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The decision to have children is arguably one of the most important decisions that a couple will ever have to make. And once that decision has been made there is much responsibility and care demanded of the parents in order to ensure a healthy and happy life for a child. Nonetheless, there are many times that couples have made the decision to have children and yet their attempts are unsuccessful. This problem is commonly referred to as infertility. Infertility is broadly defined as the state or condition of being unable to sexually reproduce. It can include the complete inability to conceive a pregnancy over one year of unprotected sex or the inability to conceive a pregnancy after a previous pregnancy has already occurred. Whatever the condition may be, infertility is a problem that plagues approximately 10-20% of couples who attempt to conceive. But why is there such a large percentage of couples that experience fertility problems? The causes of infertility cover a wide range of factors that can include both physical and emotional factors from either the male or the female partner. However, the female partner contributes to approximately 40-50% of fertility problems in couples. Infertility in women can stem from any broad range of factors from improper nutrition to dysfunction of the reproductive organs.

Specifically, polycystic ovarian disease has been identified as one of the leading causes of infertility in women (Dunaif, 1). It can severely damage the normal function of the reproductive organs and is subsequently the source of many infertility cases. Therefore, there are a variety of causes, symptoms, and treatments for polycystic ovarian disease of which people should be aware.

Polycystic ovarian disease was first detected in the early 1900’s by two gynecologists, Stein and Leventhal, and was consequently known as Stein-Leventhal Syndrome. According to David H. Barlow and Ann McPherson in the text Women’s Problems in General Practice, “this syndrome was originally ascribed to patients with amenorrhoea, hirsutism, obesity, and bilateral polycystic ovaries. It is clear, however, that any form of menstrual irregularity can occur—oligomenorrhoea, or menorrhagia with regular or irregular cycles—and the term polycystic ovarian disease or syndrome is now preferred” (38). The true nature of the disease was unknown; however, recent studies have made it easier to understand the cause of the disease and its relation to infertility in women.

In order to fully understand how this disease affects fertility in women it is necessary to understand how the reproductive system normally functions. There are two hormones that are normally required for ovulation to occur, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and both are stimulated by gonadotropin-releasing hormone (GnRH) and released from the pituitary gland. LH acts on the follicular theca cells and has the ability to convert cholesterol to testosterone. FSH then acts upon the follicular granulosa cells and converts testosterone into estrogen. The production of a threshold level of estrogen consequently stimulates the release of LH from the LH “surge center” of the brain and a follicle is then released from the ovary (ovulation). The other remaining follicles on the ovary then go through atresia and regress. These hormones are essential for maintaining normal ovarian function and ovulation.

With that in mind, it is believed that polycystic ovarian disease is a typical result of abnormal hormone levels. In fact, recent studies have revealed that there have been no abnormalities discovered in the ovaries of the women suffering from this disease. Oftentimes the ovaries remain a normal size and display no anatomical abnormalities, and thus the “focus on ovarian morphology was shifted towards the hormonal characteristics of the syndrome” (Vanderbilt, 1). According to the Vanderbilt Medical Center “PCOS is an endocrinologic disorder of undetermined etiology characterized by inappropriate gonadotropin-releasing hormone (GnRH) pulse amplitude and tonically elevated levels of luteinizing hormone (LH), but not of follicle-stimulating hormone (FSH)” (2). An abnormally high level of LH causes the overproduction of androgens, specifically testosterone, and with FSH levels unchanged, the high levels of testosterone are not converted into estrogen. Furthermore, the elevated levels of LH cause the granulosa cells to undergo atrophy, and without the granulosa cells present, FSH concentrations decrease. This phenomenon was illustrated in an experiment conducted on 12 women with polycystic ovarian disease and 6 normal women (control group). By monitoring the response of pituitary gonadotropins and ovarian steroids to specific tests it was observed that “the basal concentrations of LH, androstenedione and estrone were significantly higher and the concentration of FSH significantly lower in anovulatory PCO than in the controls (p<0.05)” (Baird, 1). The atrophy of the granulosa cells and the subsequent decrease in FSH concentrations cause an increase in the amount of unbound testosterone because testosterone is not being converted to estrogen. Without estrogen the follicle cannot be ovulated, it remains on the ovary, and the follicles develop into fluid-filled cysts. This is the basic understanding behind the development of multiple cysts on the ovaries—the characteristic trait of polycystic ovarian disease.

In addition, the department of Obstetrics and Gynecology at Columbia University College performed an experiment to study the endocrine abnormalities in women suffering from polycystic ovaries. The study included 15 ovulatory women with normal-appearing ovaries (as seen on an ultrasound), 15 ovulatory women with polycystic ovaries, and 25 women diagnosed with polycystic ovarian disease. A distinction is made between the ovulatory women with polycystic ovaries and those diagnosed with polycystic ovarian disease. The women with polycystic ovaries (as seen by an ultrasound) are still displaying ovulatory patterns and have no known endocrine disturbances whereas the women diagnosed with polycystic ovarian disease are not ovulating. The studies showed that “all the PCOS women had serum concentrations of luteinizing hormone (LH), testosterone, unbound testosterone, androstenedione and dihydroepiandrosterone sulphate (DHEAS) which were significantly higher (P<0.01) than values in the normal women, regardless of ovarian morphology” (Chang, 1). These results correspond with the idea that elevated levels of LH cause an overproduction of male androgens, which subsequently cause the development of the male-like characteristics that are typical in women suffering from polycystic ovarian disease.

The development of male-like characteristics is just one typical symptom commonly associated with polycystic ovarian disease. The elevated levels of LH, the overproduction of androgens (primarily testosterone), and the presence of multiple cysts on the ovaries bring about numerous symptoms that can be quite visible or go relatively unnoticed. The major symptoms associated with polycystic ovarian disease are irregular or absent periods, the development of male-like characteristics (hirsutism and androgenic alopecia), acne, and excessive weight gain. The absence or irregularity of menstrual periods is the most common symptom among women with the disease (Dunaif, 1). Menstruation is the shedding of the inner layer of the uterus and is typically a monthly occurrence if pregnancy is not initiated. Women with polycystic ovarian disease can experience periods of heavy or persistent bleeding or the complete lack of bleeding (Polycystic, 1). These irregularities in the menstrual cycle are caused by anovulation: “without ovulation, the uterus does not receive the regular signals to properly develop and shed this lining” (Polycystic, 1). In this disease, the hormone levels are in a constant state of elevation and do not undergo the normal fluctuation patterns of surges and drop-offs that are required to maintain proper reproductive functions of ovulation and menstruation. On the other hand, another study performed by the Department of Obstetrics and Gynecology at Columbia University College revealed that 74% of hyperandrogenic women who display regular menstruations have evidence for the diagnosis of polycystic ovarian disease (Carmina, 1). This suggests that anovulation is not always present in women suffering from this disease and indicates the strong variability of symptoms in different patients. Although certain symptoms associated with polycystic ovarian disease are quite common, ultimately, symptoms of this disease differ from patient to patient.

As previously stated, a symptom commonly associated with this disease is the development of male characteristics such as excessive hair growth or hirsutism and the loss of hair (also referred to androgenic alopecia). Both symptoms are linked to the increased levels of androgens, specifically testosterone, in the circulatory system. As previously discussed, LH initiates the conversion of cholesterol to testosterone. The elevated levels of LH cause an overproduction of testosterone, and the atrophy of the granulosa cells inhibits the subsequent conversion of testosterone to estrogen. In turn, excessive testosterone causes male pattern baldness and extreme hair growth on the face, chest, and abdomen. Increased levels of testosterone can even contribute to the development of acne (Spryszak, 3). This is another instance of the strong impacts that unbalanced hormone levels can have on the body.

Excessive weight gain or obesity is not only a common symptom of polycystic ovarian disease but it can actually contribute to the disease. In fact, obesity actually intensifies the abnormal estrogen and androgen production (Spryszak, 3). The Vanderbilt Medical Center relates that “obesity contributes to chronic estrogen stimulation because there is increased peripheral conversion of androgen to estrogens in these patients” (Vanderbilt, 1). Obesity is also thought to increase the effects of hirsutism. Excessive fat distribution is associated with decreased sex hormone binding globulin (SHBG), which, causes an increase of unbound testosterone throughout the body, and therefore male patterns are observed (Vanderbilt, 1). Thus, if left untreated this disease presents a vicious cycle—obesity is a common result of the abnormal hormone levels yet this excessive weight further contributes to these abnormal levels.

The causes and symptoms of polycystic ovarian disease make it quite clear how this disease causes fertility problems in women. The elevated levels of LH and the overproduction of androgens can potentially cause chronic anovulation. If ovulation does not occur then pregnancy is not possible. Fortunately there are a variety of treatments for this disease that help reduce the affects of the symptoms and restore fertility. Common treatments for hirsutism are anti-androgen therapy, which blocks the effects of excess androgens, and oral contraceptives: “oral contraceptives are simple and relatively safe method of ovarian suppression, in addition the estrogen component increases the sex hormone binding globulin with a resultant decrease in free testosterone” (Vanderbilt, 3). Dietary changes can help to control obesity and fertility drugs are often used to control regular ovulations. A common drug used to induce ovulation is clomiphene citrate and causes 80% of the women treated to ovulate, however only 30% actually become pregnant (Spryszak, 3). Other fertility drugs are in the form of injectable hormones and provide stimulation to the ovaries in order for pregnancy to occur. Alternative methods of fertility treatments can include intrauterine insemination or in-vitro fertilization (Spryszak, 4). So, there are a variety of treatments available for women suffering from polycystic ovarian disease both to reduce the affects of the symptoms and restore fertility.

Overall, polycystic ovarian disease is one of the major causes of infertility in women that can oftentimes go unnoticed and untreated. The lack of general knowledge about polycystic ovarian disease by the patient can cause unnecessary delays in the diagnosis and treatment of this disease. Therefore, as this is a common occurrence in today’s society it is necessary that people are fully aware of the causes, symptoms, and treatments available for this disease in order to prevent further health complications and help restore fertility.


SELECTED BIBLIOGRAPHY

Baird, DT. et al. “Pituitary-Ovarian
Relationships in Polycystic Ovary Syndrome.”
Journal of Clinical Endocrinology and
Metabolism. Oct. 1977: 798-801.
Available MEDLINE Online Electronic Journals
http://www.ncbi.nlm.nih.gov/

Carmina, E. “Do Hyperandrogenic Women With
Normal Menses Have Polycystic
Ovary Syndrome?” Fertility and Sterility
Feb. 1999: 319-322. Available
MEDLINE Online Electronic Journals
http://www.ncbi.nlm.nih.gov/

Chang, L. et al. “Endocrine Abnormalities in
Ovulatory Women With Polycystic Ovaries on
Ultrasound.” Human Reproduction May 1997:
905-909. Available
MEDLINE Online Electronic Journals
http://www.ncbi.nlm.nih.gov/

Dunaif, Andrea. Polycystic Ovary Syndrome.
1998: 1-5. Online. OnHealth Network
Company. 4 April 2000. Available
http://www.onhealth.com/ch1/in
depth/item/item,4717_1_1.asp.

McPherson, Ann, ed. Women’s Problems in General
Practice. New York: Oxford University
Press, 1988.

Polycystic Ovary Syndrome General Infomation. 1-
3. Online. Internet. Available
http://collmed.psu.edu

Spryszak, DeLois Cooke. Polycystic Ovarian
Syndrome: An Overview. 1-8. 4 April 2000.
Online. Internet. Available
http://infertility.about.com/health/infertility/library/weekly/aa02209.htm

Vanderbilt Medical Center Website. Polycystic
Ovary Syndrome. 1998: 1-4. Online. 4 April
2000. Available
http://www.mc.vanderbilt.edu/peds/pidl/adolesc/polycysov.htm.