperandrogenism, and ovarian sonography. PCOS is assigned to ICD-9-CM code 256.4. As of 2013 the three recognized criteria for PCOS diagnosis includes, the NIH Criteria, the Rotterdam criteria and the Androgen Excess and Polycystic Ovarian Syndrome Society Criteria. The clinical presentation of these criteria are illustrated in the Table.2


      The phenotypic expression varies through time, depending on several internal (e.g. ovarian/adrenal steroidogenesis, insulin resistance) and external factors (e.g. quality and quantity of food, exercise). The new guidelines endorse the Rotterdam criteria, which is widely accepted and used for diagnosis of PCOS. It includes three factors Chronic anovulation(CA), Hyperandrogenism(H), and Polycystic Ovaries on ultrasonography(PCO). With these criteria four possible phenotypes may be distinguished. Figure.5

Figure.4. Phenotypes of PCOS

• Type A, Classic PCOS: Hyperandrogenism, Chronic Anovulation and Polycystic Ovaries.
• Type B, Ovulatory PCOS: Hyperandrogenism and Polycystic ovaries.
• Type C, Normoandrogenic PCOS: Chronic Anovulation and Polycystic ovaries.
• Type D, Non-PCO PCOS: Hyperandrogenism and Chronic Anovulation.

      The most common first type, including at least two-thirds of the patients, is classic PCOS with an anovulatory hyperandrogenic phenotype. In 90% of the patients, polycystic ovaries are present. Obesity is common, but the prevalence varies largely among populations. Diabetes, altered glucose tolerance, metabolic syndrome, and increased circulating cardiovascular risk factors are also present, but their prevalence is largely influenced by body weight. The second phenotype, ovulatory PCOS, identifies patients presenting with hyperandrogenism and polycystic ovaries but ovulatory cycles. These patients seem to present a mild form of PCOS with insulin resistance and hyperinsulinemia being less severe and with a lower prevalence of metabolic and cardiovascular risk factors than in patients with classic PCOS. In these patients, body weight is often normal or only slightly increased, and changes in body weight may move the patients from one hyperandrogenic phenotype to another. The third phenotype, normoandrogenic PCOS, is present in women with chronic anovulation and polycystic ovaries but normal androgen levels. Data on this group of patients are few and more studies are needed. The fourth type, Non-PCO Type is with clinical signs of Hyperandrogenism and Chronic anovulation.

Differential Diagnosis

      The clinical conditions reflecting the clinical signs of PCOS should be considered for differential diagnosis. The main feature of PCOS is clinical hyperandrogenism or laboratory hyperandrogenaemia. In diagnosing PCOS one must always exclude other causes of androgen excess. The common differential diagnosis and their screening tests are listed in the Table.3

Investigations and assessment in PCOS

      The diagnosis of PCOS is made principally on clinical grounds, supported by ultrasonography and by some of the biochemical investigations. The choice of investigations in PCOS depends primarily on the mode of presentation. Key investigations include testosterone, SHBG, LH, FSH and free androgen index to assess androgen status and prolactin and thyroid stimulating hormone to exclude other disorders. The pelvic ultrasound is done for ovarian morphology and endometrial thickness. An oral glucose tolerance test and lipid profiles are appropriate in all women at diagnosis. The important investigations to be done in suspected cases of PCOS is displayed in the Table.4

Modern Medical Therapies

      There are a number of different medical therapies used for managing the different symptoms of PCOS like menses, fertility, excess hair, acne, weight, psychological complaints. The treatment is often focused on individual symptoms, not the syndrome itself. These therapies may include the oral contraceptive pills, insulin sensitizing drugs, hormones therapies, Ovulation induction with drugs, Laparoscopic ovarian drilling, Electrocautery, testosterone lowering drugs, weight loss drugs, Topical anti-hair-growth medications, laser hair removal techniques, antidepressants, anti-anxiety drugs etc. Conventional treatment varies as per the symptoms and also has some side effects.

Homoeopathic Perspective of Management

      As the syndrome is multi faceted the different roles of an internist, family physician, endocrinologist, dermatologist, dietitian, gynecologist etc is successfully performed by a unique responsible homoeopathic physician. It is considered as the illness of the suffering woman but not as the disease of ovaries. A fundamental and clear understanding of underlying pathophysiology with multi-factorial evaluation improves treatment success and overall management of patients. The patient is treated as a whole by taking into contemplation all the symptoms she suffers from. If erroneously she is treated for any particular symptoms like acne or hirsutism or hair loss or irregular menses or infertility or any other symptom then her disease condition will be unending never true healing results in. When any woman presents to a physician with any one of the clinical signs of PCOS; strives to elicit and probe the condition to arrive at a right diagnosis by ruling out other similar conditions. Taking care as an entity by a holistic constitutional approach facilitates to treat optimistically. Homoeopathy acts dynamically on the medium of the sentient faculty of the nerves (Aphorism 16) and induces our own body to regulate the hormone imbalance and brings back the perfect equilibrium of health. In a PCOS woman a dynamic homeopathic remedy corrects hormonal imbalances, regularizes ovulation, restores menstrual normalcy, handles obesity, manages infertility and treats positively.

Disease Classification and Miasm

      According to Hahnemannian classification of disease, PCOS falls under dynamic chronic disease with fully developed symptoms of complex miasmatic origin. PCOS is predominantly the combination of “Psora – Sycotic miasm”. Initially when there are functional changes at the level of neuro-hormonal axis it belongs to Psora and then moves on to sycotic with the proliferation by development of cysts.

Homoeopathic Therapeutics

      As such there are no specifics in homoeopathy but some of the common remedies employed to treat a PCOS women include the following. Treating of a PCOS patient is not limited and never ends within this list of remedies. A holistic constitutional approach with indicated dynamic remedy is essential for permanent cure.

Apis Melfica - Helps in cases of ovaritis and ovarian cysts which is worse on the right side with soreness and stinging pains. Indicated in suppressed and painful menses especially in young girls who is prone to emotional outbursts. She is a woman of strumous constitution, weeping disposition, irritable, nervous with fidgety and hard to please.
Natrum Muriaticum - Indicated to nervous anaemic women with irregular menses and oily shiny skin. Irritable and depressed wants to be alone, worse by consolation. Will have excessively hot sensation, aversion to heat of sun and craving for extra salt in the diet.
Thuja occidentalis - Constitutional anti- sycotic remedy corrects retarded menstrual flow with multiple cysts in ovaries. It has the inherent ability to dissolve abnormal growth or cysts or accretions anywhere in the body. It is employed, when cystic growths are evident in the left-side ovary. Corrects hormone imbalance and regulates hair growth. Clears scaly dandruff and treats hair fall.
Pulsatilla – Re-establishes the suppressed menstrual flow and helps the young girls with irregular menses at the time of puberty. Employed in sensitive women weeps at slightest instance; better with consolation and open air.
Radium Bromatum- Effective to treat acne rosacea. Apprehensive, depressed woman; fear of being alone in the dark. Regulates delayed irregular menstruation and relieves backache
Calcarea Carb-Suited to a woman suffering from profuse prolonged menses; associated with obesity. Excessive sweating on head with extreme sensitiveness to cold. Women who are averse to work and low - spirited
Sepia-Suited to women with yellow saddle across the upper part of the cheeks and nose; a "tell tale face" of uterine ailments. Acts very efficiently to regulate the menses in indifferent anxious women. Treats hair fall.
Cimicifuga Racemosa- Acts well in nervous women with ovarian irritation, amenorrhea and great depression. Clears facial blemishes of young women.
Lilium Tigrinum- Regulates dark scanty menses and relieves pain in ovaries. Suits to all pathological conditions of uterus and ovaries. This remedy can restore fertility in cases of congestion and ante-version of uterus with bearing down sensation.
Ovininum- Has significant action in woman with ovarian cyst and acne rosacea
Fraxinus Americana-Mother tincture has beneficial action in PCOS treatment when administered along with constitutional remedy

A Case of PCOS

      A girl aged 21 years presented with irregular periods since 5 years. She complains of pimples in both cheeks with pitting scars. She has hair fall, less densed with dandruff. She has unwanted hair growth in abdomen, chin, and chest. She also has two small warts on the left side of the neck since 2 years. She was diagnosed with bilateral polycystic ovaries (Refer Plate I) 5 years back. She was under allopathic treatment for more than 4 years for acne and irregular menses and now stopped everything since last 6 months. Now her menstrual cycle was erratic once in 60 -80 days with scanty clotted flow lasts for 1- 3 days. She has severe back pain during the first day of menses. She is very talkative in nature. Always concerned about her complaints moves on to depression easily. She suffers from constipation occasionally. With a constitutional and miasmatic approach she was prescribed with Thuja 1M. She was followed with Radium Brom 200 based on her totality. In her further follow up she felt better with her generals and acne, Warts on neck disappeared. But her menses was still irregular. She was prescribed with Fraxinus Americana Q additionally. She was under regular follow up for 2 years with indicated medicines. Her menses became regular, acne and hair fall reduced. No dandruff, hair growth in chin reduced. She was advised to do Ultrasonogram. Her USG reports shows normal study (Refer Plate II). Dynamic remedies has induced regular ovulation, brought back her menses and soothed her wellbeing. A complex disorder which is hardly handled by different specialty physicians is effectively treated by a unique homoeopathic physician with a simple simlimum. An integrated approach with dynamic homeopathic remedies, good lifestyle changes along with diet and exercise can be most effective in helping a woman suffering with polycystic ovarian syndrome.

Diet Regulation and Life style Management
A woman with PCOS has to adopt some diet plans along with healthy life style changes which will assist to overcome the condition and to combat obesity and hormone imbalance. The things to include and avoid is listed in Table.5


      As PCOS is an intricate condition a multidisciplinary approach is pivotal to combat and overcome it. Our dynamic remedies arouse our own immunity which fights the syndrome as an entity dynamically and re- establishes the health and harmony. Thus in a PCOS suffering woman, a dynamic homeopathic similimum clears hormonal imbalances, regularizes natural ovulation, restores menstrual normalcy, handles obesity, manages infertility and treats as a whole positively.

Organon of Medicine, Dr.Samuel Hahnemann, B Jain Publishers
Key Notes, Dr. H.C.Allen, B Jain Publishers, 2011
Shaw’s Textbook of Gynaecology, VG Padubidri and SN Daftary
Polycystic Ovary Syndrome. Novel Insights into Causes & Therapy, Vol 40.
International journal of obesity Volume 26, Issue July 2002