Abstract
Endometriosis is a debilitating condition whose pathophysiology includes hormonal, genetic, anatomic, and immune factors. The disease’s risk factors alter the frequency and duration of retrograde menstruation, and enhance the growth of endometrial tissue. Risk factors include environment, genetics, history of pelvic infection, uterine abnormalities, family history, medical conditions that thwart the normal passage of menstrual flow, age, nullipara, and diet. Few modifiable risk factors have been identified even though strategies to manage the disease are numerous.
Introduction
Endometriosis is a chronic disorder that involves the growth of the endometrium outside the uterus and affects various areas in the body including the bowel, ovaries, fallopian tubes, and the pelvic region (Price & Thomas, 2015). The disease affects more than 6 million females in the United States alone. The misplaced tissue develops, grows, breaks down and sheds every month in a manner similar to the menstrual cycle (Juarez & Tomas, 2013). Symptoms of the disorder include infertility, pelvic pain, fatigue, dysmenorrhea, dyspareunia, dyschezia, dysuria, and gastrointestinal upsets such as diarrhea and nausea (Juarez & Tomas, 2013). The precise etiology of endometriosis remains unknown. However, scientists have developed some theories to explain its development. For example, the retrograde menstruation theory suggests that the disease results from the growth of menstrual tissue that backs up during menstruation, moves to the abdomen, and grows (Juarez & Tomas, 2013
Risk factors
There are several risk factors that predispose women and girls to the development of endometriosis. They include environment, genetics, menstrual history, family history, age, nullipara, lifestyle, and diet (Juarez & Tomas, 2013). These risk factors can be grouped into modifiable and non-modifiable factors. Modifiable risk factors include environment, lifestyle, and diet. Non-modifiable factors include genetics, family history, not having children, and menstrual history.
Environment
In the medical field, several theories have been postulated to explain the probable cause or factors that could put women at risk of developing the disease. One theory suggests that endometriosis is an environmental disease while the other suggests that it is a genetic disease (Juarez & Tomas, 2013). The major risk factors for endometriosis are environment and genetics. The theory on environment as a risk factor was developed based on the findings of a 1993 seminal study. The results of the study established a relationship between endometriosis and environmental toxins. The study found out that dioxins and polychlorinated biphenyls (PCBs) contribute to the development of the disease (Juarez & Tomas, 2013). The toxins weaken the body’s immune system rendering it unable to resist the growth of wayward endometrial tissue. These toxins are classified under substances referred to as xeno-oestrogens that mimic the function of estrogen in the body. Studies have suggested that women who are exposed to these toxins are subjected to increased risk of developing endometriosis. This risk factor is modifiable because exposure can be reduced through proper incineration of contaminated material and strict control of industrial processes that release the toxins.
Genetics
The other theory involving genetics suggests that women who posses certain genes are at risk of developing endometriosis. A large portion of current research regarding the disease is directed toward establishing the relationship between the disease and genes. One such study is the Oxford Endometriosis Gene Study (OXEGENE) (Juarez & Tomas, 2013). The main goal of the study is to isolate specific genes that predispose women to endometriosis. Endometriosis is associated with genomic changes on chromosomes 1, 2, 6, 7, 9, 10, and 12. In addition, changes in the fibronectin gene have been linked to the disease. It is impossible to modify genetics in order to protect women against endometriosis because it is very difficult to alter the process of DNA replication.
Age
Endometriosis affects women of all ages. However, it is more common among women between the ages of 25 and 40. In older women, it occurs due to prolonged exposure to menstruation. In younger women, it mainly occurs because of nullipara. This risk factor in non-modifiable.
Culture
Some studies have established that endometriosis is more common among Asian women that women from other racial or ethnic origins (Price & Thomas, 2015). This risk factor is non-modifiable.
Nullipara
Nulliparous women are at a higher risk of endometriosis than parous women. Certain studies have shown that early pregnancy lowers the risk of developing the disease because of the absence of retrograde menstruation. During pregnancy, the distension of the cervix prevents the backward movement of menses and as such, lowers the risk of endometriosis. This risk factor is non-modifiable. Studies conducted have not found any protection against endometriosis with pregnancy.
Family history
A woman belonging to a family with a history of endometriosis is more likely to develop the disease than a woman from a family without such a history. For example, a woman with a mother or sister with the disease is at a high risk of developing it. Studies have suggested that the risk of the disease is six times higher in first-degree relatives of women win endometriosis (Schrager, Falleroni, & Edgoose, 2013). This suggestion was invalidated by a study that found no relationship between family history and the incidence of endometriosis. This risk factor is non-modifiable.
Menstrual history
The risk of developing endometriosis increases depending on a woman’s menstrual history. Menstruation problems such as heavier periods, longer periods, and irregular menstrual cycles are associated with the disease (Price & Thomas, 2015). Women who start menstruating at younger ages than the average are also at risk (Schrager et al., 2013). Irregular periods increase the risk for retrograde menstruation that is associated with the initial development of endometriosis. This risk factor is non-modifiable.
Dietary factors and lifestyle
Certain studies have shown that women who eat red meat and trans fats subject themselves to high risk of endometriosis (Parazzini, Vigano, Candiani, & Fedele, 2013). In contrast, women who consume lots of fruits, vegetables, and healthy fatty acids lower the risk of developing the disease. The role of diet in the development of endometriosis is modifiable and women can lower the risk of developing endometriosis by eating healthy foods (Parazzini et al., 2013). For example, consumption of fish is a great source of omega-3 fatty acids. It is also important for women to modify their lifestyles to include physical activity. This is because diet and physical exercise affect estrogen-dependent conditions that have a great role to play in the development of endometriosis. Examples of these conditions include menstruation, menopausal symptoms, and fibroids (Parazzini et al., 2013). A study that involved 1008 women (504 healthy and 504 with endometriosis) found out that women who included beef in their daily meals were twice as likely to develop the disease. In contrast, women who included seven servings of fruits or vegetables in their daily diets lowered the risk of developing the disease by about 40% (Parazzini et al., 2013).
Use of risk factor information
Professionals can sue the information derived from the foregoing risk assessment to communicate risks to women and how they can modify certain risk factors to lower the risk of the disease’s development. In addition, they can use the information to educate women about endometriosis in order to promote good health. The information can be used to develop individualized and preventative approaches to endometriosis (Schrager et al., 2013). For example, healthcare professionals can teach women about the importance of avoiding environments that are polluted by toxins associated with the development of endometriosis. The information can also be used by to develop programs that sensitize communities about the significance of implementing preventative strategies, as well as the various measures that can be taken to avoid endometriosis. Finally, the information can be used to identify areas that need extensive research. There is little information regarding the risk factors for endometriosis because many of the studies that have been conducted gave conflicting results. Professional understanding of the pathophysiologic process of endometriosis is necessary for the development of effective diagnostic and treatment remedies for the disease (Schrager et al., 2013). The disease affects more than 6 million women in the United States. Therefore, developing effective treatment approaches is necessary.
Conclusion
Endometriosis is a debilitating condition that affects more than 6 million women in the United States. Its risk factors include age, environment, genetics, diet, family history, not having babies, menstrual history, and lifestyle. The most studied factors are environment and genetics. Scientists have not yet agreed on the main cause of endometriosis. Modifiable risk factors include environment, diet and lifestyle. Non-modifiable factors include genetics, family history, menstrual history, and not having babies. Nurses and health care professionals can use the risk assessment information to develop efficacious treatment and diagnostic approaches, and educate women regarding the various strategies that they can use to lower the risk of endometriosis.
References
Juarez, M., & Tomas, L. (2013). Endometriosis: Risk Factors, Symptoms and Management. New York, NY: Nova Science Publishers, Incorporated.
Parazzini, F., Vigano, P., Candiani, M., & Fedele, L. (2013). Diet Endometriosis Risk: A Literature Review. Reproductive Biomedicine Online, 26(4), 323-336. Web.
Price, D. L., & Thomas, V. (2015). The Pathogenesis of Endometriosis: Still Searching for Answers. Obstetrics and Gynecology Forum 25(4), 31-38.
Schrager, S., Falleroni, J., & Edgoose, J. (2013). Evaluation and Treatment of Endometriosis. American Family Physician, 87(2), 107-113.